BIOLOGICAL SCIENCE # ZOOLOGY # Genetics & Molecular Biology

Cell cycle.

 

  1. Which phase consumes the maximum time in the cell cycle?
    A. G1 phase
    B. S phase
    C. G2 phase
    D. M phase
    Answer: A
    Explanation: The G1 (Gap 1) phase is typically the longest phase in the cell cycle, involving cell growth and preparation for DNA synthesis. In mammalian cells, it lasts 8–10 hours.
  2. Synapsis of homologous chromosomes occurs during:
    A. Leptotene
    B. Zygotene
    C. Pachytene
    D. Diplotene
    Answer: B
    Explanation: Synapsis (pairing of homologous chromosomes) begins in Zygotene of Prophase I in meiosis.
  3. The “restriction point” where the cell commits to division is in:
    A. G1 phase
    B. S phase
    C. G2 phase
    D. M phase
    Answer: A
    Explanation: The G1 restriction point (in animal cells) is where cells decide to divide based on growth factors, nutrients, and DNA integrity.
  4. Which cyclin-CDK complex triggers the G2/M transition?
    A. Cyclin D-CDK4
    B. Cyclin E-CDK2
    C. Cyclin A-CDK2
    D. Cyclin B-CDK1
    Answer: D
    Explanation: Cyclin B-CDK1 (MPF) promotes entry into mitosis by phosphorylating nuclear lamins, histones, and other proteins.
  5. In mitosis, spindle fibers attach to chromosomes via:
    A. Centrioles
    B. Kinetochores
    C. Centromeres
    D. Telomeres
    Answer: B
    Explanation: Kinetochores (protein structures on centromeres) serve as attachment sites for spindle microtubules.
  6. Crossing over occurs during:
    A. Pachytene
    B. Diplotene
    C. Diakinesis
    D. Metaphase I
    Answer: A
    Explanation: Pachytene (Prophase I) involves crossing over between non-sister chromatids of homologous chromosomes.
  7. Cytokinesis in plant cells occurs via:
    A. Cleavage furrow
    B. Cell plate formation
    C. Septum formation
    D. Binary fission
    Answer: B
    Explanation: Plant cells form a cell plate (from Golgi vesicles) that develops into the cell wall during cytokinesis.
  8. The phase where DNA replication occurs is:
    A. G1
    B. S
    C. G2
    D. M
    Answer: B
    Explanation: S phase (Synthesis) is dedicated to DNA replication, resulting in duplicate chromatids.
  9. Which checkpoint verifies DNA integrity before mitosis?
    A. G1/S
    B. G2/M
    C. Spindle assembly
    D. Metaphase-anaphase
    Answer: B
    Explanation: The G2/M checkpoint ensures DNA is fully replicated and undamaged before mitosis.
  10. Meiosis II resembles mitosis because:
    A. DNA replicates before division
    B. Homologous chromosomes pair
    C. Sister chromatids separate
    D. Crossing over occurs
    Answer: C
    Explanation: In Meiosis II, sister chromatids separate (as in mitosis), but without DNA replication beforehand.
  11. The term “cell cycle” was coined by:
    A. Walther Flemming
    B. Howard & Pelc
    C. Sutton & Boveri
    D. Robert Hooke
    Answer: B
    Explanation: Howard & Pelc (1953) defined the G1, S, G2, and M phases after studying radioactive DNA in beans.
  12. Inactive cells (e.g., neurons) reside in which phase?
    A. G0
    B. G1
    C. G2
    D. S
    Answer: A
    Explanation: G0 phase is a quiescent state where metabolically active cells (e.g., liver/heart cells) exit the cycle.
  13. The stage where chromosomes align equatorially:
    A. Prophase
    B. Metaphase
    C. Anaphase
    D. Telophase
    Answer: B
    Explanation: In Metaphase, chromosomes align at the metaphase plate via spindle fibers.
  14. Which enzyme prevents telomere shortening?
    A. DNA polymerase
    B. Telomerase
    C. Ligase
    D. Helicase
    Answer: B
    Explanation: Telomerase (an RNA-dependent polymerase) adds telomeric repeats to chromosome ends to prevent shortening.
  15. Chiasmata are observed during:
    A. Leptotene
    B. Zygotene
    C. Diplotene
    D. Pachytene
    Answer: C
    Explanation: Diplotene features chiasmata—X-shaped sites where homologous chromosomes remain attached after crossing over.
  16. Cytokinesis in animal cells involves:
    A. Phragmoplast
    B. Cell plate
    C. Cleavage furrow
    D. Karyokinesis
    Answer: C
    Explanation: Cleavage furrow (formed by actin-myosin contractile ring) pinches animal cells during cytokinesis.
  17. The number of chromatids in a human cell during G2 phase is:
    A. 23
    B. 46
    C. 92
    D. 184
    Answer: C
    Explanation: After S phase, each of the 46 chromosomes duplicates into two chromatids → 92 chromatids in G2.
  18. Which protein regulates the G1/S transition?
    A. p53
    B. Rb (Retinoblastoma protein)
    C. Cyclin D
    D. Caspase
    Answer: B
    Explanation: Rb protein inhibits the G1/S transition; when phosphorylated by Cyclin D-CDK4/6, it releases E2F for S-phase entry.
  19. Spindle formation in animal cells is initiated by:
    A. Centrosomes
    B. Kinetochores
    C. Centromeres
    D. Nucleolus
    Answer: A
    Explanation: Centrosomes (containing centrioles) organize microtubules to form the mitotic spindle in animal cells.
  20. Apoptosis is controlled by:
    A. Cyclins
    B. Caspases
    C. Kinases
    D. Phosphatases
    Answer: B
    Explanation: Caspases are proteases that execute apoptosis by cleaving cellular components.
    21. Which is NOT a stage of mitosis?
    A. Interphase
    B. Prophase
    C. Anaphase
    D. Telophase
    Answer: A
    Explanation: Interphase is not part of mitosis. It occurs before mitosis and includes G1, S, and G2 phases.
  21. Meiosis produces:
    A. Two identical diploid cells
    B. Four identical haploid cells
    C. Four genetically distinct haploid cells
    D. Two genetically distinct diploid cells
    Answer: C
    Explanation: Meiosis results in four genetically diverse haploid gametes due to crossing over and independent assortment.
  22. DNA damage halts the cell cycle at:
    A. G1/S checkpoint
    B. G2/M checkpoint
    C. Both A and B
    D. Spindle checkpoint
    Answer: C
    Explanation: DNA damage activates checkpoints at both G1/S and G2/M to prevent progression until repaired.
  23. The shortest phase of mitosis is:
    A. Prophase
    B. Metaphase
    C. Anaphase
    D. Telophase
    Answer: C
    Explanation: Anaphase is the shortest, lasting only a few minutes, during which sister chromatids are rapidly pulled apart.
  24. Recombination nodules appear in:
    A. Leptotene
    B. Zygotene
    C. Pachytene
    D. Diplotene
    Answer: C
    Explanation: Recombination nodules, essential for crossing over, appear in pachytene.
  25. In meiosis, disjunction of chromosomes occurs in:
    A. Anaphase I
    B. Anaphase II
    C. Metaphase I
    D. Telophase I
    Answer: A
    Explanation: In Anaphase I, homologous chromosomes separate (disjunction), while sister chromatids remain joined.
  26. Which cyclin is degraded via the anaphase-promoting complex (APC/C)?
    A. Cyclin A
    B. Cyclin B
    C. Cyclin D
    D. Cyclin E
    Answer: B
    Explanation: Cyclin B is targeted by APC/C for degradation, facilitating the exit from mitosis.
  27. The term “mitosis” was introduced by:
    A. Walther Flemming
    B. Strasburger
    C. Boveri
    D. Sutton
    Answer: A
    Explanation: Walther Flemming coined the term “mitosis” in the 19th century based on his observations.
  28. During which stage does the nucleolus reappear?
    A. Prophase
    B. Metaphase
    C. Anaphase
    D. Telophase
    Answer: D
    Explanation: In Telophase, the nuclear envelope reforms and the nucleolus reappears.
  29. Polyploidy arises due to failure in:
    A. Karyokinesis
    B. Cytokinesis
    C. Synapsis
    D. Crossing over
    Answer: B
    Explanation: Polyploidy results from failure in cytokinesis, leading to cells with multiple chromosome sets.
  30. The “quiescent center” in plant roots is in:
    A. G0 phase
    B. G1 phase
    C. S phase
    D. G2 phase
    Answer: A
    Explanation: Cells in the quiescent center are metabolically active but non-dividing, residing in G0 phase.
  31. Which phase is absent in meiosis?
    A. Interkinesis
    B. S phase
    C. G2 phase
    D. G1 phase
    Answer: B
    Explanation: There is no S phase between Meiosis I and II; DNA is not replicated again.
  32. Lampbrush chromosomes are observed in:
    A. Mitotic prophase
    B. Meiotic prophase I
    C. Oocytes of amphibians
    D. Polytene chromosomes
    Answer: C
    Explanation: Lampbrush chromosomes are extended meiotic chromosomes found in oocytes of amphibians and birds.
  33. The spindle assembly checkpoint ensures:
    A. DNA replication is complete
    B. Chromosomes are aligned at metaphase plate
    C. Chromosomes condense
    D. Centrosomes duplicate
    Answer: B
    Explanation: This checkpoint prevents progression to anaphase until all kinetochores are attached to spindle fibers.
  34. Which structure disappears during prophase?
    A. Chromatin
    B. Nucleolus
    C. Spindle fibers
    D. Chromatids
    Answer: B
    Explanation: The nucleolus disappears in prophase, and chromatin condenses into chromosomes.
  35. Kinetochore is located on:
    A. Chromosome arms
    B. Telomeres
    C. Centromere
    D. Nucleolus
    Answer: C
    Explanation: The kinetochore forms on the centromere and serves as an attachment site for spindle fibers.
  36. Cytokinesis in animals is aided by:
    A. Cell wall
    B. Phragmoplast
    C. Actin-myosin ring
    D. Vesicle fusion
    Answer: C
    Explanation: An actin-myosin contractile ring constricts to form a cleavage furrow during cytokinesis in animals.
  37. Centrosome duplicates during:
    A. G0 phase
    B. G1 phase
    C. S phase
    D. M phase
    Answer: C
    Explanation: The centrosome (containing centrioles) duplicates during S phase alongside DNA replication.
  38. Which phase involves the separation of sister chromatids?
    A. Anaphase
    B. Telophase
    C. Prophase
    D. Metaphase
    Answer: A
    Explanation: During Anaphase, sister chromatids are pulled to opposite poles by spindle fibers.
  39. Meiosis ensures:
    A. Chromosome duplication
    B. Diploid zygote formation
    C. Genetic uniformity
    D. Genetic variation
    Answer: D
    Explanation: Meiosis promotes genetic variation through crossing over and independent assortment.
  40. DNA content doubles in:
    A. G1 phase
    B. G2 phase
    C. M phase
    D. S phase
    Answer: D
    Explanation: DNA replication occurs during S phase, doubling the DNA content.
  41. Chiasmata function in:
    A. Chromatid cohesion
    B. Spindle formation
    C. Genetic recombination
    D. Nuclear envelope breakdown
    Answer: C
    Explanation: Chiasmata are points where homologous chromosomes exchange genetic material.
  42. How many cell divisions occur in meiosis?
    A. One
    B. Two
    C. Three
    D. Four
    Answer: B
    Explanation: Meiosis involves two successive cell divisions: Meiosis I and Meiosis II.
  43. Colchicine blocks cell division at:
    A. Prophase
    B. Metaphase
    C. Anaphase
    D. Telophase
    Answer: B
    Explanation: Colchicine inhibits microtubule formation, arresting cells in metaphase.
  44. Spindle fibers are composed of:
    A. Actin
    B. Tubulin
    C. Myosin
    D. Lamin
    Answer: B
    Explanation: Spindle fibers are made of tubulin microtubules that segregate chromosomes.
  45. Number of chromosomes in human gametes:
    A. 23
    B. 46
    C. 44
    D. 22
    Answer: A
    Explanation: Gametes (sperm/egg) are haploid, containing 23 chromosomes.
  46. Nondisjunction leads to:
    A. Genetic recombination
    B. Aneuploidy
    C. Polyploidy
    D. Mutation
    Answer: B
    Explanation: Nondisjunction is failure of chromosomes to separate properly, resulting in aneuploid cells.
  47. Which organelle plays a role in spindle formation?
    A. Golgi body
    B. Nucleus
    C. Centrosome
    D. Lysosome
    Answer: C
    Explanation: The centrosome organizes spindle fibers for chromosome segregation.
  48. How many chromatids are there in a human cell after S phase?
    A. 46
    B. 92
    C. 23
    D. 69
    Answer: B
    Explanation: Post-S phase, each of 46 chromosomes has two chromatids = 92 chromatids total.
  49. Programmed cell death is termed:
    A. Necrosis
    B. Apoptosis
    C. Lysis
    D. Phagocytosis
    Answer: B
    Explanation: Apoptosis is a regulated process to eliminate damaged or unnecessary cells.

