Molecular Biology and Genomics Practice Questions

Q: Which of the following is not a stop codon?

UGG. ### Explanation In the genetic code, **stop codons** (also known as nonsense codons) are specific nucleotide triplets within messenger RNA (mRNA) that signal the termination of translation. When a ribosome encounters a stop codon, no corresponding transfer RNA (tRNA) binds; instead, **release factors** bind to the ribosome, causing the newly synthesized polypeptide chain to be released. **Why UGG is the correct answer:** **UGG** is not a stop codon; it is the specific codon that codes for the amino acid **Tryptophan**. Tryptophan and Methionine (AUG) are unique because they are the only two amino acids encoded by a single codon each. **Analysis of incorrect options:** There are three standard stop codons in the universal genetic code: * **UAG (Amber):** A stop codon that signals the end of translation. * **UAA (Ochre):** The most common stop codon used in bacteria. * **UGA (Opal):** A stop codon in the universal code (though it notably codes for Selenocysteine in specific contexts). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** To remember the stop codons, use: **U** **A**re **G**one (UAG), **U** **A**re **A**way (UAA), and **U** **G**o **A**way (UGA). * **Nonsense Mutation:** A point mutation that changes a functional codon into a stop codon, leading to a truncated, usually non-functional protein (e.g., in some forms of β-thalassemia). * **Mitochondrial Exception:** In human mitochondria, the genetic code differs slightly; **UGA** codes for Tryptophan instead of acting as a stop codon, and **AGA/AGG** act as stop codons instead of coding for Arginine. * **21st Amino Acid:** **Selenocysteine** is often referred to as the 21st amino acid and is encoded by the UGA codon when a specific insertion sequence (SECIS) is present.

Q: Which of the following is false about telomerase?

Telomerase leads to premature aging.. **Explanation:** Telomerase is a specialized enzyme responsible for maintaining the length of telomeres (repetitive DNA sequences at the ends of linear chromosomes). **Why Option D is the correct (false) statement:** Telomerase activity is associated with **immortality and cellular longevity**, not premature aging. It prevents the "end-replication problem" by adding TTAGGG repeats to the 3' end of DNA. **Premature aging syndromes** (like Progeria or Werner syndrome) are actually caused by **shortened telomeres** or a **deficiency/absence** of telomerase activity. When telomeres become critically short, the cell enters senescence (the Hayflick limit). **Analysis of other options:** * **Option A (True):** Telomerase is a specialized **reverse transcriptase** (specifically TERT: Telomerase Reverse Transcriptase). It uses an RNA template to synthesize DNA. * **Option B (True):** It contains an **intrinsic RNA template** (TERC: Telomerase RNA Component) that acts as a guide/primer for the synthesis of telomeric repeats. * **Option C (True):** It is a **ribonucleoprotein** because it is a complex consisting of both a protein catalytic subunit (TERT) and an RNA molecule (TERC). **Clinical Pearls for NEET-PG:** * **Cancer Connection:** Telomerase is highly active in **85-90% of cancer cells**, allowing them to divide indefinitely (immortality). * **Stem Cells:** It is normally active in germ cells, stem cells, and lymphocytes, but absent in most somatic cells. * **Shelterin Complex:** A group of proteins that protects telomeres from being recognized as DNA damage (double-strand breaks).

Q: A 10-year-old female patient with a known history of beta-thalassemia complains of tiredness and shortness of breath. Beta-thalassemia is caused by faulty splicing of which of the following?

