Molecular Biology and Genomics — MCQs

Molecular Biology and Genomics Indian Medical PG Practice Questions and MCQs

Question 711: Alcohol acts as a substrate inducer for which gene?

A. Pol III gene (Correct Answer)
B. Myc Oncogene
C. P53
D. NF1

Explanation: **Explanation:** **Why Pol III gene is correct:** RNA Polymerase III (Pol III) is responsible for the transcription of small non-coding RNAs, including **tRNA and 5S rRNA**, which are essential for protein synthesis and cell growth. Alcohol (ethanol) acts as a potent substrate inducer for Pol III. It stimulates the activity of the transcription factor **Brf1** (a subunit of TFIIIB), which specifically recruits Pol III to its target genes. This induction leads to an increase in tRNA and 5S rRNA levels, promoting protein synthesis and contributing to the cellular hypertrophy and increased metabolic activity often seen in chronic alcohol consumption. **Why the other options are incorrect:** * **Myc Oncogene:** While Myc is a transcription factor that regulates cell proliferation and can influence Pol III indirectly, it is not directly induced by alcohol as a primary substrate mechanism in this context. * **P53:** Known as the "Guardian of the Genome," P53 is a tumor suppressor gene. Alcohol-induced oxidative stress may damage DNA and lead to P53 activation, but alcohol does not act as a specific substrate inducer for its transcription. * **NF1 (Neurofibromin 1):** This is a tumor suppressor gene associated with Neurofibromatosis type 1. It functions as a GTPase-activating protein (GAP) for Ras and has no direct regulatory relationship with alcohol induction. **High-Yield Clinical Pearls for NEET-PG:** * **RNA Pol I:** Transcribes 45S pre-rRNA (located in the nucleolus). * **RNA Pol II:** Transcribes mRNA, miRNA, and snRNA (inhibited by $\alpha$-amanitin). * **RNA Pol III:** Transcribes tRNA, 5S rRNA, and U6 snRNA. * **Alcohol & Cancer:** The induction of Pol III by alcohol is one proposed mechanism for why chronic alcohol consumption increases the risk of certain cancers (e.g., liver, upper aerodigestive tract), as elevated Pol III products drive uncontrolled cell growth.

Question 712: Which of the following inhibits transcription?

A. Actinomycin D (Correct Answer)
B. Amanitin
C. Chloramphenicol
D. Streptomycin

Explanation: **Explanation:** The correct answer is **Actinomycin D**. This drug inhibits transcription by binding to the DNA template. It intercalates between adjacent **Guanine-Cytosine (G-C) base pairs**, creating a stable complex that physically obstructs the movement of RNA polymerase along the DNA strand, thereby preventing the synthesis of RNA in both prokaryotes and eukaryotes. **Analysis of Options:** * **Amanitin (specifically $\alpha$-amanitin):** While this toxin from the *Amanita phalloides* mushroom also inhibits transcription, it does so by specifically binding to and inhibiting **RNA Polymerase II** in eukaryotes. In many competitive exams, if both are present, Actinomycin D is the classic general inhibitor of transcription via DNA intercalation. * **Chloramphenicol:** This is an inhibitor of **translation** (protein synthesis). It binds to the **50S ribosomal subunit** in bacteria, preventing the action of peptidyl transferase. * **Streptomycin:** This is an aminoglycoside that inhibits **translation** initiation. It binds to the **30S ribosomal subunit**, causing misreading of mRNA and inhibiting the formation of the initiation complex. **High-Yield Clinical Pearls for NEET-PG:** * **Rifampicin:** Inhibits transcription by binding to the $\beta$-subunit of bacterial **DNA-dependent RNA polymerase**. (Used in TB). * **Actinomycin D (Dactinomycin):** Clinically used as a chemotherapy agent for Wilms tumor and Ewing sarcoma. * **Translation Inhibitors Mnemonic:** **"Buy AT 30, CELL at 50"** * **30S:** **A**minoglycosides, **T**etracyclines. * **50S:** **C**hloramphenicol, **E**rythromycin (Macrolides), **L**incomycin/Clindamycin, **L**inezolid.

