Molecular Biology and Genomics — MCQs

Molecular Biology and Genomics Indian Medical PG Practice Questions and MCQs

Question 91: Which of the following is a non-sense codon?

A. UGG
B. AUG
C. UGA (Correct Answer)
D. CCA

Explanation: ### Explanation **Correct Option: C (UGA)** In molecular biology, a **nonsense codon** (or stop codon) is a trinucleotide sequence within messenger RNA (mRNA) that signals the termination of translation. There are three nonsense codons in the standard genetic code: 1. **UAA** (Ochre) 2. **UAG** (Amber) 3. **UGA** (Opal) These codons do not code for any amino acid. Instead, they are recognized by **release factors**, which trigger the hydrolysis of the ester bond linking the tRNA to the polypeptide chain, effectively ending protein synthesis. **Analysis of Incorrect Options:** * **A. UGG:** This is a sense codon that codes for the amino acid **Tryptophan**. It is unique because, along with Methionine, it is one of only two amino acids coded by a single codon. * **B. AUG:** This is the **initiation (start) codon**. It codes for **Methionine** in eukaryotes and N-formylmethionine (fMet) in prokaryotes. It sets the reading frame for translation. * **D. CCA:** This codes for the amino acid **Proline**. All codons ending in "A" are not necessarily stop codons; the specific sequence matters. **NEET-PG High-Yield Pearls:** * **Nonsense Mutation:** A point mutation that changes a sense codon into a nonsense codon, leading to a truncated (shortened) and usually non-functional protein. * **Exceptions to the Code:** In human **mitochondria**, UGA is not a stop codon; it codes for **Tryptophan**. Conversely, AGA and AGG (normally Arginine) serve as stop codons in mitochondria. * **Ambigous vs. Degenerate:** The genetic code is **unambiguous** (one codon = one amino acid) and **degenerate/redundant** (one amino acid can have multiple codons).

Question 92: Which enzyme is responsible for DNA repair proofreading in prokaryotes?

A. DNA Polymerase I
B. DNA Polymerase II (Correct Answer)
C. DNA Polymerase III
D. Gyrase

Explanation: **Explanation:** **Correct Answer: B. DNA Polymerase II** In prokaryotes (*E. coli*), **DNA Polymerase II** is specifically specialized for **DNA repair**. While it possesses $5' \to 3'$ polymerase activity, its primary role is triggered when the replication fork stalls due to DNA damage. It acts as a backup enzyme in the SOS repair mechanism and possesses $3' \to 5'$ exonuclease activity for proofreading, ensuring high fidelity during the repair of inter-strand cross-links and bulky lesions. **Analysis of Incorrect Options:** * **A. DNA Polymerase I:** Known as the "Kornberg enzyme," its primary roles are **primer removal** (via $5' \to 3'$ exonuclease activity) and filling gaps during lagging strand synthesis. While it participates in excision repair, it is not the primary "specialized" repair polymerase. * **C. DNA Polymerase III:** This is the **primary replicative enzyme** responsible for the bulk of de novo DNA synthesis. Although it has $3' \to 5'$ proofreading activity during replication, its main function is elongation, not dedicated DNA repair. * **D. Gyrase (Topoisomerase II):** This enzyme does not have polymerase or proofreading activity. Its function is to relieve **torsional strain** (supercoiling) ahead of the replication fork by creating double-stranded breaks. **High-Yield Clinical Pearls for NEET-PG:** * **Prokaryotic Proofreading:** All three major DNA polymerases (I, II, and III) possess $3' \to 5'$ exonuclease activity (proofreading). * **Unique Feature:** Only **DNA Polymerase I** has $5' \to 3'$ exonuclease activity (essential for removing RNA primers). * **Eukaryotic Counterpart:** DNA Polymerase $\beta$ is the eukaryotic enzyme primarily involved in Base Excision Repair (BER). * **Quinolones:** Drugs like Ciprofloxacin target **DNA Gyrase** in bacteria, inhibiting replication.