hnRNA. **Explanation:** **1. Why hnRNA is Correct:** Beta-thalassemia is a genetic blood disorder characterized by reduced or absent synthesis of the beta-globin chains of hemoglobin. In many cases, the underlying molecular defect is a mutation in the **introns** or at the **splice site junctions** of the beta-globin gene. The primary transcript produced immediately after transcription is **hnRNA (heterogeneous nuclear RNA)**, also known as pre-mRNA. This hnRNA contains both exons (coding) and introns (non-coding). For functional mRNA to be formed, introns must be removed via **splicing**. Mutations in beta-thalassemia often create "cryptic" splice sites, leading to incorrect splicing of the hnRNA. This results in defective mRNA, which is either degraded or translated into non-functional proteins, leading to a deficiency of beta-globin. **2. Why Other Options are Incorrect:** * **snRNA (small nuclear RNA):** These molecules complex with proteins to form **snRNPs** ("snurps"), which are the *machinery* (spliceosome) that performs the splicing. While they facilitate the process, they are not the molecule being spliced. * **scRNA (small cytoplasmic RNA):** These are involved in protein targeting (e.g., Signal Recognition Particle) and are not involved in the splicing of globin genes. * **snoRNA (small nucleolar RNA):** These play a role in the post-transcriptional modification of **rRNA** (ribosomal RNA) within the nucleolus, not mRNA splicing. **Clinical Pearls for NEET-PG:** * **Post-transcriptional modifications** of hnRNA include: 5' Capping, 3' Polyadenylation, and Splicing. * **Splice site mutations** are a classic cause of $\beta^+$-thalassemia (reduced synthesis) or $\beta^0$-thalassemia (total absence). * **High-yield association:** Systemic Lupus Erythematosus (SLE) involves antibodies against snRNPs (**Anti-Smith antibodies**).

Q: Actinomycin D interferes with enzyme induction by combining with which of the following?

Deoxyribonucleic acid (DNA). ### Explanation **Correct Answer: B. Deoxyribonucleic acid (DNA)** **Mechanism of Action:** Actinomycin D (also known as Dactinomycin) is a potent polypeptide antibiotic that functions as a **transcription inhibitor**. It exerts its effect by binding specifically to **double-stranded DNA**. It intercalates between adjacent **Guanine-Cytosine (G-C) base pairs**, forming a stable complex. This physical obstruction prevents the movement of **RNA Polymerase** along the DNA template, thereby blocking the synthesis of messenger RNA (mRNA). Since enzyme induction requires the transcription of new mRNA to produce specific proteins, Actinomycin D effectively interferes with this process. **Analysis of Incorrect Options:** * **A. Transfer RNA (tRNA):** Actinomycin D does not bind to tRNA. tRNA is involved in the translation phase (carrying amino acids), whereas this drug acts at the transcriptional level. * **C. Ribosomal RNA (rRNA):** While Actinomycin D can inhibit the synthesis of rRNA (especially at low doses in the nucleolus), its primary site of binding is the DNA template itself, not the RNA product. * **D. Repressor protein:** Repressor proteins bind to the operator region of DNA to inhibit transcription naturally (e.g., in the Lac operon). Actinomycin D is an exogenous chemical agent that binds to DNA directly, not a protein-protein regulator. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Use:** Actinomycin D is a key chemotherapeutic agent used in pediatric oncology, specifically for **Wilms tumor**, **Ewing sarcoma**, and **Rhabdomyosarcoma**. It is also used in **Gestational Trophoblastic Neoplasia (Choriocarcinoma)**. * **Key Distinction:** Unlike **Rifampicin** (which binds directly to bacterial RNA Polymerase), Actinomycin D binds to the **DNA template**. * **Toxicity:** It is a potent vesicant and can cause significant bone marrow suppression and "radiation recall" phenomenon.

Q: The CAP protein in the lac operon serves as an example of which of the following?