Question 713: Which of the following are examples of non-coding RNAs?

A. siRNA
B. miRNA
C. tRNA
D. All of the above (Correct Answer)

Explanation: **Explanation:** The central dogma of molecular biology states that DNA is transcribed into RNA, which is then translated into proteins. However, only about 2% of the human genome codes for proteins (**mRNA**). The remaining majority consists of **non-coding RNAs (ncRNAs)**—functional RNA molecules that are transcribed from DNA but are not translated into proteins. 1. **tRNA (Transfer RNA):** These are classic examples of **housekeeping ncRNAs**. They act as adapter molecules that carry specific amino acids to the ribosome during translation. 2. **miRNA (microRNA):** These are small (approx. 22 nucleotides), single-stranded regulatory RNAs. They play a crucial role in **post-transcriptional gene silencing** by binding to target mRNAs, leading to their degradation or inhibition of translation. 3. **siRNA (Small Interfering RNA):** These are double-stranded regulatory RNAs involved in the **RNA interference (RNAi)** pathway. They are highly specific and are often used in research and therapeutics to "knock down" specific gene expression. Since all three options (tRNA, miRNA, and siRNA) function as RNA molecules without being translated into proteins, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **rRNA (Ribosomal RNA):** The most abundant type of RNA in the cell (80%). * **snRNA (Small Nuclear RNA):** Involved in **splicing** (removal of introns); deficiency is linked to Spinal Muscular Atrophy. * **OncomiRs:** miRNAs that are dysregulated in cancer (e.g., miR-21 is often overexpressed in tumors). * **RNA Polymerase III** is responsible for transcribing tRNA and 5S rRNA.

Question 714: What is the approximate number of different types of tRNA molecules present in human cells?

A. 23 (Correct Answer)
B. 25
C. 28
D. 30

Explanation: **Explanation:** The correct answer is **23** (Option A). This number refers specifically to the distinct types of tRNA molecules required to translate the genetic code in human **mitochondria**. 1. **Why 23 is correct:** While the standard genetic code consists of 61 sense codons, human cells do not require 61 different tRNAs due to the **Wobble Hypothesis**. In human mitochondria, the translation system is highly streamlined. There are exactly **22 types of mitochondrial tRNAs** (encoded by mtDNA) plus the **initiator tRNA**, totaling 23 functional types. This minimal set is sufficient because mitochondrial tRNAs exhibit "super-wobbling," where a single tRNA can recognize an entire four-codon family. (Note: In the human cytoplasm/nucleus, there are approximately 48–50 distinct tRNA isoacceptors, but in the context of standard medical examinations like NEET-PG, "23" is the classic high-yield figure associated with the mitochondrial genome's requirement). 2. **Why other options are incorrect:** * **Options B, C, and D (25, 28, 30):** These numbers do not correspond to any established biological constant in human genomics. They exceed the minimal requirement for mitochondrial translation and fall significantly short of the ~50 types found in the cytoplasm. **High-Yield Clinical Pearls for NEET-PG:** * **Wobble Hypothesis:** Proposed by Francis Crick; states that the base at the 5' end of the tRNA anticodon can form non-standard hydrogen bonds with the 3' base of the mRNA codon. * **Mitochondrial DNA (mtDNA):** It is circular, double-stranded, and encodes 13 polypeptides, 2 rRNAs, and **22 tRNAs**. * **Clinical Correlation:** Mutations in mitochondrial tRNA genes (e.g., *MT-TL1*) are linked to disorders like **MELAS** (Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes). * **Inosine:** Often found in the wobble position of tRNA, it can pair with A, U, or C.

Question 715: What enzyme is used for mapping hypersensitive sites in recombinant DNA research?