 

 


Allele concept, multiple allele (ABO blood group); pseudo allele; isoallele; allelic interaction.

 

  1. ABO blood groups in humans are controlled by:
    A. Multiple alleles
    B. Lethal genes
    C. Complementary genes
    D. Linked genes
    Answer: A
    Explanation: ABO blood groups involve three alleles (I<sup>A</sup>, I<sup>B</sup>, i) of a single gene, making it a classic example of multiple allelism.
  2. A person with blood group AB has the genotype:
    A. I<sup>A</sup>I<sup>A</sup>
    B. I<sup>B</sup>I<sup>B</sup>
    C. I<sup>A</sup>I<sup>B</sup>
    D. ii
    Answer: C
    Explanation: Codominance between I<sup>A</sup> and I<sup>B</sup> alleles results in AB phenotype.
  3. Isoalleles are defined as:
    A. Alleles expressing identical phenotypes
    B. Mutated alleles with lethal effects
    C. Alleles with identical function but different protein sequences
    D. Alleles that mask pseudoalleles
    Answer: C
    Explanation: Isoalleles produce functionally identical proteins but differ in DNA sequence, detectable only through molecular analysis.
  4. Which allelic interaction explains the AB blood group?
    A. Incomplete dominance
    B. Codominance
    C. Epistasis
    D. Complementary genes
    Answer: B
    Explanation: I<sup>A</sup> and I<sup>B</sup> are codominant, expressing both antigens (A and B) equally.
  5. Pseudoalleles are:
    A. Non-functional alleles
    B. Closely linked genes mimicking alleles
    C. Alleles with identical mutations
    D. Alleles showing incomplete dominance
    Answer: B
    Explanation: Pseudoalleles are tightly linked genes (e.g., in Drosophila eye color) that behave like alleles due to rare recombination.
  6. A cross between blood group A (I<sup>A</sup>i) and B (I<sup>B</sup>i) parents can produce offspring with blood group:
    A. A only
    B. AB only
    C. O, A, B, AB
    D. O and AB only
    Answer: C
    Explanation: Genotypes: I<sup>A</sup>i × I<sup>B</sup>i → 25% I<sup>A</sup>I<sup>B</sup> (AB), 25% I<sup>A</sup>i (A), 25% I<sup>B</sup>i (B), 25% ii (O).
  7. The allele for sickle-cell anemia shows:
    A. Codominance
    B. Overdominance
    C. Incomplete dominance
    D. Lethal dominance
    Answer: A
    Explanation: Heterozygotes (Hb<sup>A</sup>Hb<sup>S</sup>) express both normal and sickle hemoglobin, demonstrating codominance.
  8. Which is NOT a feature of multiple alleles?
    A. Occupy same locus
    B. Arise from repeated mutations
    C. Control same trait
    D. Present in different individuals
    Answer: D
    Explanation: Multiple alleles exist in a population, but an individual diploid organism can possess only two alleles at a locus.
  9. In chickens, the gene for feather color exhibits incomplete dominance: BB (black), Bb (blue), bb (white). A cross between blue chickens gives:
    A. All blue
    B. 1 black : 2 blue : 1 white
    C. 3 blue : 1 white
    D. 1 black : 1 white
    Answer: B
    Explanation: Bb × Bb → 25% BB (black), 50% Bb (blue), 25% bb (white).
  10. The term “allele” was coined by:
    A. Gregor Mendel
    B. William Bateson
    C. Thomas Morgan
    D. Carl Correns
    Answer: B
    Explanation: William Bateson introduced “allele” in 1905 to describe variant forms of a gene.
  11. Which phenomenon is observed in the Drosophila Bar eye mutation?
    A. Multiple alleles
    B. Pseudoallelism
    C. Isoallelism
    D. Overdominance
    Answer: B
    Explanation: Bar eye results from pseudoalleles (duplicated genes B<sup>+</sup> and B) where unequal crossing over causes phenotypic variation.
  12. A gene with over 100 alleles in humans is:
    A. ABO blood group
    B. HLA complex
    C. Rh factor
    D. Hemoglobin gene
    Answer: B
    Explanation: The HLA complex (MHC) has >100 alleles per locus, crucial for immune diversity.
  13. Complementary genes require:
    A. Two dominant alleles to express a trait
    B. One dominant allele to suppress another
    C. Interaction of non-allelic genes
    D. Multiple alleles at a single locus
    Answer: A
    Explanation: Complementary genes (e.g., sweet pea flower color) need dominant alleles of two different genes for trait expression.
  14. Bombay phenotype arises due to:
    A. Mutation in ABO gene
    B. Epistasis by hh genotype
    C. Codominance failure
    D. Pseudoallelism
    Answer: B
    Explanation: Recessive hh genotype (epistatic gene) prevents ABO antigen formation, resulting in O phenotype regardless of ABO genotype.
  15. Alleles I<sup>A</sup> and I<sup>B</sup> produce:
    A. Antigens
    B. Antibodies
    C. Enzymes
    D. Hormones
    Answer: C
    Explanation: I<sup>A</sup> encodes glycosyltransferase A (adds N-acetylgalactosamine), I<sup>B</sup> adds galactose to H antigen.
  16. In mice, agouti coat color (AA) is dominant to black (aa). Heterozygotes (Aa) show intermediate phenotype. This is:
    A. Codominance
    B. Incomplete dominance
    C. Epistasis
    D. Lethal alleles
    Answer: B
    Explanation: Incomplete dominance results in an intermediate phenotype (e.g., yellow-brown) in heterozygotes.
  17. Which represents allelic exclusion?
    A. Random X-chromosome inactivation
    B. Expression of only one immunoglobulin allele
    C. Genomic imprinting
    D. Overdominance
    Answer: B
    Explanation: Allelic exclusion ensures B-cells express only one heavy/light chain allele, producing monospecific antibodies.
  18. The Rh<sup>+</sup> allele is:
    A. Dominant
    B. Recessive
    C. Codominant
    D. Incompletely dominant
    Answer: A
    Explanation: Rh<sup>+</sup> is dominant (DD/Dd); Rh<sup>-</sup> is recessive (dd).
  19. Lethal alleles were first discovered in:
    A. Drosophila
    B. Mice
    C. Snapdragon
    D. Neurospora
    Answer: B
    Explanation: Cuenot (1905) observed yellow coat lethality in mice (Agouti gene).
  20. In ABO system, universal donor is O because:
    A. It lacks A/B antigens
    B. It produces anti-A and anti-B antibodies
    C. Both A and B
    D. It is codominant
    Answer: C
    Explanation: Group O RBCs lack A/B antigens and plasma has anti-A/B antibodies, minimizing transfusion reactions.
  21. Pseudoalleles can be distinguished by:
    A. Phenotypic ratios
    B. Complementation test
    C. High recombination frequency
    D. Lethal effects
    Answer: B
    Explanation: Complementation test reveals if mutations are in the same gene (fail to complement) or different genes (complement).
  22. Epistasis differs from dominance in that:
    A. It involves inter-genic interactions
    B. It alters Mendelian ratios
    C. Both A and B
    D. It is intra-allelic
    Answer: C
    Explanation: Epistasis is inter-genic (non-allelic genes interact), often modifying 9:3:3:1 ratios.
  23. The ABO gene is located on chromosome:
    A. 1
    B. 9
    C. 11
    D. 19
    Answer: B
    Explanation: ABO gene locus is on chromosome 9q34.2.
  24. Which shows overdominance?
    A. Sickle-cell trait in malaria zones
    B. AB blood group
    C. Pink snapdragons
    D. Bombay phenotype
    Answer: A
    Explanation: Overdominance occurs when heterozygotes (Hb<sup>A</sup>Hb<sup>S</sup>) have higher fitness than homozygotes in malaria-endemic regions.
  25. Isoalleles are identified through:
    A. Phenotypic analysis