Question 93: After digestion by restriction endonucleases, DNA strands can be joined again by which enzyme?

A. DNA polymerase
B. DNA ligase (Correct Answer)
C. DNA topoisomerase
D. DNA gyrase

Explanation: **Explanation:** **DNA ligase** is the correct answer because it acts as the "molecular glue" of the cell. After restriction endonucleases cut DNA (producing either "sticky" or "blunt" ends), DNA ligase facilitates the joining of these strands by catalyzing the formation of a **phosphodiester bond** between the 3'-hydroxyl group of one nucleotide and the 5'-phosphate group of another. This process requires energy, typically in the form of **ATP** (in eukaryotes and T4 phage) or **NAD+** (in some bacteria). **Analysis of Incorrect Options:** * **DNA polymerase:** Its primary role is the synthesis of new DNA strands by adding deoxynucleotides to a pre-existing primer during replication or repair; it cannot join two independent double-stranded fragments. * **DNA topoisomerase:** These enzymes regulate the overwinding or underwinding of DNA. They relieve torsional strain by making transient single-strand (Type I) or double-strand (Type II) breaks, but they do not function to permanently join recombinant DNA fragments. * **DNA gyrase:** A specific type of bacterial Topoisomerase II that introduces negative supercoils. It is a target for fluoroquinolone antibiotics (e.g., Ciprofloxacin) but is not used for joining DNA strands in cloning. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Genetic Engineering:** DNA ligase is indispensable in recombinant DNA technology for inserting a gene of interest into a plasmid vector. * **Okazaki Fragments:** In vivo, DNA ligase is essential for joining Okazaki fragments on the lagging strand during DNA replication. * **Clinical Correlation:** Mutations in the *LIG4* gene (DNA Ligase IV) lead to **LIG4 syndrome**, characterized by immunodeficiency, microcephaly, and sensitivity to ionizing radiation due to defective double-strand break repair.

Question 94: If codon no 302 UAG is replaced by UAA, then this mutation is:

A. Missense
B. Silent (Correct Answer)
C. Nonsense
D. Given information is not sufficient to identify

Explanation: **Explanation:** The correct answer is **Silent mutation** because both **UAG** and **UAA** are **Stop Codons** (Nonsense codons). 1. **Why it is Silent:** In the genetic code, there are three termination codons: **UAA** (Ochre), **UAG** (Amber), and **UGA** (Opal). These codons do not code for any amino acid; instead, they signal the termination of translation. Since the mutation changes one stop codon (UAG) to another stop codon (UAA), the resulting polypeptide chain remains identical in length and composition. Because there is no change in the final protein product, it is classified as a silent mutation. 2. **Why other options are incorrect:** * **Missense:** This occurs when a point mutation changes a codon such that it codes for a *different* amino acid (e.g., GAA to GUA). * **Nonsense:** This occurs when a codon coding for an amino acid is changed into a stop codon, leading to premature termination. Here, the site was *already* a stop codon. * **Insufficient Information:** The identity of all three stop codons is a fundamental fact in molecular biology, making the information provided sufficient. **High-Yield NEET-PG Pearls:** * **Stop Codons:** UAA (Ochre), UAG (Amber), UGA (Opal). *Mnemonic: **U** **A**re **A**way, **U** **A**re **G**one, **U** **G**o **A**way.* * **Degeneracy of Genetic Code:** Multiple codons coding for the same amino acid (usually differing at the 3rd base/Wobble position) is the most common cause of silent mutations. * **Transition vs. Transversion:** UAG to UAA is a **transversion** (G is a purine, A is a purine—wait, G to A is actually a **transition**). *Correction:* Purine to Purine (A↔G) or Pyrimidine to Pyrimidine (C↔U) is a **Transition**.

Question 95: The ends of chromosomes are replicated by which enzyme?