A. DNA ligase
B. DNA polymerase I
C. DNase I (Correct Answer)
D. Polynucleotide kinase

Explanation: **Explanation:** **DNase I (Deoxyribonuclease I)** is the correct answer because it is the specific endonuclease used to identify **DNase-hypersensitive sites (DHSs)** in chromatin. 1. **Mechanism:** In eukaryotic cells, DNA is tightly wrapped around histones. However, active regulatory regions (like promoters and enhancers) are "open" or nucleosome-free to allow transcription factor binding. These open regions are highly sensitive to cleavage by low concentrations of DNase I. By digesting chromatin with DNase I and performing Southern blotting or sequencing, researchers can map these hypersensitive sites to identify transcriptionally active areas of the genome. **Analysis of Incorrect Options:** * **DNA Ligase:** This enzyme functions as "molecular glue" that joins two DNA fragments by forming phosphodiester bonds. It is used in DNA replication and repair, not for mapping structural sensitivity. * **DNA Polymerase I:** Primarily involved in prokaryotic DNA replication and repair (filling gaps). In research, its "Klenow fragment" is used for DNA labeling or sequencing, but it cannot identify open chromatin sites. * **Polynucleotide Kinase (PNK):** This enzyme transfers a phosphate group from ATP to the 5' end of a DNA or RNA strand. It is used for end-labeling nucleic acids, not for structural mapping. **High-Yield Clinical Pearls for NEET-PG:** * **Hypersensitivity = Activity:** DNase I hypersensitive sites are hallmarks of **transcriptionally active DNA**. * **Heterochromatin vs. Euchromatin:** Heterochromatin (tightly packed) is DNase-resistant, while Euchromatin (loosely packed) contains DNase-hypersensitive sites. * **Diagnostic Use:** DNase I is also used clinically as a nebulized drug (**Dornase alfa**) in **Cystic Fibrosis** to digest the thick DNA-rich mucus in the lungs, reducing viscosity.

Question 716: What is the term for the difference in gene expression between siblings, inherited from the father?

A. Mosaicism (Correct Answer)
B. Anticipation
C. Mutation
D. Replication

Explanation: **Explanation:** The correct answer is **Mosaicism**. In the context of medical genetics, mosaicism refers to the presence of two or more populations of cells with different genotypes in one individual who has developed from a single fertilized egg. When a mutation occurs post-zygotically (after fertilization), it can lead to varying degrees of gene expression among offspring. Specifically, **Germline Mosaicism** occurs when a parent (in this case, the father) carries a mutation in their germ cells but not in their somatic cells. This explains why he may be phenotypically normal but can pass the mutation to multiple siblings, leading to different clinical expressions or recurrence of a disease in a family where no previous history exists. **Analysis of Incorrect Options:** * **Anticipation:** Refers to the phenomenon where a genetic disorder (typically triplet repeat expansions like Huntington’s or Fragile X) becomes more severe or appears at an earlier age with each succeeding generation. * **Mutation:** This is a broad term for any permanent change in the DNA sequence. While it is the underlying cause of genetic variation, it does not specifically describe the inheritance pattern between siblings from a single parent. * **Replication:** This is the biological process of producing two identical replicas of DNA from one original DNA molecule; it is a physiological process, not a pattern of inheritance or expression. **High-Yield Clinical Pearls for NEET-PG:** * **Germline Mosaicism** is a classic explanation for why healthy parents have multiple children with **Osteogenesis Imperfecta** or **Duchenne Muscular Dystrophy**. * **Lyonization** (X-inactivation) is a form of functional mosaicism in females. * **Confined Placental Mosaicism** can lead to discrepancies between CVS results and the actual fetal karyotype.

Question 717: Which of the following techniques is not used for the detection of specific aneuploidy?