    B. Biochemical assays
    C. DNA sequencing
    D. Complementation tests
    Answer: C
    Explanation: DNA sequencing detects subtle nucleotide differences in isoalleles producing identical phenotypes.
  26. A type O mother and type AB father can have children with blood group:
    A. A or B only
    B. AB only
    C. O only
    D. A, B, AB, or O
    Answer: A
    Explanation: Mother (ii) × Father (I<sup>A</sup>I<sup>B</sup>) → offspring I<sup>A</sup>i (A) or I<sup>B</sup>i (B).
  27. The H antigen in ABO system is synthesized by:
    A. FUT1 gene
    B. ABO gene
    C. Rh gene
    D. HLA gene
    Answer: A
    Explanation: FUT1 (H gene) on chromosome 19 encodes fucosyltransferase to produce H antigen.
  28. Allelic exclusion in immunology ensures:
    A. Self-tolerance
    B. Clonal selection
    C. Antibody specificity
    D. MHC diversity
    Answer: C
    Explanation: By expressing only one allele, B-cells produce monospecific antibodies against a single epitope.
  29. Which is an example of recessive lethal alleles?
    A. Huntington’s disease
    B. Tay-Sachs disease
    C. Sickle-cell anemia
    D. Cystic fibrosis
    Answer: B
    Explanation: Tay-Sachs is caused by recessive lethal alleles (homozygotes die in early childhood).
  30. In Drosophila, the white-eye pseudoalleles were studied by:
    A. Morgan
    B. Lewis
    C. Bridges
    D. Sturtevant
    Answer: B
    Explanation: Edward B. Lewis demonstrated pseudoallelism in the bithorax complex using recombination studies.
  31. Which best describes codominance?
    A. One allele masks another
    B. Both alleles express partially
    C. Both alleles express fully
    D. Neither allele expresses
    Answer: C
    Explanation: In codominance, both alleles contribute equally and independently to the phenotype (e.g., AB blood group).
  32. Which blood group lacks both anti-A and anti-B antibodies?
    A. O
    B. AB
    C. A
    D. B
    Answer: B
    Explanation: AB individuals have both A and B antigens on RBCs, so they do not produce anti-A or anti-B antibodies.
  33. A person with genotype ii has which blood group?
    A. A
    B. B
    C. AB
    D. O
    Answer: D
    Explanation: Genotype ii lacks A and B antigens, resulting in O blood group.
  34. In humans, how many ABO alleles can an individual carry?
    A. 1
    B. 2
    C. 3
    D. 4
    Answer: B
    Explanation: Humans are diploid; they can have any two of the three alleles (I<sup>A</sup>, I<sup>B</sup>, i).
  35. What is the genotype of a universal plasma donor?
    A. I<sup>A</sup>I<sup>A</sup>
    B. I<sup>B</sup>I<sup>B</sup>
    C. I<sup>A</sup>I<sup>B</sup>
    D. ii
    Answer: C
    Explanation: AB blood group lacks anti-A and anti-B antibodies in plasma, making them universal plasma donors.
  36. Bombay phenotype individuals cannot express ABO antigens because:
    A. They lack ABO alleles
    B. They have IA and IB alleles
    C. They lack H antigen
    D. They produce abnormal antibodies
    Answer: C
    Explanation: The absence of H antigen (due to hh genotype) prevents expression of A or B antigens.
  37. Which condition arises from incomplete dominance in humans?
    A. Blood group AB
    B. Tay-Sachs disease
    C. Sickle-cell anemia
    D. Pink flower in snapdragon
    Answer: B
    Explanation: In Tay-Sachs carriers, heterozygotes show intermediate enzyme activity, illustrating incomplete dominance at the biochemical level.
  38. What type of interaction occurs between I<sup>A</sup> and I<sup>B</sup> alleles?
    A. Dominance
    B. Incomplete dominance
    C. Codominance
    D. Overdominance
    Answer: C
    Explanation: I<sup>A</sup> and I<sup>B</sup> alleles are codominant and both antigens are expressed in AB blood group.
  39. A person with genotype I<sup>A</sup>i and I<sup>B</sup>i may produce which blood groups in offspring?
    A. A only
    B. A and B only
    C. A, B, AB, O
    D. AB and O only
    Answer: C
    Explanation: Cross between I<sup>A</sup>i × I<sup>B</sup>i gives all four possible ABO blood types.
  40. What type of dominance is shown when heterozygote phenotype is intermediate?
    A. Codominance
    B. Incomplete dominance
    C. Complete dominance
    D. Overdominance
    Answer: B
    Explanation: In incomplete dominance, heterozygote shows a phenotype between the two homozygotes.
  41. Which is true for lethal alleles?
    A. They always cause death in heterozygous state
    B. Only dominant lethal alleles are known
    C. Homozygous individuals may not survive
    D. They always affect eye color
    Answer: C
    Explanation: Recessive lethal alleles cause death only in homozygous condition (e.g., yellow coat in mice).
  42. Which genetic principle explains why blood group O cannot receive AB blood?
    A. Epistasis
    B. Incomplete dominance
    C. Antigen-antibody reaction
    D. Codominance
    Answer: C
    Explanation: Blood group O has anti-A and anti-B antibodies which attack AB donor antigens.
  43. The term ‘multiple alleles’ means:
    A. Genes located on different chromosomes
    B. More than two alternative forms of a gene
    C. Many phenotypes in one individual
    D. Two genes influencing one trait
    Answer: B
    Explanation: Multiple alleles refer to more than two allelic forms of a gene in a population (e.g., ABO).
  44. A cross between two heterozygous snapdragons produces what flower color ratio?
    A. 1 red : 2 pink : 1 white
    B. 3 red : 1 white
    C. 1 red : 1 white
    D. All pink
    Answer: A
    Explanation: Incomplete dominance produces a 1:2:1 phenotypic ratio (RR:red, Rr:pink, rr:white).
  45. A pseudoallele behaves like:
    A. An allele due to linkage
    B. A mutant allele
    C. A silent gene
    D. A non-functional protein
    Answer: A
    Explanation: Pseudoalleles are closely linked genes that mimic the behavior of alleles.
  46. Which test differentiates between pseudoalleles and real alleles?
    A. Punnett square
    B. Complementation test
    C. PCR
    D. Northern blot
    Answer: B
    Explanation: Complementation tests determine if mutations affect the same or different genes.
  47. In epistasis, one gene:
    A. Is incompletely dominant
    B. Masks the expression of another
    C. Is codominant
    D. Replaces another gene
    Answer: B
    Explanation: Epistasis is when one gene interferes with or suppresses the expression of another gene.
  48. Allelic exclusion ensures:
    A. Immunoglobulin diversity
    B. Expression of both alleles
    C. Single specificity of B-cells
    D. Somatic recombination
    Answer: C
    Explanation: Allelic exclusion ensures each B-cell produces only one type of antibody.
  49. In Rh incompatibility, a problem arises when:
    A. Both parents are Rh-
    B. Mother is Rh- and fetus is Rh+
    C. Father is Rh- and mother is Rh+
    D. Both fetus and mother are Rh+
    Answer: B
    Explanation: Rh- mother with Rh+ fetus may develop antibodies that attack fetal RBCs in later pregnancies.
  50. Which gene is necessary for ABO antigen expression?
    A. ABO
    B. Rh
    C. FUT1
    D. MHC
    Answer: C
    Explanation: FUT1 gene encodes the enzyme that forms the H antigen, the base for ABO antigen development.

 

 

Sex determination with special reference to Drosophila and Man.