Positive regulator. ### Explanation **1. Why Option A is Correct:** The **Catabolite Activator Protein (CAP)**, also known as cAMP Receptor Protein (CRP), is a classic example of a **positive regulator**. In the absence of glucose, levels of cyclic AMP (cAMP) rise. cAMP binds to CAP, forming a cAMP-CAP complex. This complex binds to a specific site near the *lac* promoter, enhancing the affinity of RNA polymerase for the promoter. This "recruitment" significantly increases the rate of transcription. Therefore, CAP acts as an activator that "turns on" or upregulates gene expression. **2. Why Other Options are Incorrect:** * **B. Negative Regulator:** This refers to the **Lac Repressor protein** (encoded by the *lacI* gene). The repressor binds to the operator to block transcription; CAP does the opposite. * **C. Attenuation:** This is a regulatory mechanism seen in the **Tryptophan (*trp*) operon**, involving premature termination of transcription based on the speed of translation. It is not a feature of the *lac* operon. * **D. Constitutive Expression:** This refers to genes that are expressed at a constant rate regardless of environmental conditions (e.g., "housekeeping genes"). The *lac* operon is **inducible**, not constitutive. **3. High-Yield Clinical Pearls for NEET-PG:** * **Glucose Effect:** The *lac* operon is subject to "Catabolite Repression." Even if lactose is present, the operon is not fully active if glucose is available, because glucose inhibits Adenylate Cyclase, lowering cAMP levels and preventing CAP binding. * **Dual Control:** Remember that for maximal *lac* operon expression, two conditions must be met: **High Lactose** (to remove the repressor) and **Low Glucose** (to allow CAP binding). * **DNA Binding Motif:** CAP utilizes a **Helix-turn-helix** motif to bind to DNA, a common feature in prokaryotic regulatory proteins.

Q: A study of peripheral blood smears shows that neutrophil nuclei of women have a Barr body, whereas those of men do not. The Barr body is an inactivated X chromosome. Which of the following forms of RNA is most likely to play a role in Barr body formation?

lncRNA. **Explanation:** The correct answer is **lncRNA (Long non-coding RNA)**. **1. Why lncRNA is correct:** The Barr body represents an inactivated X chromosome (Lyonization), a process essential for dosage compensation in females. This inactivation is mediated by the **XIST gene** (*X-inactive specific transcript*), located in the X-inactivation center (XIC). The XIST gene produces a unique type of RNA that does not code for proteins; instead, it is a **long non-coding RNA (lncRNA)** [1]. XIST lncRNA "coats" the X chromosome from which it is transcribed, triggering gene silencing through chromatin remodeling and DNA methylation, resulting in the formation of heterochromatin (the Barr body) [1]. **2. Why other options are incorrect:** * **mRNA (Messenger RNA):** These are coding RNAs that serve as templates for protein synthesis. * **miRNA (microRNA):** These are small (approx. 22 nucleotides) non-coding RNAs that typically regulate gene expression post-transcriptionally by causing mRNA degradation or inhibiting translation [2]. * **siRNA (Small interfering RNA):** These are double-stranded RNAs involved in the RNA interference (RNAi) pathway, primarily acting to silence specific target genes by mRNA cleavage. **Clinical Pearls for NEET-PG:** * **Formula for Barr Bodies:** Number of Barr bodies = (Total X chromosomes - 1). * *Turner Syndrome (45,XO):* 0 Barr bodies [1]. * *Klinefelter Syndrome (47,XXY):* 1 Barr body. * **Morphology:** In neutrophils, the Barr body appears as a **"Drumstick"** appendage on the nucleus. * **XIST vs. TSIX:** While XIST promotes inactivation, its antisense transcript **TSIX** prevents inactivation on the active X chromosome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 16-17.

Q: Which of the following is NOT a disease of defective DNA repair?