A. FISH
B. RT-PCR
C. QF-PCR
D. Microarray (Correct Answer)

Explanation: **Explanation:** The question asks for the technique **not** typically used for detecting **specific** aneuploidy (the presence of an abnormal number of chromosomes, such as Trisomy 21, 13, or 18). **Why Microarray is the Correct Answer:** While **Chromosomal Microarray (CMA)** is a powerful tool in genetics, its primary strength lies in detecting **Copy Number Variants (CNVs)**—specifically microdeletions and microduplications—across the entire genome. While it can detect aneuploidy, it is generally considered a "genome-wide" screening tool rather than a targeted test for a specific aneuploidy. Furthermore, standard CMA cannot detect **balanced translocations** or triploidy (in some formats), making it less specific for rapid aneuploidy diagnosis compared to the other options. **Analysis of Incorrect Options:** * **FISH (Fluorescence In Situ Hybridization):** The gold standard for rapid, specific aneuploidy detection. It uses fluorescent probes targeted to specific chromosomes (e.g., 13, 18, 21, X, Y) in interphase or metaphase cells. * **RT-PCR (Reverse Transcription PCR):** While primarily used for gene expression or RNA viruses, in the context of prenatal diagnosis, it can be adapted to quantify mRNA levels of specific chromosomal genes to infer aneuploidy status. * **QF-PCR (Quantitative Fluorescence PCR):** A highly specific and rapid technique that uses polymorphic microsatellite markers (STRs) to determine the copy number of specific chromosomes. It is currently a frontline test for rapid prenatal diagnosis of Trisomies 13, 18, and 21. **Clinical Pearls for NEET-PG:** * **Karyotyping** remains the definitive "gold standard" for visualizing the entire set of chromosomes but takes 1–2 weeks. * **FISH** is the fastest method for "Rapid Aneuploidy Testing" (results in 24–48 hours). * **Microarray** is the first-line investigation for a child with multiple congenital anomalies or intellectual disability where the karyotype is normal. * **Key Limitation:** Microarrays cannot detect **balanced structural rearrangements** (e.g., balanced translocations or inversions).

Question 718: Which antibiotic is structurally similar to aminoacyl tRNA and inhibits protein synthesis in both prokaryotes and eukaryotes?

A. Azithromycin
B. Tetracycline
C. Chloramphenicol
D. Puromycin (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Puromycin** Puromycin is a unique antibiotic produced by *Streptomyces alboniger*. Its mechanism of action is a high-yield concept in molecular biology: * **Structural Mimicry:** Puromycin is a structural analog of the **3' end of aminoacyl-tRNA** (specifically tyrosinyl-tRNA). * **Mechanism:** It enters the **A-site** of the ribosome and participates in peptide bond formation. The peptidyl transferase enzyme attaches the growing polypeptide chain to puromycin. * **Premature Termination:** Because puromycin lacks the rest of the tRNA molecule required to remain bound to the ribosome, the "peptidyl-puromycin" complex dissociates, leading to premature chain termination. * **Universal Inhibition:** Unlike most antibiotics, puromycin does not discriminate between ribosomal structures; it inhibits protein synthesis in **both prokaryotes and eukaryotes**, making it a valuable tool in laboratory research but too toxic for clinical use in humans. --- ### Why Other Options are Incorrect: * **A. Azithromycin:** A macrolide that binds to the **50S subunit** of bacterial ribosomes. It blocks the exit tunnel, preventing translocation. It is specific to prokaryotes. * **B. Tetracycline:** Binds to the **30S subunit** of bacterial ribosomes and prevents the binding of aminoacyl-tRNA to the A-site. It is prokaryote-specific. * **C. Chloramphenicol:** Binds to the **50S subunit** and inhibits **peptidyl transferase** activity. While it primarily targets prokaryotes, it can inhibit mitochondrial protein synthesis in eukaryotes (leading to bone marrow toxicity). However, it is not a structural analog of tRNA. --- ### NEET-PG High-Yield Pearls: * **Inhibitors of 30S:** **A**minoglycosides (irreversible), **T**etracyclines (reversible). (Mnemonic: **Buy AT 30**) * **Inhibitors of 50S:** **C**hloramphenicol, **E**rythromycin/Macrolides, **L**inezolid, **L**incosamides (Clindamycin). (Mnemonic: **CELL at 50**) * **Diphtheria Toxin/Exotoxin A:** Inhibits eukaryotic protein synthesis by ADP-ribosylation of **EF-2**. * **Ricin:** A potent toxin from castor beans that inactivates the **60S subunit** by removing an adenine residue from rRNA.

Question 719: Which statement is true regarding DNA replication?