  1. In humans, sex is determined by:
    A. X chromosome in sperm
    B. Y chromosome in sperm
    C. X chromosome in egg
    D. Cytoplasm of egg
    Answer: B
    Explanation: Human sex determination follows the XY system. A sperm carrying a Y chromosome determines male development by contributing the SRY gene.
  2. Drosophila sex determination relies on:
    A. Number of X chromosomes
    B. Presence of Y chromosome
    C. Temperature
    D. Hormones
    Answer: A
    Explanation: Drosophila determines sex based on the X:A ratio (number of X chromosomes relative to autosomes), not the presence of a Y chromosome.
  3. The master regulator of male development in humans is:
    A. DAX1 gene
    B. SOX9 gene
    C. SRY gene
    D. WNT4 gene
    Answer: C
    Explanation: The SRY gene on the Y chromosome triggers male development by initiating testis formation.
  4. A Drosophila with genotype XXY will be:
    A. Male
    B. Female
    C. Intersex
    D. Sterile male
    Answer: B
    Explanation: In Drosophila, the presence of two X chromosomes (X:A ratio = 1.0) determines female development, regardless of the Y chromosome.
  5. Dosage compensation in humans occurs via:
    A. Hypertranscription of X in males
    B. Inactivation of one X in females
    C. Y chromosome gene amplification
    D. Autosome silencing
    Answer: B
    Explanation: One X chromosome in females is inactivated (Barr body) to balance gene dosage with males.
  6. Klinefelter syndrome results from:
    A. 44 + XXY
    B. 44 + XO
    C. 44 + XXX
    D. 44 + YY
    Answer: A
    Explanation: Klinefelter syndrome (47,XXY) is a male with an extra X chromosome, resulting in infertility and feminized traits.
  7. The Drosophila gene Sex-lethal (Sxl) is activated in:
    A. Males (XY)
    B. Females (XX)
    C. Both sexes
    D. Only in mutants
    Answer: B
    Explanation: Sxl is activated in XX embryos, initiating the female developmental pathway through alternative RNA splicing.
  8. Turner syndrome is characterized by:
    A. 45,XO karyotype
    B. Male phenotype with infertility
    C. Trisomy of X
    D. XXY genotype
    Answer: A
    Explanation: Turner syndrome (45,XO) results in a sterile female with physical abnormalities such as short stature and webbed neck.
  9. In Drosophila, the Y chromosome is essential for:
    A. Male development
    B. Sperm motility
    C. Dosage compensation
    D. Oogenesis
    Answer: B
    Explanation: While not involved in sex determination, the Y chromosome in Drosophila carries fertility genes required for sperm production.
  10. The SRY gene encodes a:
    A. Hormone receptor
    B. Transcription factor
    C. RNA-splicing protein
    D. Membrane protein
    Answer: B
    Explanation: SRY encodes a transcription factor that promotes SOX9 expression, leading to testis formation.
  11. A Drosophila gynandromorph occurs due to:
    A. Non-disjunction
    B. Loss of X chromosome during mitosis
    C. Mutation in Sxl
    D. Temperature sensitivity
    Answer: B
    Explanation: Gynandromorphs form when one X chromosome is lost in an early mitotic division, producing XX (female) and XO (male) cell lineages.
  12. Androgen Insensitivity Syndrome (AIS) results from:
    A. SRY deletion
    B. Defective androgen receptors
    C. Estrogen deficiency
    D. XXY karyotype
    Answer: B
    Explanation: In AIS, individuals are genetically male (XY) but develop female phenotypes due to nonfunctional androgen receptors.
  13. The Drosophila gene transformer (tra) is spliced into active form only in:
    A. Males
    B. Females
    C. Both sexes
    D. Larvae
    Answer: B
    Explanation: Sxl protein promotes female-specific splicing of tra mRNA, producing Tra protein only in females.
  14. In humans, the default sex development pathway is:
    A. Male
    B. Female
    C. Bisexual
    D. Environment-dependent
    Answer: B
    Explanation: In the absence of SRY, the bipotential gonad develops into ovaries, making the female pathway default.
  15. Drosophila males compensate for single X by:
    A. X-inactivation
    B. Hypertranscription of X
    C. Y chromosome gene expression
    D. Autosome silencing
    Answer: B
    Explanation: Drosophila males double the transcriptional output of their single X chromosome to equalize gene expression with females.
  16. Swyer syndrome (46,XY female) is caused by:
    A. SRY mutation
    B. Extra X chromosome
    C. Aromatase deficiency
    D. Androgen excess
    Answer: A
    Explanation: Mutation in the SRY gene prevents testis development, leading to a female phenotype in an XY individual.
  17. The Drosophila gene doublesex (dsx):
    A. Determines X:A ratio
    B. Is sex-specifically spliced
    C. Activates Sxl
    D. Encodes a hormone
    Answer: B
    Explanation: dsx mRNA is spliced into male- or female-specific isoforms depending on the sex, influencing sexual differentiation.
  18. Which karyotype is non-viable?
    A. 45,XO
    B. 47,XXY
    C. 47,XYY
    D. 45,YO
    Answer: D
    Explanation: 45,YO embryos lack an X chromosome, which is essential for development, and are not viable.
  19. Drosophila females with genotype tra/tra develop as:
    A. Normal females
    B. Males
    C. Intersex
    D. Sterile females
    Answer: B
    Explanation: tra is essential for female development. XX tra/tra mutants follow the male pathway due to lack of functional Tra protein.
  20. The Barr body in human cells is:
    A. An activated X chromosome
    B. An inactivated Y chromosome
    C. An inactivated X chromosome
    D. A degenerate autosome
    Answer: C
    Explanation: In female cells, one X chromosome condenses into a Barr body and is transcriptionally inactive.
  21. Drosophila with genotype X:AA = 0.5 will be:
    A. Male
    B. Female
    C. Metafemale
    D. Intersex
    Answer: A
    Explanation: An X:A ratio of 0.5 (e.g., XY or XO with diploid autosomes) results in male development in Drosophila.
  22. SRY gene is located on:
    A. Short arm of Y chromosome
    B. Long arm of X chromosome
    C. Autosome 7
    D. Pseudoautosomal region
    Answer: A
    Explanation: The SRY gene is located on the short arm of the Y chromosome (Yp11.3 region).
  23. In Drosophila, the msl-2 gene is repressed in females by:
    A. Sxl protein
    B. Tra protein
    C. Dsx protein
    D. Y chromosome
    Answer: A
    Explanation: Sxl protein inhibits translation of msl-2 mRNA in females, preventing dosage compensation machinery from acting.
  24. Turner syndrome patients lack:
    A. Barr bodies
    B. Ovarian follicles
    C. Both A and B
    D. Functional SRY
    Answer: C
    Explanation: Turner syndrome individuals (45,XO) lack a second X chromosome (no Barr body) and functional ovaries.
  25. Drosophila males have:
    A. One Barr body
    B. Hyperactive X chromosome
    C. Inactive Y chromosome
    D. Sxl gene expression
    Answer: B
    Explanation: Male Drosophila upregulate transcription of their single X chromosome to match female gene dosage.
  26. The testis-determining factor (TDF) is produced by:
    A. Leydig cells
    B. SRY gene
    C. Pituitary gland
    D. Wolffian ducts
    Answer: B
    Explanation: The SRY gene encodes TDF, a transcription factor that initiates testis formation from bipotential gonads.
  27. Drosophila with X:A ratio = 1.5 are:
    A. Males
    B. Females
    C. Metafemales
    D. Intersex
    Answer: C
    Explanation: A ratio of 1.5 (e.g., XXX:AA) produces metafemales—abnormal females with low fertility.
  28. In humans, the Wolffian ducts develop into:
    A. Ovaries
    B. Uterus
    C. Epididymis
    D. Clitoris
    Answer: C
    Explanation: In male development, testosterone stimulates Wolffian ducts to form epididymis, vas deferens, and seminal vesicles.
  29. The Drosophila gene fruitless (fru) controls:
    A. Ovary development
    B. Male courtship behavior
    C. X:A ratio sensing
    D. Dosage compensation
    Answer: B
    Explanation: The fru gene is essential for male courtship behavior and is expressed in a male-specific manner.
  30. SRY activates which downstream gene?
    A. DAX1
    B. WNT4
    C. SOX9
    D. FOXL2
    Answer: C
    Explanation: SRY induces expression of SOX9, which promotes testis development and suppresses ovarian pathways.

Gene as a structural & functional unit  cistron concept; one gene – one polypeptide; sickle cell anemia; thalassemia.

 