Adenosis polyposis coli. **Explanation:** The correct answer is **Adenosis polyposis coli (APC)**. **1. Why APC is the correct answer:** Familial Adenomatous Polyposis (FAP) is caused by a mutation in the **APC gene**, which is a **tumor suppressor gene** involved in the **Wnt signaling pathway**. The APC protein normally promotes the degradation of β-catenin. When mutated, β-catenin accumulates, translocates to the nucleus, and triggers the transcription of genes (like *c-myc*) that drive cell proliferation. It is a defect in **cell signaling and growth regulation**, not a direct defect in DNA repair mechanisms. **2. Analysis of incorrect options (DNA Repair Defects):** * **Severe Combined Immunodeficiency (SCID):** Specifically, the **RS-SCID** variant is caused by mutations in genes like *DCLRE1C* (Artemis), which are essential for **Non-Homologous End Joining (NHEJ)** during V(D)J recombination. * **Bloom Syndrome:** Caused by a mutation in the *BLM* gene, which encodes a **DNA Helicase**. This leads to genomic instability due to defective repair during DNA replication (homologous recombination). * **BRCA 1:** This gene is critical for the repair of double-strand breaks via **Homologous Recombination**. Mutations lead to an inability to repair DNA damage, significantly increasing the risk of breast and ovarian cancers. **Clinical Pearls for NEET-PG:** * **Hereditary Non-Polyposis Colorectal Cancer (HNPCC/Lynch Syndrome):** Often confused with APC, this *is* a DNA repair defect (specifically **Mismatch Repair/MMR**). * **Xeroderma Pigmentosum:** Defect in **Nucleotide Excision Repair (NER)**; inability to repair UV-induced thymine dimers. * **Ataxia Telangiectasia:** Defect in the *ATM* gene, which senses double-strand breaks. * **Fanconi Anemia:** Defect in the repair of DNA inter-strand cross-links.

Question 1

Which of the following is not a stop codon?

Accepted Answer

UGG

Answer

UAG

Answer

UAA

Answer

UGA

Question 2

A cell is placed in a medium containing radioactively labelled thymidine. After the cells undergo replication 3 times, what percentage of the cells will have both strands of DNA labelled?

Accepted Answer

75%

Answer

25%

Answer

50%

Answer

100%

Question 3

Which of the following is false about telomerase?

Accepted Answer

Telomerase leads to premature aging.

Answer

Has reverse transcriptase activity.

Answer

Has an intrinsic primer.

Answer

It is a ribonucleoprotein.

Question 4

A 10-year-old female patient with a known history of beta-thalassemia complains of tiredness and shortness of breath. Beta-thalassemia is caused by faulty splicing of which of the following?

Accepted Answer

hnRNA

Answer

snRNA

Answer

scRNA

Answer

snoRNA

Question 5

Which of the following statements about transposons is NOT true?

Accepted Answer

They modulate the translation of target messenger RNAs into their corresponding proteins.

Answer

They are popularly known as jumping genes.

Answer

They are mobile genetic elements.

Answer

They are implicated in gene regulation and chromatin organization.

Question 6

Actinomycin D interferes with enzyme induction by combining with which of the following?

Accepted Answer

Deoxyribonucleic acid (DNA)

Answer

Transfer RNA (tRNA)

Answer

Ribosomal RNA (rRNA)

Answer

Repressor protein

Question 7

The CAP protein in the lac operon serves as an example of which of the following?

Accepted Answer

Positive regulator

Answer

Negative regulator

Answer

Attenuation

Answer

Constitutive expression

Question 8

A study of peripheral blood smears shows that neutrophil nuclei of women have a Barr body, whereas those of men do not. The Barr body is an inactivated X chromosome. Which of the following forms of RNA is most likely to play a role in Barr body formation?

Accepted Answer

lncRNA

Answer

mRNA

Answer

miRNA

Answer

siRNA

Question 9

What is the common feature of Nuclear Localization Signals?

Accepted Answer

Rich in basic amino acid residues and may be located anywhere in the protein sequence

Answer

Rich in acidic amino acid residues and located at the C-terminus of the protein

Answer

Rich in basic amino acid residues and located at the C-terminus of the protein

Answer

Rich in acidic amino acid residues and may be located anywhere in the protein sequence

Question 10

Which of the following is NOT a disease of defective DNA repair?

Accepted Answer

Adenosis polyposis coli

Answer

Severe combined immunodeficiency disease

Answer

Bloom syndrome

Answer

Breast cancer susceptibility 1 (BRCA 1)

Molecular Biology and Genomics — MCQs

Molecular Biology and Genomics — MCQs

On this page

Practice by Chapter

Want unlimited practice?