Genetic Code and Codon Usage — MCQs
What is the function of the UGA codon?
Mark the false statement regarding mitochondrial DNA:
If a sequence of 4 nucleotides codes for 1 amino acid, how many amino acids can be theoretically formed?
Which condition is associated with defects in pre-mRNA splicing and SMN protein dysfunction?
What is the primary function of exonuclease in DNA replication?
Which type of bonds are represented by the dotted lines in the image? (AIIMS Nov 2017)
During DNA replication, if the template strand has the sequence 5'-GATTACA-3', what is the sequence of the complementary strand?
Nucleotides serve all of the following roles, EXCEPT:
What is the end product of pyrimidine catabolism?
Which of the following compounds is an analogue of hypoxanthine?
Genetic Code and Codon Usage Indian Medical PG Practice Questions and MCQs
Question 1: What is the function of the UGA codon?
- A. Initiates transcription
- B. Translates
- C. Terminates protein synthesis (Correct Answer)
- D. None of the options
Explanation: ***Terminates protein synthesis*** - The **UGA codon** is one of the three **stop codons** (UAA, UAG, UGA) that signal the termination of translation. - When a ribosome encounters a UGA codon, there is no corresponding **tRNA** with an anticodon, leading to the binding of release factors and dissociation of the ribosomal complex. *Initiates transcription* - **Transcription initiation** involves RNA polymerase binding to a promoter region, which is a DNA sequence, not a specific mRNA codon. - The UGA codon is part of an mRNA sequence and functions during translation. *Translates* - While translation is the process of synthesizing protein from an mRNA template, the **UGA codon** specifically acts as a signal to **stop** this process. - It does not directly code for an amino acid, unlike other codons that are "translated" into specific amino acids. *None of the options* - This option is incorrect because **UGA** has a very specific and critical function in **terminating protein synthesis**.
Question 2: Mark the false statement regarding mitochondrial DNA:
- A. AGA and AGG are stop codons in mitochondrial DNA
- B. Kearns-Sayre Syndrome is a large deletion in mitochondrial DNA
- C. Does not show heteroplasmy (Correct Answer)
- D. 1% of cellular DNA, 13 proteins of respiratory chain
Explanation: ***Does not show heteroplasmy*** - This statement is false because **mitochondrial DNA (mtDNA)** commonly exhibits **heteroplasmy**, meaning the presence of more than one type of mitochondrial genome within a cell or individual. - **Heteroplasmy** arises due to the presence of both normal and mutated mtDNA, which can be passed down from the mother. *AGA and AGG are stop codons in mitochondrial DNA* - This statement is true; in the **universal genetic code**, AGA and AGG code for **arginine**, but in **human mitochondrial DNA**, they serve as **stop codons**. - This is an example of the **differences** in genetic code interpretation between the nuclear genome and the mitochondrial genome. *Kearns-Sayre Syndrome is a large deletion in mitochondrial DNA* - This statement is true; **Kearns-Sayre Syndrome** is a well-known mitochondrial disorder caused by a **large single deletion** in the mitochondrial DNA. - This deletion often leads to chronic progressive **external ophthalmoplegia**, **retinal pigmentary degeneration**, and **cardiac conduction defects**. *1% of cellular DNA, 13 proteins of respiratory chain* - This statement is true; **mitochondrial DNA constitutes** approximately **1% of the total cellular DNA** by mass. - It codes for **13 essential proteins** that are part of the **electron transport chain** (respiratory chain) complexes in the mitochondrion, along with ribosomal RNAs (rRNAs) and transfer RNAs (tRNAs).
Question 3: If a sequence of 4 nucleotides codes for 1 amino acid, how many amino acids can be theoretically formed?
- A. 4
- B. 64
- C. 16
- D. 256 (Correct Answer)
Explanation: ***256*** - With **4 distinct nucleotides** and a code sequence of **4 nucleotides** per amino acid, the number of possible unique combinations is calculated as 4^4. - This results in 4 × 4 × 4 × 4 = **256 theoretically possible amino acids**. - This is a mathematical combinatorics calculation: with 4 choices at each of 4 positions, total combinations = 4^4 = 256. *64* - This number represents the combinations if **3 nucleotides** coded for one amino acid (4^3 = 64), which is the actual case in the **standard genetic code** (triplet codons). - However, the question specifies a hypothetical sequence of **4 nucleotides** per amino acid, making this option incorrect. *16* - This number would be correct if **2 nucleotides** coded for one amino acid (4^2 = 16). - The problem explicitly states that **4 nucleotides** code for each amino acid in this theoretical scenario. *4* - This would only be the case if each **single nucleotide** coded for one amino acid (4^1 = 4). - Given **4 distinct nucleotides** and a sequence length of 4, the potential for combinations is much higher.