  1. The term “cistron” was coined by:
    A. T.H. Morgan
    B. Seymour Benzer
    C. Beadle & Tatum
    D. Jacob & Monod
    Answer: B
    Explanation: Seymour Benzer introduced “cistron” (1957) using complementation tests in bacteriophage T4, defining the smallest functional genetic unit.
  2. The “one gene–one polypeptide” hypothesis emerged from studies on:
    A. Drosophila eye color
    B. Neurospora crassa mutants
    C. E. coli lac operon
    D. Human hemoglobin
    Answer: B
    Explanation: Beadle & Tatum’s work on Neurospora (1941) showed each gene controls a specific enzyme (later refined to polypeptide).
  3. Sickle cell anemia results from a mutation in:
    A. α-globin gene
    B. β-globin gene
    C. Heme synthesis enzyme
    D. Spectrin protein
    Answer: B
    Explanation: A point mutation (GAG→GTG) in the β-globin gene (chromosome 11) substitutes valine for glutamic acid at position 6.
  4. The cistron concept is validated by:
    A. Recombination frequency
    B. Complementation test
    C. DNA sequencing
    D. Transcription assays
    Answer: B
    Explanation: The complementation test determines if two mutations are in the same cistron (fail to complement) or different cistrons (complement).
  5. Which is an exception to “one gene–one polypeptide”?
    A. Alternative splicing
    B. Sickle cell anemia
    C. Thalassemia
    D. Cistronic genes
    Answer: A
    Explanation: Alternative splicing allows one gene to produce multiple polypeptides (e.g., DSCAM gene in Drosophila yields 38,016 isoforms).
  6. In sickle cell anemia, hemoglobin forms polymers due to:
    A. Hydrophilic substitution
    B. Hydrophobic valine at position 6
    C. Frameshift mutation
    D. Deletion in β-globin
    Answer: B
    Explanation: Hydrophobic valine causes HbS molecules to polymerize into rigid fibers under low oxygen.
  7. β-thalassemia major results from:
    A. Mutations in one β-globin allele
    B. Complete absence of β-globin chains
    C. Reduced α-globin synthesis
    D. HbC mutation
    Answer: B
    Explanation: Homozygous mutations in β-globin genes cause severe anemia due to absent/nonfunctional β-chains.
  8. The functional unit of a gene that specifies a polypeptide is a:
    A. Muton
    B. Recon
    C. Cistron
    D. Operon
    Answer: C
    Explanation: A cistron is the smallest unit of DNA that codes for a complete polypeptide (equivalent to a gene).
  9. Heterozygote advantage is seen in:
    A. β-thalassemia
    B. Sickle cell trait (HbAS)
    C. Cystic fibrosis
    D. Hemophilia
    Answer: B
    Explanation: HbAS heterozygotes are resistant to Plasmodium falciparum malaria, providing selective advantage.
  10. α-thalassemia is caused by:
    A. β-globin mutations
    B. Deletions in α-globin genes
    C. Iron deficiency
    D. Chromosome 11 defects
    Answer: B
    Explanation: Deletions in one or more of the four α-globin genes (chromosome 16) reduce α-chain synthesis.
  11. Benzer’s work on rII mutants of T4 phage demonstrated:
    A. Gene recombination
    B. Cistron as a functional unit
    C. One gene–one enzyme
    D. Colinearity of gene and protein
    Answer: B
    Explanation: Complementation tests with rII mutants defined the cistron as the smallest genetic unit.
  12. In sickle cell anemia, red blood cells become:
    A. Biconcave discs
    B. Crescent-shaped
    C. Spherocytes
    D. Target cells
    Answer: B
    Explanation: HbS polymerization deforms RBCs into sickle/crescent shapes, causing vaso-occlusion.
  13. The “Hb Bart’s” hydrops fetalis syndrome results from:
    A. β-thalassemia major
    B. Deletion of all four α-globin genes
    C. HbS homozygosity
    D. Iron overload
    Answer: B
    Explanation: Deletion of all four α-globin genes causes severe γ4 tetramers (Hb Bart’s), leading to fetal death.
  14. Which concept is challenged by overlapping genes?
    A. Cistron
    B. One gene–one polypeptide
    C. Central dogma
    D. Genetic code universality
    Answer: B
    Explanation: Overlapping genes (e.g., in ΦX174 phage) share nucleotides, allowing one DNA sequence to code for multiple polypeptides.
  15. Sickle cell anemia inheritance is:
    A. Autosomal dominant
    B. X-linked recessive
    C. Autosomal recessive
    D. Mitochondrial
    Answer: C
    Explanation: Requires homozygous recessive (HbSS) genotype for full disease expression.
  16. In β-thalassemia, excess unpaired α-globin chains:
    A. Form stable tetramers
    B. Precipitate in RBCs
    C. Enhance oxygen transport
    D. Degrade heme
    Answer: B
    Explanation: Excess α-chains precipitate, causing hemolysis and ineffective erythropoiesis.
  17. The minimal genetic element defined by a complementation test is a:
    A. Gene
    B. Cistron
    C. Exon
    D. Operon
    Answer: B
    Explanation: Cistron is defined by complementation: mutations in the same cistron fail to complement.
  18. Treatment for β-thalassemia major involves:
    A. Iron supplements
    B. Hydroxyurea
    C. Regular blood transfusions
    D. Gene therapy
    Answer: C
    Explanation: Lifelong blood transfusions correct anemia but cause iron overload, requiring chelation.
  19. The genetic defect in sickle cell anemia is a:
    A. Silent mutation
    B. Missense mutation
    C. Nonsense mutation
    D. Frameshift mutation
    Answer: B
    Explanation: Missense mutation changes codon 6 (GAG→GTG), substituting valine for glutamate.
  20. α-thalassemia silent carrier has:
    A. One α-globin gene deleted
    B. Two α-globin genes deleted
    C. Three α-globin genes deleted
    D. HbH disease
    Answer: A
    Explanation: Silent carriers lose one α-globin gene (e.g., -α/αα), showing no symptoms.
  21. Which supports “one gene–one polypeptide”?
    A. RNA editing
    B. Collagen (trimeric protein)
    C. Polycistronic mRNA
    D. Monomeric enzymes
    Answer: D
    Explanation: Monomeric enzymes (e.g., lysozyme) are encoded by single genes, aligning with the hypothesis.
  22. Hydroxyurea treats sickle cell disease by:
    A. Correcting the β-globin mutation
    B. Increasing fetal hemoglobin (HbF)
    C. Chelating iron
    D. Preventing RBC sickling
    Answer: B
    Explanation: Hydroxyurea induces HbF (γ-globin), which dilutes HbS and inhibits polymerization.
  23. In humans, the β-globin gene cluster is on chromosome:
    A. 11
    B. 16
    C. 9
    D. X
    Answer: A
    Explanation: β-globin genes (HBB) are located on chromosome 11p15.4.
  24. Hemoglobin Lepore is a fusion product seen in:
    A. α-thalassemia
    B. β-thalassemia
    C. Sickle cell anemia
    D. HbC disease
    Answer: B
    Explanation: Unequal crossover between δ- and β-globin genes creates a δβ fusion protein, causing β-thalassemia.
  25. The cistron concept applies to:
    A. Prokaryotes only
    B. Eukaryotes only
    C. Both prokaryotes and eukaryotes
    D. Viruses only
    Answer: C
    Explanation: Complementation tests work in all organisms to define functional gene units.
  26. Target cells and microcytosis are hallmarks of:
    A. Sickle cell anemia
    B. Thalassemia
    C. Hemophilia
    D. Leukemia
    Answer: B
    Explanation: Thalassemia causes microcytic, hypochromic RBCs with target cells due to imbalanced globin chains.
  27. Which gene therapy product is approved for β-thalassemia?
    A. Zynteglo (betibeglogene autotemcel)
    B. Luxturna
    C. Spinraza
    D. Kymriah
    Answer: A
    Explanation: Zynteglo uses autologous CD34+ cells transduced with functional β-globin gene.
  28. The molecular basis of “one gene–one polypeptide” is:
    A. Colinearity of DNA and protein
    B. Genetic code degeneracy
    C. Polyribosomes
    D. RNA interference
    Answer: A
    Explanation: Colinearity (e.g., in E. coli tryptophan synthetase) shows nucleotide sequence directly corresponds to amino acid sequence.
  29. In α-thalassemia, HbH disease results from deletion of:
    A. One α-globin gene
    B. Two α-globin genes
    C. Three α-globin genes
    D. Four α-globin genes
    Answer: C
    Explanation: Three-gene deletion (e.g., –/-α) causes β4 tetramers (HbH), leading to hemolytic anemia.
  30. Which confirms sickle cell diagnosis?
    A. Complete blood count (CBC)
    B. Hemoglobin electrophoresis
    C. Peripheral smear
    D. Iron studies
    Answer: B
    Explanation: Hemoglobin electrophoresis shows HbS migration pattern (slower than HbA) for definitive diagnosis.

 

 

 

Genetics and molecular biology of replication, transcription and translation.

 