A. Telomerase (Correct Answer)
B. Centromere
C. Restriction endonuclease
D. Exonuclease

Explanation: ### Explanation **1. Why Telomerase is Correct:** DNA polymerase requires a RNA primer to initiate synthesis and can only add nucleotides in a 5' to 3' direction. During lagging strand synthesis, once the terminal RNA primer is removed, there is no upstream 3'-OH group available for DNA polymerase to fill the gap. This is known as the **"End Replication Problem."** To prevent the progressive shortening of chromosomes, the enzyme **Telomerase** (a specialized **Reverse Transcriptase**) adds repetitive DNA sequences (TTAGGG in humans) to the 3' end. It carries its own internal RNA template, making it a **ribonucleoprotein**. **2. Why Other Options are Incorrect:** * **Centromere:** This is a structural region of the chromosome (not an enzyme) that joins sister chromatids and serves as the attachment site for spindle fibers during cell division. * **Restriction Endonuclease:** These are bacterial enzymes used in recombinant DNA technology to cut DNA at specific palindromic sequences. They are not involved in normal cellular DNA replication. * **Exonuclease:** These enzymes remove nucleotides one at a time from the ends of a DNA molecule (e.g., 3'→5' proofreading activity of DNA Polymerase). They degrade or trim DNA rather than replicating chromosome ends. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Cellular Aging:** Telomerase activity is high in germ cells and stem cells but low or absent in somatic cells, leading to "replicative senescence" (Hayflick limit). * **Cancer:** Approximately 85-90% of cancer cells upregulate telomerase to achieve immortality. * **Shelterin Complex:** A group of proteins that protect telomeres from being recognized as DNA double-strand breaks. * **Dyskeratosis Congenita:** A genetic disorder caused by mutations in telomerase components, leading to premature aging and bone marrow failure.

Question 96: What is the term for a segment of DNA that codes for a functional product, such as a protein or RNA molecule?

A. Codon
B. Anticodon
C. Cistron (Correct Answer)
D. Okazaki fragment

Explanation: ### Explanation **Correct Answer: C. Cistron** **1. Why Cistron is Correct:** A **cistron** is the functional unit of DNA that contains the genetic information required to synthesize a single polypeptide chain or a functional RNA molecule. The term is derived from the "cis-trans" test, which historically defined a genetic unit of function. In molecular biology, it is often used interchangeably with "gene." * **High-Yield Concept:** Prokaryotic mRNA is typically **polycistronic** (one mRNA codes for multiple proteins), whereas eukaryotic mRNA is **monocistronic** (one mRNA codes for a single protein). **2. Why Other Options are Incorrect:** * **A. Codon:** A sequence of three consecutive nucleotides in DNA or mRNA that specifies a single amino acid or a termination signal during protein synthesis. It is a subunit of a cistron, not the whole functional unit. * **B. Anticodon:** A sequence of three nucleotides found on **tRNA** that is complementary to a specific codon on mRNA. It ensures the correct amino acid is added to the growing polypeptide chain. * **D. Okazaki fragment:** Short sequences of DNA nucleotides synthesized discontinuously on the **lagging strand** during DNA replication. These are later joined by DNA ligase. **3. NEET-PG Clinical Pearls & High-Yield Facts:** * **Introns vs. Exons:** In eukaryotes, cistrons are interrupted by non-coding sequences called **introns** (intervening sequences), which are removed during splicing. **Exons** are the expressed sequences. * **Polycistronic mRNA:** This is a hallmark of bacterial operons (e.g., *Lac operon*), allowing for the coordinated regulation of enzymes in a single metabolic pathway. * **Muton and Recon:** Occasionally asked terms; a **Muton** is the smallest unit of DNA capable of mutation, and a **Recon** is the smallest unit capable of recombination.

Question 97: What does ORF stand for?