Question 4: Which condition is associated with defects in pre-mRNA splicing and SMN protein dysfunction?
- A. Sickle cell disease
- B. Huntington's disease
- C. Spinal muscular atrophy (Correct Answer)
- D. α-Thalassemia
Explanation: ***Spinal muscular atrophy*** - **Spinal muscular atrophy (SMA)** is primarily caused by mutations in the **SMN1 gene**, leading to insufficient production of the **survival motor neuron (SMN) protein**. - Without adequate SMN protein, defects occur in the **pre-mRNA splicing** of motor neuron genes, leading to the degeneration of **alpha motor neurons** in the spinal cord. *Sickle cell disease* - **Sickle cell disease** is an inherited **hemoglobinopathy** caused by a point mutation in the beta-globin gene, leading to the production of abnormal **hemoglobin S**. - This condition does not involve defects in pre-mRNA splicing or SMN protein dysfunction, but rather the **polymerization of hemoglobin S** under low oxygen conditions. *Huntington's disease* - **Huntington's disease** (formerly called Huntington chorea) is a neurodegenerative disorder caused by an **expanded CAG trinucleotide repeat** in the huntingtin gene. - Huntington's disease involves protein misfolding and aggregation, but not primary defects in pre-mRNA splicing or SMN protein dysfunction. *α-Thalassemia* - **α-Thalassemia** is a group of inherited blood disorders characterized by reduced or absent production of **alpha-globin chains**, typically due to **gene deletions** on chromosome 16. - This condition affects the assembly of hemoglobin and does not involve pre-mRNA splicing defects or SMN protein dysfunction.
Question 5: What is the primary function of exonuclease in DNA replication?
- A. Polymerization
- B. Proofreading (Correct Answer)
- C. Chain elongation
- D. Termination
Explanation: ***Proofreading*** - Exonucleases, particularly those associated with **DNA polymerases**, are crucial for **proofreading** during DNA replication. - They remove incorrectly paired nucleotides from the 3' end of the growing DNA strand, ensuring high fidelity of replication. *Polymerization* - **DNA polymerase** is primarily responsible for the **polymerization** of new DNA strands by adding nucleotides. - While exonucleases can be part of the polymerase complex, their main function is not polymerization itself. *Chain elongation* - **Chain elongation** refers to the process of adding nucleotides to the growing DNA strand, which is performed by **DNA polymerase**. - Exonucleases act as a quality control mechanism during this elongation process, rather than carrying out the elongation. *Termination* - **Termination** of DNA replication involves specific sequences and proteins that signal the end of replication, not the primary function of exonucleases. - Exonucleases are active throughout the replication process to maintain accuracy.
Question 6: Which type of bonds are represented by the dotted lines in the image? (AIIMS Nov 2017)
- A. Hydrogen bond (Correct Answer)
- B. Covalent bond
- C. Ionic bond
- D. Phosphodiester
Explanation: ***Hydrogen bond*** - The dotted lines in the image represent the weak, non-covalent interactions between the **nitrogenous bases** on opposite strands of the DNA double helix. - Specifically, these are **hydrogen bonds** formed between complementary base pairs (Adenine with Thymine via two hydrogen bonds, and Guanine with Cytosine via three hydrogen bonds). *Covalent bond* - **Covalent bonds** involve the sharing of electron pairs between atoms and are much stronger than hydrogen bonds. - In DNA, covalent bonds form the **sugar-phosphate backbone** of each strand and link the nitrogenous bases to the deoxyribose sugars. *Ionic bond* - **Ionic bonds** involve the electrostatic attraction between oppositely charged ions, formed by the complete transfer of electrons. - While ions (like magnesium or sodium) interact with DNA, the dotted lines specifically represent the inter-strand forces between bases, which are not ionic. *Phosphodiester* - A **phosphodiester bond** is a specific type of covalent bond that links the 3' carbon of one deoxyribose sugar to the 5' carbon of the next deoxyribose sugar via a phosphate group, forming the backbone of a single DNA strand. - The dotted lines are between the two DNA strands, not within a single strand's backbone.
Question 7: During DNA replication, if the template strand has the sequence 5'-GATTACA-3', what is the sequence of the complementary strand?