  1. Semi-conservative DNA replication was demonstrated by:
    A. Watson & Crick
    B. Meselson & Stahl
    C. Hershey & Chase
    D. Taylor et al.
    Answer: B
    Explanation: Meselson & Stahl (1958) used ⁿ¹⁵N labeling in E. coli to show each daughter DNA has one parental strand.
  2. The enzyme that synthesizes RNA primers during DNA replication is:
    A. DNA polymerase III
    B. Primase
    C. Helicase
    D. Ligase
    Answer: B
    Explanation: Primase synthesizes short RNA primers for DNA polymerase to initiate replication.
  3. In eukaryotes, transcription of mRNA is performed by:
    A. RNA polymerase I
    B. RNA polymerase II
    C. RNA polymerase III
    D. Primase
    Answer: B
    Explanation: RNA pol II transcribes protein-coding genes into pre-mRNA.
  4. The Shine-Dalgarno sequence functions in:
    A. DNA replication initiation
    B. Translation initiation in prokaryotes
    C. Transcription termination
    D. mRNA splicing
    Answer: B
    Explanation: This ribosome-binding site (AGGAGG) aligns mRNA with the 16S rRNA in prokaryotes.
  5. Okazaki fragments are synthesized during:
    A. Leading strand replication
    B. Lagging strand replication
    C. Transcription
    D. Translation
    Answer: B
    Explanation: Lagging strand synthesis produces short, discontinuous Okazaki fragments (1,000-2,000 nt in prokaryotes).
  6. The genetic code is degenerate because:
    A. Multiple codons specify one amino acid
    B. Codons are non-overlapping
    C. AUG is the start codon
    D. Stop codons terminate translation
    Answer: A
    Explanation: Degeneracy allows multiple codons (e.g., UCU, UCC, UCA) to code for serine.
  7. Telomerase is a:
    A. DNA-dependent DNA polymerase
    B. RNA-dependent DNA polymerase
    C. RNA-dependent RNA polymerase
    D. Reverse transcriptase
    Answer: D
    Explanation: Telomerase (a reverse transcriptase) uses its RNA template to add telomeric repeats (e.g., TTAGGG) to chromosome ends.
  8. Rho (ρ)-dependent termination occurs in:
    A. DNA replication
    B. Prokaryotic transcription
    C. Eukaryotic transcription
    D. Translation
    Answer: B
    Explanation: ρ-factor binds RNA and terminates transcription in E. coli by unwinding RNA-DNA hybrids.
  9. Aminoacyl-tRNA synthetases catalyze:
    A. Peptide bond formation
    B. Charging tRNA with amino acids
    C. mRNA splicing
    D. Transcription initiation
    Answer: B
    Explanation: These enzymes link amino acids to their cognate tRNAs (ATP-dependent).
  10. The TATA box is a component of:
    A. Prokaryotic promoters
    B. Eukaryotic promoters
    C. Ribosome binding sites
    D. Transcriptional enhancers
    Answer: B
    Explanation: TATA box (consensus TATAAA) in eukaryotes binds TFIID to position RNA pol II.
  11. Proofreading during DNA replication is performed by:
    A. 3’→5′ exonuclease activity of DNA pol
    B. Primase
    C. DNA ligase
    D. Topoisomerase
    Answer: A
    Explanation: DNA pol I/III remove mismatched nucleotides via 3’→5′ exonuclease activity.
  12. The initiator tRNA in bacteria carries:
    A. Methionine
    B. Formylmethionine (fMet)
    C. N-formyl serine
    D. Alanine
    Answer: B
    Explanation: fMet-tRNAⁿ⁺⁾⁺ initiates translation in prokaryotes.
  13. CRISPR-Cas9 is derived from a:
    A. Prokaryotic immune system
    B. Eukaryotic RNAi pathway
    C. Viral replication mechanism
    D. Transposon-based system
    Answer: A
    Explanation: CRISPR-Cas9 is adapted from bacterial/archaeal adaptive immunity against viruses.
  14. Introns are removed by:
    A. RNA polymerase
    B. Ribosomes
    C. Spliceosomes
    D. Aminoacyl-tRNA synthetases
    Answer: C
    Explanation: Spliceosomes (snRNPs) catalyze intron excision and exon ligation.
  15. The enzyme relieving DNA supercoiling during replication is:
    A. Helicase
    B. Ligase
    C. Topoisomerase II (DNA gyrase)
    D. Primase
    Answer: C
    Explanation: DNA gyrase (prokaryotes) and topoisomerase II (eukaryotes) introduce negative supercoils.
  16. Polycistronic mRNA is found in:
    A. Prokaryotes
    B. Eukaryotes
    C. Both
    D. Viruses only
    Answer: A
    Explanation: Prokaryotes have polycistronic mRNA (e.g., lac operon), encoding multiple proteins.
  17. The wobble hypothesis explains:
    A. Degeneracy of genetic code
    B. Transcription errors
    C. DNA repair
    D. Frameshift mutations
    Answer: A
    Explanation: Wobble base pairing (3rd codon position) allows one tRNA to recognize multiple codons.
  18. Antibiotics like streptomycin inhibit:
    A. DNA replication
    B. Transcription
    C. Translation initiation
    D. Peptide bond formation
    Answer: C
    Explanation: Streptomycin binds 30S ribosomal subunit, disrupting initiation complex formation.
  19. The Kozak sequence (GCCRCCAUGG) optimizes:
    A. Prokaryotic translation initiation
    B. Eukaryotic translation initiation
    C. Transcription termination
    D. Splicing
    Answer: B
    Explanation: Kozak sequence enhances translation initiation efficiency in eukaryotes.
  20. Huntington’s disease results from:
    A. Trinucleotide repeat expansion
    B. Point mutation in globin gene
    C. Chromosomal deletion
    D. Telomerase dysfunction
    Answer: A
    Explanation: CAG repeat expansion in HTT gene (>40 repeats) causes Huntington’s disease.
  21. DNA polymerase III holoenzyme includes:
    A. Primase activity
    B. 5’→3’ polymerase and 3’→5’ exonuclease
    C. Ligase function
    D. Helicase activity
    Answer: B
    Explanation: DNA polymerase III synthesizes DNA in the 5’→3’ direction and proofreads via 3’→5’ exonuclease activity.
  22. The lac operon is regulated by:
    A. cAMP-CRP complex
    B. TATA-binding protein
    C. Rho factor
    D. Release factors
    Answer: A
    Explanation: cAMP-CRP activates lac operon transcription in the absence of glucose by binding the promoter region.
  23. Release factors (RF1/RF2) in translation recognize:
    A. Start codons
    B. Stop codons
    C. Shine-Dalgarno sequence
    D. Promoters
    Answer: B
    Explanation: RF1 (recognizes UAA/UAG) and RF2 (UAA/UGA) bind to stop codons and facilitate release of the nascent polypeptide chain.
  24. Fragile X syndrome is caused by:
    A. Trinucleotide (CGG) repeat expansion
    B. Chromosome 15 deletion
    C. Trisomy 21
    D. Point mutation in FMR1
    Answer: A
    Explanation: Fragile X results from >200 CGG repeats in the FMR1 gene promoter, leading to gene silencing and intellectual disability.
  25. The Pribnow box in prokaryotes is analogous to:
    A. TATA box
    B. CAAT box
    C. GC box
    D. Kozak sequence
    Answer: A
    Explanation: The Pribnow box (TATAAT) is a promoter element in prokaryotes analogous to the TATA box in eukaryotes.
  26. Amino acid activation requires:
    A. GTP
    B. ATP
    C. CTP
    D. UTP
    Answer: B
    Explanation: ATP is hydrolyzed during amino acid activation to form aminoacyl-AMP before transfer to tRNA.
  27. Which antibiotic inhibits peptidyl transferase?
    A. Tetracycline
    B. Streptomycin
    C. Chloramphenicol
    D. Rifampicin
    Answer: C
    Explanation: Chloramphenicol inhibits the peptidyl transferase activity of the 50S ribosomal subunit in prokaryotes.
  28. The central dogma describes:
    A. DNA → RNA → Protein
    B. RNA → DNA → Protein
    C. Protein → RNA → DNA
    D. DNA → Protein → RNA
    Answer: A
    Explanation: Crick’s central dogma (1958) defines the unidirectional information flow from DNA to RNA to protein.
  29. RNA editing occurs in:
    A. Trypanosomes (guide RNA)
    B. E. coli
    C. Saccharomyces
    D. Drosophila
    Answer: A
    Explanation: Trypanosomes use guide RNAs (gRNAs) for RNA editing, inserting or deleting uridines in mitochondrial transcripts.
  30. The nucleolus is the site of:
    A. DNA replication
    B. rRNA synthesis and ribosome assembly
    C. mRNA splicing
    D. Protein degradation
    Answer: B
    Explanation: The nucleolus is where RNA polymerase I transcribes rRNA, and ribosomal subunits are assembled.

 

 

Mutation-types, detection, molecular mechanism, chromosomal aberration.

 

 