A. Open reading frame (Correct Answer)
B. Oncocytic removing fraction
C. Oncogenic removing frequency
D. Oil fraction in blood

Explanation: **Explanation:** **Why the correct answer is right:** An **Open Reading Frame (ORF)** is a continuous stretch of DNA sequence that has the potential to be translated into a protein. It is defined by the presence of a **Start Codon** (typically AUG) at the beginning, followed by a series of codons representing amino acids, and ending with a **Stop Codon** (UAA, UAG, or UGA) in the same reading frame. In molecular biology, identifying an ORF is the first step in gene prediction, as it indicates a protein-coding region. **Why the incorrect options are wrong:** * **Options B and C:** "Oncocytic removing fraction" and "Oncogenic removing frequency" are fabricated terms. While "oncogenic" refers to tumor formation, these specific phrases do not exist in standard biochemical or genomic nomenclature. * **Option D:** "Oil fraction in blood" is irrelevant to molecular biology. While lipids (fats) are present in blood, they are measured as lipoproteins (HDL, LDL, VLDL) or triglycerides, not as an "oil fraction." **High-Yield Clinical Pearls for NEET-PG:** * **Frameshift Mutations:** Deletion or insertion of nucleotides (not in multiples of three) shifts the reading frame, often resulting in a premature stop codon and a truncated, non-functional protein (e.g., Duchenne Muscular Dystrophy). * **Polycistronic vs. Monocistronic:** Prokaryotic mRNA often contains multiple ORFs (polycistronic), whereas eukaryotic mRNA typically contains only one (monocistronic). * **Bioinformatics:** In genomic studies, a sequence is generally considered a functional ORF if it exceeds a minimum length (e.g., 100 codons) without an intervening stop codon.

Question 98: A codon consists of how many nucleotide bases?

A. 3 base pairs (Correct Answer)
B. 2 base pairs
C. 2 nucleotides
D. 5 base pairs

Explanation: **Explanation:** The genetic code is the set of rules by which information encoded in genetic material is translated into proteins. A **codon** is defined as a sequence of **three consecutive nucleotides** (often referred to as base pairs in the context of double-stranded DNA) in DNA or mRNA that specifies a single amino acid during protein synthesis. **Why Option A is Correct:** The triplet nature of the codon is a mathematical necessity. There are 20 standard amino acids but only 4 nitrogenous bases (A, U/T, G, C). * A singlet code ($4^1$) could only code for 4 amino acids. * A doublet code ($4^2$) could code for 16. * A **triplet code ($4^3$)** provides 64 possible combinations, which is more than enough to cover all 20 amino acids plus "stop" signals. **Why Other Options are Incorrect:** * **Options B & C:** Two nucleotides/base pairs would only allow for 16 combinations, failing to account for all 20 amino acids. * **Option D:** Five base pairs would create $4^5$ (1,024) combinations, which is unnecessarily complex and biologically inefficient. **High-Yield NEET-PG Pearls:** 1. **Degeneracy/Redundancy:** Most amino acids are coded by more than one codon (e.g., Leucine has 6). 2. **Non-overlapping & Commaless:** The code is read sequentially without skipping bases or sharing bases between adjacent codons. 3. **Universality:** The code is the same in almost all organisms, with rare exceptions in **mitochondrial DNA** (e.g., UGA codes for Tryptophan instead of "Stop"). 4. **Initiation Codon:** **AUG** (Methionine) is the universal start codon. 5. **Stop Codons (Nonsense Codons):** UAA (Ochre), UAG (Amber), and UGA (Opal).

Question 99: What are the consensus sequences for the initiation and termination of a gene sequence's introns?

A. GU at initiation, AG at termination (Correct Answer)
B. AG at initiation, GU at termination
C. GA at initiation, GU at termination
D. UG at initiation, AG at termination