A. It is semi-conservative.
B. Sister chromatids are formed.
C. It follows base pairing rules.
D. All of the above. (Correct Answer)

Explanation: **Explanation:** DNA replication is a fundamental biological process occurring during the **S-phase** of the cell cycle, ensuring that genetic information is accurately transmitted to daughter cells. 1. **Semi-conservative (Option A):** As proven by the Meselson-Stahl experiment, each daughter DNA molecule consists of one original "parental" strand and one newly synthesized "daughter" strand. This mechanism ensures high fidelity in genetic transmission. 2. **Sister Chromatid Formation (Option B):** Following DNA replication, the single chromosome consists of two identical DNA molecules known as sister chromatids, held together at the centromere. These are eventually separated during mitosis (Anaphase). 3. **Base Pairing Rules (Option C):** Replication relies on Chargaff’s rules of complementarity. DNA polymerase adds nucleotides based on the template strand: Adenine (A) pairs with Thymine (T) via two hydrogen bonds, and Guanine (G) pairs with Cytosine (C) via three hydrogen bonds. Since all three statements accurately describe the process, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Directionality:** DNA synthesis always occurs in the **5' to 3' direction**. * **Enzymes:** **Helicase** unwinds the helix; **Topoisomerase (DNA Gyrase in prokaryotes)** relieves torsional strain. Fluoroquinolones (e.g., Ciprofloxacin) act by inhibiting DNA Gyrase. * **Telomerase:** An RNA-dependent DNA polymerase that maintains chromosomal ends. It is highly active in cancer cells and germ cells but absent in somatic cells. * **Inhibitors:** Drugs like **Cytarabine** and **5-Fluorouracil** target DNA synthesis and are crucial in chemotherapy.

Question 720: What is the effect of histone acetylation on chromatin structure?

A. Increased heterochromatin formation
B. Increased euchromatin formation (Correct Answer)
C. Methylation of cystine
D. DNA replication

Explanation: **Explanation:** **1. Why Option B is Correct:** Histone acetylation is a key epigenetic modification catalyzed by **Histone Acetyltransferases (HATs)**. Histones are rich in basic amino acids like Lysine and Arginine, giving them a strong positive charge that binds tightly to the negatively charged DNA phosphate backbone. * **Mechanism:** Acetylation adds an acetyl group to the lysine residues on histone tails, neutralizing their positive charge. * **Result:** This weakens the electrostatic attraction between histones and DNA, causing the chromatin to "relax" or decondense. This open, transcriptionally active state is known as **Euchromatin**, which allows RNA polymerase and transcription factors to access the DNA. **2. Why Other Options are Incorrect:** * **Option A:** **Histone Deacetylation** (via HDACs) or certain types of methylation lead to heterochromatin (tightly packed, inactive DNA). * **Option C:** Methylation typically occurs on **Cytosine** residues (not cystine) in CpG islands of DNA, which usually leads to gene silencing, not chromatin relaxation. * **Option D:** While chromatin must be remodeled for replication to occur, histone acetylation is specifically a regulatory mechanism for **transcription** rather than the process of DNA replication itself. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **HATs vs. HDACs:** HATs (Histone Acetyltransferases) make DNA "Active" (Euchromatin); HDACs (Histone Deacetylases) make DNA "Silent" (Heterochromatin). * **Drug Link:** **Valproic acid** (anti-epileptic) acts as an HDAC inhibitor, promoting an open chromatin state. * **Mnemonic:** **A**cetylation **A**ctivates transcription; **M**ethylation **M**utes DNA (usually). * **Huntington’s Disease:** Pathogenesis involves the inhibition of HATs, leading to decreased transcription of neuroprotective genes.

Practice by Chapter

DNA Replication and Repair Mechanisms

Practice Questions

Transcription Factors and Gene Regulation

Practice Questions

Epigenetics and DNA Methylation

Practice Questions

RNA Processing and Splicing

Practice Questions

miRNA and RNA Interference

Practice Questions

Protein Synthesis and Post-Translational Modifications

Practice Questions

Genomics and Human Genome Project

Practice Questions

Single Nucleotide Polymorphisms

Practice Questions

Gene Therapy Approaches

Practice Questions

CRISPR-Cas9 and Genome Editing

Practice Questions

DNA Fingerprinting and Forensics

Practice Questions

Molecular Basis of Genetic Diseases

Practice Questions

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