  1. A point mutation that changes a codon to a stop codon is called:
    A. Missense mutation
    B. Nonsense mutation
    C. Silent mutation
    D. Frameshift mutation
    Answer: B
    Explanation: Nonsense mutations (e.g., CAG→UAG) create premature stop codons, truncating proteins.
  2. The Ames test detects:
    A. Carcinogens
    B. Aneuploidy
    C. Chromosomal deletions
    D. Polyploidy
    Answer: A
    Explanation: This bacterial reverse mutation assay (using Salmonella His⁻ mutants) identifies mutagens that may be carcinogens.
  3. Cri-du-chat syndrome results from:
    A. 5p⁻ deletion
    B. Trisomy 18
    C. Philadelphia chromosome
    D. Fragile X expansion
    Answer: A
    Explanation: Terminal deletion of 5p causes microcephaly and cat-like cry due to CTNND2 gene loss.
  4. UV radiation primarily causes DNA damage by forming:
    A. Thymine dimers
    B. 8-oxoguanine
    C. AP sites
    D. Single-strand breaks
    Answer: A
    Explanation: Thymine dimers (cyclobutane pyrimidine dimers) distort the DNA helix, blocking replication.
  5. Which mutation is NOT a frameshift?
    A. Insertion of 1 bp
    B. Deletion of 2 bp
    C. Insertion of 3 bp
    D. Deletion of 4 bp
    Answer: C
    Explanation: Insertion/deletion of 3 bp (multiples of 3) maintains the reading frame, causing in-frame mutation.
  6. Philadelphia chromosome is a:
    A. Reciprocal translocation (9;22)
    B. Deletion in chromosome 22
    C. Inversion in chromosome 9
    D. Trisomy 21
    Answer: A
    Explanation: t(9;22)(q34;q11) fuses BCR and ABL genes, producing oncogenic tyrosine kinase in CML.
  7. Mutagens like 5-bromouracil cause:
    A. Transitions
    B. Transversions
    C. Deletions
    D. Insertions
    Answer: A
    Explanation: Base analogs (5-BU) induce A-T → G-C or G-C → A-T transitions by tautomeric shifts.
  8. Klinefelter syndrome (47,XXY) is an example of:
    A. Autopolyploidy
    B. Autosomal trisomy
    C. Sex chromosome aneuploidy
    D. Triploidy
    Answer: C
    Explanation: Extra X chromosome (47,XXY) causes sex chromosome aneuploidy, leading to male infertility.
  9. Fluorescence In Situ Hybridization (FISH) detects:
    A. Point mutations
    B. Chromosomal aberrations
    C. Protein misfolding
    D. mRNA expression
    Answer: B
    Explanation: FISH uses fluorescent probes to visualize specific DNA sequences for deletions/translocations.
  10. A silent mutation:
    A. Alters amino acid sequence
    B. Creates a stop codon
    C. Changes codon without altering amino acid
    D. Shifts reading frame
    Answer: C
    Explanation: Synonymous mutations exploit codon degeneracy (e.g., UCU→UCC, both code for serine).
  11. Down syndrome is most commonly caused by:
    A. Robertsonian translocation
    B. 21q21q translocation
    C. Mosaicism
    D. Free trisomy 21
    Answer: D
    Explanation: 95% of cases involve free trisomy 21 due to maternal meiotic non-disjunction.
  12. Alkylating agents (e.g., EMS) cause mutations by:
    A. Cross-linking DNA strands
    B. Adding methyl/ethyl groups to bases
    C. Intercalating into DNA
    D. Breaking phosphodiester bonds
    Answer: B
    Explanation: Alkylation (e.g., O⁶-methylguanine) leads to mispairing (e.g., with T instead of C).
  13. Pericentric inversions involve:
    A. Centromere excluded
    B. Centromere included
    C. Telomeric regions
    D. p-arm only
    Answer: B
    Explanation: Pericentric inversions include the centromere, altering chromosome arm ratios.
  14. Sickle cell anemia results from a:
    A. Missense mutation (Glu→Val)
    B. Nonsense mutation
    C. Frameshift mutation
    D. Splice-site mutation
    Answer: A
    Explanation: β-globin codon 6 mutation (GAG→GTG) substitutes valine for glutamic acid.
  15. Mutations in tumor suppressor genes typically exhibit:
    A. Dominant inheritance
    B. Recessive loss-of-function
    C. Gain-of-function
    D. X-linked dominance
    Answer: B
    Explanation: Knudson’s two-hit hypothesis: Both alleles must be inactivated (e.g., RB1, TP53).
  16. Aneuploidy arises from:
    A. Non-disjunction
    B. Inversion loops
    C. Transposition
    D. Base excision repair
    Answer: A
    Explanation: Meiotic/mitotic non-disjunction causes abnormal chromosome numbers (e.g., trisomy, monosomy).
  17. Which mutation detection method uses PCR and gel electrophoresis?
    A. Karyotyping
    B. FISH
    C. RFLP analysis
    D. Comet assay
    Answer: C
    Explanation: RFLP detects mutations via altered restriction enzyme sites visualized on gels.
  18. Huntington’s disease is caused by:
    A. CAG trinucleotide expansion
    B. CTG repeat expansion
    C. FMR1 deletion
    D. Chromosome 4 translocation
    Answer: A
    Explanation: >40 CAG repeats in HTT exon 1 lead to toxic polyglutamine aggregates.
  19. Reciprocal translocations may cause:
    A. Position effect variegation
    B. Balanced gametes only
    C. Reduced fertility due to unbalanced gametes
    D. Triploidy
    Answer: C
    Explanation: Adjacent-1/2 segregation produces gametes with duplications/deletions, causing infertility.
  20. Xeroderma pigmentosum results from defects in:
    A. Mismatch repair
    B. Nucleotide excision repair (NER)
    C. Base excision repair
    D. Double-strand break repair
    Answer: B
    Explanation: NER deficiency impairs thymine dimer removal, increasing UV-induced skin cancer risk.
  21. A robertsonian translocation involves:
    A. Acrocentric chromosomes
    B. Telomeric fusions
    C. X and Y chromosomes
    D. Paracentric inversion
    Answer: A
    Explanation: Fusion of acrocentric chromosomes (13,14,15,21,22) at centromeres forms derivative chromosomes.
  22. Triploidy (69,XXY) commonly results from:
    A. Dispermy
    B. Meiotic non-disjunction
    C. Mitotic error
    D. Robertsonian translocation
    Answer: A
    Explanation: Dispermy (two sperm fertilizing one egg) is the most frequent cause of triploidy.
  23. Mutagens causing frameshifts include:
    A. Ethyl methanesulfonate (EMS)
    B. Proflavin
    C. 5-Bromouracil
    D. UV light
    Answer: B
    Explanation: Intercalating agents (proflavin, acridine orange) insert between bases, causing insertions/deletions.
  24. In pedigree analysis, autosomal dominant disorders show:
    A. Vertical transmission
    B. Skips generations
    C. Male-to-male transmission absent
    D. Higher male prevalence
    Answer: A
    Explanation: Vertical transmission (affected parent → child) with 50% recurrence risk.
  25. Isochromosomes arise from:
    A. Horizontal centromere division
    B. Robertsonian translocation
    C. Inversion
    D. Deletion
    Answer: A
    Explanation: Transverse centromere cleavage creates mirror-image chromosomes with identical arms (e.g., i(17q)).
  26. The “comet assay” detects:
    A. Chromosomal translocations
    B. DNA strand breaks
    C. Point mutations
    D. Telomere length
    Answer: B
    Explanation: Single-cell gel electrophoresis visualizes DNA fragmentation (“comet tail”) from strand breaks.
  27. Which is a chromosomal duplication syndrome?
    A. Charcot-Marie-Tooth disease (CMT1A)
    B. Cri-du-chat
    C. Williams syndrome
    D. Angelman syndrome
    Answer: A
    Explanation: CMT1A involves 1.5 Mb duplication of PMP22 on 17p11.2, causing peripheral neuropathy.
  28. Mutagenesis via oxidative damage commonly produces:
    A. 8-oxoguanine
    B. Thymine dimers
    C. AP sites
    D. Methylated cytosine
    Answer: A
    Explanation: 8-oxoG mispairs with adenine, causing G→T transversions.
  29. Uniparental disomy (UPD) causes:
    A. Prader-Willi syndrome
    B. Down syndrome
    C. Turner syndrome
    D. Klinefelter syndrome
    Answer: A
    Explanation: Maternal UPD15 silences paternally expressed genes (e.g., SNRPN), causing Prader-Willi.
  30. Which technique detects microdeletions?
    A. Karyotyping
    B. FISH
    C. Southern blot
    D. All of the above
    Answer: D
    Explanation:
  • Karyotyping: Detects >5 Mb deletions
  • FISH: Detects 1–10 Mb deletions
  • Southern blot: Detects smaller deletions if probe-targeted

 

 

 

Elementary idea of DNA finger printing, PCR, cloning, oncogene.

 