Explanation: ### Explanation **1. The Concept: The GT-AG Rule (GU-AG in RNA)** In eukaryotic gene expression, pre-mRNA undergoes splicing to remove non-coding regions (introns) and join coding regions (exons). This process is governed by highly conserved consensus sequences at the intron-exon boundaries. * **5' Splice Site (Donor Site):** The intron begins with the dinucleotide **GU** (DNA equivalent: GT). * **3' Splice Site (Acceptor Site):** The intron ends with the dinucleotide **AG**. This is known as the **Chambon’s Rule** or the **GU-AG rule**. These sequences are recognized by the spliceosome (snRNPs) to ensure precise cleavage and ligation. **2. Analysis of Incorrect Options** * **Option B (AG at initiation, GU at termination):** This is a reversal of the actual sequence. AG is the signal for the end (acceptor site), not the start. * **Option C (GA at initiation, GU at termination):** GA is not a conserved consensus sequence for the 5' donor site. * **Option D (UG at initiation, AG at termination):** While "U" and "T" are interchangeable in RNA/DNA contexts, the standard biological convention for the donor site is GU, not UG. **3. High-Yield Clinical Pearls for NEET-PG** * **Splice Site Mutations:** Mutations in these consensus sequences (e.g., a G → A transition at the 5' site) lead to **aberrant splicing**. This can result in "exon skipping" or the retention of introns, leading to non-functional proteins. * **Clinical Example:** **β-Thalassemia** is frequently caused by mutations in the GU-AG splice sites of the β-globin gene. * **The Lariat Loop:** During splicing, the 5' GU end attaches to an internal **Adenine (Branch point)**, forming a lariat-shaped structure before the 3' AG site is cleaved. * **Autoimmunity:** Antibodies against snRNPs (e.g., **Anti-Smith antibodies**) are highly specific diagnostic markers for **Systemic Lupus Erythematosus (SLE)**.

Question 100: Which of the following is NOT true about DNA supercoiling?

A. Underwinding results in negative superhelical density and supercoiling.
B. Superhelical density depends on the length of DNA.
C. Underwinding strain is normally accommodated by strand separation. (Correct Answer)
D. Topoisomerase II changes linking number in increments of 2.

Explanation: ### Explanation **1. Why Option C is the correct (NOT true) statement:** While underwinding (negative supercoiling) does facilitate strand separation (e.g., during replication and transcription), the strain is **normally accommodated by the formation of supercoils**, not by permanent strand separation. In a cellular environment, DNA is maintained in a negatively supercoiled state because it is more compact and energetically stores the tension required to open the helix when enzymes need access. Strand separation is a local, transient event, whereas supercoiling is the global structural solution to underwinding. **2. Analysis of other options:** * **Option A:** True. Underwinding (fewer helical turns than the B-form relaxed state) leads to **negative supercoiling**. This is the predominant form of DNA in both prokaryotes and eukaryotes. * **Option B:** True. Superhelical density ($\sigma$) is defined as the change in linking number ($\Delta Lk$) divided by the linking number of the relaxed DNA ($Lk_0$). Since $Lk_0$ is directly proportional to the number of base pairs, superhelical density is dependent on the **length of the DNA**. * **Option D:** True. **Topoisomerase II** (e.g., DNA Gyrase) works by breaking both strands of the double helix, passing another segment through the break, and resealing it. This mechanism changes the Linking Number ($Lk$) by **steps of 2**. (Note: Topoisomerase I changes $Lk$ by increments of 1). ### High-Yield Clinical Pearls for NEET-PG * **DNA Gyrase:** A bacterial Type II Topoisomerase that introduces negative supercoils. It is the specific target of **Fluoroquinolones** (e.g., Ciprofloxacin). * **Topoisomerase II Inhibitors:** Drugs like **Etoposide** and **Teniposide** inhibit human Topo II and are used as anticancer agents. * **Topoisomerase I Inhibitors:** **Irinotecan** and **Topotecan** target Topo I. * **Linking Number ($Lk$):** An invariant topological property of covalently closed circular DNA; it can only be changed by breaking and rejoining the DNA backbone via Topoisomerases.

Practice by Chapter

DNA Replication and Repair Mechanisms

Practice Questions

Transcription Factors and Gene Regulation

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Epigenetics and DNA Methylation

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RNA Processing and Splicing

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miRNA and RNA Interference

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Protein Synthesis and Post-Translational Modifications

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Genomics and Human Genome Project

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Single Nucleotide Polymorphisms

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Gene Therapy Approaches

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CRISPR-Cas9 and Genome Editing

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DNA Fingerprinting and Forensics

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Molecular Basis of Genetic Diseases

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