  1. DNA fingerprinting is based on the principle of:
    A. Variable Number Tandem Repeats (VNTRs)
    B. Single Nucleotide Polymorphisms (SNPs)
    C. Copy Number Variations (CNVs)
    D. DNA methylation patterns
    Answer: A
    Explanation: VNTRs (hypervariable regions) show high polymorphism between individuals, forming the basis of DNA fingerprinting.
  2. The enzyme used in PCR to synthesize DNA is:
    A. Taq DNA polymerase
    B. Reverse transcriptase
    C. DNA ligase
    D. Restriction endonuclease
    Answer: A
    Explanation: Taq polymerase from Thermus aquaticus is thermostable and synthesizes DNA during PCR amplification.
  3. The first cloned mammal, Dolly the sheep, was produced by:
    A. Somatic Cell Nuclear Transfer (SCNT)
    B. Embryo splitting
    C. CRISPR-Cas9
    D. mRNA vaccination
    Answer: A
    Explanation: SCNT involved transferring a nucleus from an adult mammary cell into an enucleated egg, cloned in 1996.
  4. Oncogenes are derived from:
    A. Proto-oncogenes
    B. Tumor suppressor genes
    C. Viral genes
    D. Housekeeping genes
    Answer: A
    Explanation: Proto-oncogenes regulate normal cell growth; mutations convert them into oncogenes that cause cancer.
  5. In DNA fingerprinting, restriction enzymes are used to:
    A. Cut DNA into fragments
    B. Amplify DNA
    C. Join DNA fragments
    D. Sequence DNA
    Answer: A
    Explanation: Restriction enzymes (e.g., HaeIII) cut DNA at specific sites, generating VNTR fragments for analysis.
  6. The denaturation step in PCR involves:
    A. Heating to 94–98°C to separate DNA strands
    B. Cooling to 50–65°C for primer annealing
    C. Heating to 72°C for DNA synthesis
    D. Adding probes for detection
    Answer: A
    Explanation: Denaturation (94–98°C) breaks hydrogen bonds, separating double-stranded DNA into single strands.
  7. The p53 gene is a:
    A. Tumor suppressor gene
    B. Proto-oncogene
    C. Retroviral oncogene
    D. DNA repair enzyme
    Answer: A
    Explanation: p53 (“guardian of the genome”) arrests the cell cycle for DNA repair or triggers apoptosis if damage is irreparable.
  8. Plasmid vectors used in cloning typically contain:
    A. Origin of replication (ori)
    B. Ribosomal RNA genes
    C. Telomeric sequences
    D. Centromeric DNA
    Answer: A
    Explanation: ori allows autonomous replication of plasmids in host cells (e.g., E. coli).
  9. Short Tandem Repeats (STRs) are preferred over VNTRs in forensic DNA fingerprinting because they:
    A. Are smaller and more amenable to PCR
    B. Show higher mutation rates
    C. Require radioactive probes
    D. Are found only in exons
    Answer: A
    Explanation: STRs (2–6 bp repeats) are shorter, allowing robust PCR amplification and automated analysis.
  10. The ras oncogene is activated by:
    A. Point mutations
    B. Chromosomal translocations
    C. Gene amplification
    D. Viral integration
    Answer: A
    Explanation: Point mutations (e.g., codon 12 in KRAS) lock the protein in a GTP-bound “ON” state, promoting proliferation.
  11. RT-PCR is used to amplify:
    A. DNA
    B. RNA
    C. Proteins
    D. Carbohydrates
    Answer: B
    Explanation: Reverse Transcriptase PCR converts RNA to cDNA before amplification, enabling gene expression studies.
  12. The main application of therapeutic cloning is to produce:
    A. Genetically identical animals
    B. Embryonic stem cells
    C. Recombinant proteins
    D. Vaccines
    Answer: B
    Explanation: Therapeutic cloning generates patient-specific embryonic stem cells for regenerative medicine.
  13. In DNA fingerprinting, Southern blotting is used to:
    A. Transfer DNA fragments to a membrane
    B. Amplify DNA
    C. Sequence DNA
    D. Visualize proteins
    Answer: A
    Explanation: Southern blotting transfers gel-separated DNA to a nitrocellulose membrane for hybridization with probes.
  14. The Philadelphia chromosome results from:
    A. t(9;22) translocation
    B. 5p⁻ deletion
    C. Trisomy 21
    D. BRCA1 mutation
    Answer: A
    Explanation: t(9;22) fuses BCR and ABL genes, producing a hyperactive tyrosine kinase in chronic myeloid leukemia.
  15. Primers in PCR are:
    A. Short synthetic oligonucleotides
    B. Restriction enzymes
    C. DNA ligases
    D. Thermostable polymerases
    Answer: A
    Explanation: Primers (18–22 bp) are designed to flank the target DNA and initiate synthesis.
  16. The HER2/neu oncogene is overexpressed in:
    A. Breast cancer
    B. Lung cancer
    C. Colon cancer
    D. Leukemia
    Answer: A
    Explanation: HER2/neu amplification occurs in 20–30% of breast cancers and is targeted by trastuzumab (Herceptin).
  17. A common vector for cloning large DNA fragments is:
    A. Bacterial Artificial Chromosome (BAC)
    B. Plasmid
    C. Cosmid
    D. Phagemid
    Answer: A
    Explanation: BACs can carry inserts up to 300 kb, used in genome sequencing projects.
  18. The number of cycles required to amplify a single DNA molecule into 1,048,576 copies is:
    A. 20
    B. 25
    C. 30
    D. 35
    Answer: A
    Explanation: After n cycles, copies = 2ⁿ. 2²⁰ = 1,048,576.
  19. Which virus carries the src oncogene?
    A. Rous sarcoma virus (RSV)
    B. Human papillomavirus (HPV)
    C. Epstein-Barr virus (EBV)
    D. Hepatitis B virus (HBV)
    Answer: A
    Explanation: RSV carries v-src, a viral oncogene derived from the cellular c-src proto-oncogene.
  20. The function of DNA ligase in cloning is to:
    A. Join DNA fragments
    B. Cut DNA
    C. Synthesize DNA
    D. Degrade RNA
    Answer: A
    Explanation: DNA ligase seals nicks between adjacent nucleotides, joining insert and vector DNA.
  21. STR analysis in DNA fingerprinting detects variations in:
    A. Number of tandem repeats
    B. Single base substitutions
    C. Methylation patterns
    D. Telomere length
    Answer: A
    Explanation: STR loci vary in repeat number (e.g., 5–20 repeats), creating unique profiles.
  22. BRCA1 is a:
    A. Tumor suppressor gene
    B. Proto-oncogene
    C. Retroviral gene
    D. Housekeeping gene
    Answer: A
    Explanation: BRCA1 repairs DNA double-strand breaks; mutations increase breast/ovarian cancer risk.
  23. The purpose of the annealing step in PCR is to:
    A. Allow primers to bind to DNA
    B. Separate DNA strands
    C. Synthesize new DNA strands
    D. Digest non-specific products
    Answer: A
    Explanation: Annealing (50–65°C) enables primers to hybridize with complementary template sequences.
  24. Agrobacterium-mediated gene transfer is used in cloning for:
    A. Plants
    B. Mammals
    C. Bacteria
    D. Yeast
    Answer: A
    Explanation: Agrobacterium tumefaciens transfers T-DNA to plant cells, making it a key tool in plant biotechnology.
  25. Real-time PCR (qPCR) differs from standard PCR by:
    A. Quantifying DNA during amplification
    B. Using RNA templates exclusively
    C. Omitting primers
    D. Requiring gel electrophoresis
    Answer: A
    Explanation: qPCR uses fluorescent dyes/probes to measure DNA accumulation in real-time, enabling quantification.
  26. Knudson’s “two-hit hypothesis” explains the mechanism of:
    A. Tumor suppressor genes
    B. Proto-oncogenes
    C. Viral oncogenes
    D. DNA repair genes
    Answer: A
    Explanation: Knudson’s model requires both alleles of a tumor suppressor gene (e.g., RB1) to be inactivated.
  27. In DNA fingerprinting, the probability of two individuals having identical profiles is:
    A. Extremely low (1 in billions)
    B. 50%
    C. 10%
    D. 1%
    Answer: A
    Explanation: High polymorphism in 13–20 STR loci makes matches exceedingly rare (e.g., 1 in 10¹⁵ for CODIS).
  28. The MYC oncogene is activated by:
    A. Translocation in Burkitt lymphoma
    B. Point mutation in lung cancer
    C. Deletion in neuroblastoma
    D. Viral integration in cervical cancer
    Answer: A
    Explanation: t(8;14) places MYC under immunoglobulin enhancer control, causing overexpression in lymphoma.
  29. Electroporation is a method used in cloning to:
    A. Introduce DNA into host cells
    B. Amplify DNA
    C. Digest DNA
    D. Sequence DNA
    Answer: A
    Explanation: Electroporation uses electrical pulses to create pores in cell membranes for DNA uptake.
  30. The main ethical concern regarding reproductive cloning is:
    A. Health risks to clones
    B. Cost of the procedure
    C. Difficulty of the technique
    D. Low success rate
    Answer: A
    Explanation: Health risks include premature aging, organ defects, and high miscarriage rates, as seen in animal cloning.
  31. Inverse PCR is used to amplify:
    A. DNA flanking known sequences
    B. RNA templates
    C. Whole genomes
    D. Mitochondrial DNA
    Answer: A
    Explanation: Inverse PCR amplifies unknown regions adjacent to known sequences by circularizing and cutting DNA with restriction enzymes.
  32. The primary function of a selectable marker in plasmid vectors is to:
    A. Identify transformed cells
    B. Promote DNA replication
    C. Enhance transcription
    D. Facilitate DNA sequencing
    Answer: A
    Explanation: Antibiotic resistance genes (e.g., ampᵣ) allow growth of only transformed cells in selective media.
  33. Which oncogene encodes a transcription factor activated in Burkitt lymphoma?
    A. MYC
    B. RAS
    C. SRC
    D. FOS
    Answer: A
    Explanation: t(8;14) translocation places MYC under immunoglobulin enhancer control, causing overexpression.
  34. In multiplex PCR:
    A. Multiple genes are amplified in one reaction
    B. PCR products are cloned directly
    C. RNA is reverse transcribed
    D. DNA is sequenced in real-time
    Answer: A
    Explanation: Uses multiple primer pairs to amplify several targets simultaneously (e.g., pathogen detection).
  35. The “VNTR” in DNA fingerprinting refers to:
    A. Variable Number Tandem Repeats
    B. Viral Nucleotide Transfer RNA
    C. Verified Non-Transcribed Region
    D. Vector-mediated Nucleotide Transfer
    Answer: A
    Explanation: VNTRs (10–100 bp repeats) were used in early DNA fingerprinting but largely replaced by STRs.
  36. TP53 gene mutations are most commonly associated with:
    A. Li-Fraumeni syndrome
    B. Familial adenomatous polyposis
    C. Neurofibromatosis type 1
    D. Von Hippel-Lindau syndrome
    Answer: A
    Explanation: Germline TP53 mutations cause Li-Fraumeni syndrome, increasing risk of multiple cancers.
  37. The main advantage of nanopore sequencing over PCR is:
    A. Direct long-read sequencing without amplification
    B. Higher error rate
    C. Requirement for DNA amplification
    D. Limited to short DNA fragments
    Answer: A
    Explanation: Nanopore tech (e.g., Oxford Nanopore) sequences DNA/RNA directly in real-time, avoiding PCR bias.
  38. Induced pluripotent stem cells (iPSCs) are generated by:
    A. Reprogramming somatic cells with transcription factors
    B. Somatic cell nuclear transfer
    C. Embryo splitting
    D. CRISPR-Cas9 editing
    Answer: A
    Explanation: Yamanaka factors (OCT4, SOX2, KLF4, c-MYC) reprogram adult cells to pluripotent state.
  39. The APC gene is a tumor suppressor associated with:
    A. Colorectal cancer
    B. Breast cancer
    C. Melanoma
    D. Glioblastoma
    Answer: A
    Explanation: APC mutations cause familial adenomatous polyposis (FAP), leading to colorectal cancer.
  40. In DNA fingerprinting, the Combined DNA Index System (CODIS) utilizes:
    A. 13 core STR loci
    B. VNTR polymorphisms
    C. Mitochondrial DNA SNPs
    D. Whole-genome sequencing
    Answer: A
    Explanation: CODIS database uses 13 STR loci for forensic identification with high discrimination power.
  41. Gateway cloning relies on:
    A. Site-specific recombination (λ phage)
    B. Restriction enzyme digestion
    C. T4 DNA ligase
    D. Homologous recombination
    Answer: A
    Explanation: Uses λ phage att sites and BP/LR clonase enzymes for rapid, high-efficiency cloning.
  42. The MDM2 oncogene promotes cancer by:
    A. Degrading p53 protein
    B. Activating DNA repair
    C. Inhibiting angiogenesis
    D. Promoting apoptosis
    Answer: A
    Explanation: MDM2 ubiquitinates p53 for proteasomal degradation, inactivating tumor suppression.
  43. Digital PCR (dPCR) differs from qPCR in its ability to:
    A. Quantify absolute copy number without standards
    B. Measure fluorescence in real-time
    C. Amplify RNA targets
    D. Detect large chromosomal deletions
    Answer: A
    Explanation: dPCR partitions samples into nanoreactors for endpoint quantification, enabling absolute copy number measurement.
  44. The ethical concern specific to reproductive cloning is:
    A. Identity and autonomy of the clone
    B. Cost of the procedure
    C. Efficiency of somatic cell transfer
    D. Use of embryonic stem cells
    Answer: A
    Explanation: Primary issues include loss of genetic uniqueness and psychological impact on the cloned individual.
  45. CRISPR-Cas9 gene editing was adapted from:
    A. Bacterial adaptive immunity
    B. Retroviral replication
    C. Eukaryotic RNA interference
    D. Archaeal DNA repair
    Answer: A
    Explanation: Based on CRISPR arrays in bacteria that store viral DNA memories for targeted cleavage.

 

 

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