- A. 5'-GATTACA-3'
- B. 3'-GATTACA-5'
- C. 5'-ACATTAG-3'
- D. 5'-TGTAATC-3' (Correct Answer)
Explanation: **5'-TGTAATC-3'** - DNA replication involves **base pairing rules**: **adenine (A)** pairs with **thymine (T)**, and **guanine (G)** pairs with **cytosine (C)**. - The complementary strand is synthesized in an **antiparallel direction**: if the template is 5'-GATTACA-3', the new strand will be 3'-CTAATGT-5'. When written in the conventional 5' to 3' direction, this becomes 5'-TGTAATC-3'. *5'-GATTACA-3'* - This sequence is identical to the template strand, which would only occur if the DNA were to replicate in a **non-complementary manner**, violating base pairing rules. - Direct duplication of the template sequence does not produce a complementary strand. *3'-GATTACA-5'* - This sequence is the **template sequence written in the antiparallel direction** but is not the complementary strand. - It fails to apply the correct base pairing rules (A with T, G with C). *5'-ACATTAG-3'* - This sequence incorrectly pairs the bases and does not maintain the **antiparallel orientation** correctly. - For example, the first base G in the template would pair with C, not A.
Question 8: Nucleotides serve all of the following roles, EXCEPT:
- A. Monomeric units of nucleic acids
- B. Mediators in cellular signalling
- C. Source of energy
- D. Structural component of membrane (Correct Answer)
Explanation: ### Explanation **Nucleotides** are versatile molecules consisting of a nitrogenous base, a pentose sugar, and one or more phosphate groups. While they are central to genetic and metabolic processes, they do **not** serve as structural components of cell membranes. Cell membranes are primarily composed of phospholipids, cholesterol, and proteins. #### Why Option D is Correct: **Structural component of membrane:** Nucleotides are highly hydrophilic (polar) due to their phosphate groups and sugar moieties. This makes them unsuitable for forming the hydrophobic core of the lipid bilayer. Membranes require amphipathic molecules like phospholipids; nucleotides lack the long-chain fatty acids necessary for membrane integrity. #### Why Other Options are Incorrect: * **A. Monomeric units of nucleic acids:** This is the primary role of nucleotides. DNA and RNA are polymers formed by phosphodiester bonds between deoxyribonucleotides and ribonucleotides, respectively. * **B. Mediators in cellular signaling:** Nucleotides act as crucial secondary messengers. Examples include **cAMP** (cyclic AMP) and **cGMP**, which relay signals from hormones and neurotransmitters. Additionally, ATP and adenosine act as extracellular signaling molecules (purinergic signaling). * **C. Source of energy:** **ATP** (Adenosine triphosphate) is the "universal energy currency" of the cell. Other nucleotides like GTP are also used in specific pathways (e.g., protein synthesis and gluconeogenesis). --- ### High-Yield Clinical Pearls for NEET-PG: * **Synthetic Analogues:** Many chemotherapeutic drugs are nucleotide/nucleoside analogues (e.g., **5-Fluorouracil, Methotrexate**) that inhibit DNA synthesis. * **Activated Intermediates:** Nucleotides serve as carriers for biosynthetic precursors, such as **UDP-Glucose** (glycogen synthesis) and **CDP-Choline** (phospholipid synthesis). * **Coenzyme Components:** Many essential coenzymes like **NAD+, FAD, and Coenzyme A** contain an adenine nucleotide moiety as part of their structure.
Question 9: What is the end product of pyrimidine catabolism?
- A. Ammonia (NH3)
- B. Carbon dioxide (CO2) and water (H2O) (Correct Answer)
- C. Both ammonia and carbon dioxide/water
- D. None of the above
Explanation: **Explanation:** The catabolism of pyrimidines (Cytosine, Uracil, and Thymine) differs significantly from purine catabolism. While purines are degraded into insoluble uric acid, pyrimidines are broken down into highly soluble products that are easily excreted or utilized by the body. **1. Why Option B is Correct:** The pyrimidine ring is cleaved to produce **CO₂ and H₂O** as the ultimate metabolic end products. Specifically: * **Cytosine and Uracil** are degraded into **β-alanine**, which is further converted into CO₂, H₂O, and NH₃. * **Thymine** is degraded into **β-aminoisobutyrate**, which eventually breaks down into CO₂, H₂O, and NH₃. Because these products are simple, non-toxic molecules, pyrimidine catabolism does not lead to clinical disorders like gout. **2. Why Other Options are Incorrect:** * **Option A:** While ammonia (NH₃) is produced during the deamination steps of pyrimidine breakdown, it is an intermediate that is quickly diverted to the **Urea Cycle** for detoxification. It is not considered the final "end product" of the carbon skeleton. * **Option C:** Although both are produced, standard biochemical nomenclature identifies the final respiratory/metabolic disposal of the carbon skeleton as CO₂ and H₂O. **High-Yield Clinical Pearls for NEET-PG:** * **β-aminoisobutyrate:** The excretion of this metabolite in urine is a specific marker for high DNA turnover (e.g., leukemia or post-radiation therapy). * **Solubility:** Unlike purine end-products (uric acid), pyrimidine end-products are **highly water-soluble**. * **Rate-limiting enzyme:** Dihydropyrimidine dehydrogenase (DPD) is the key enzyme in pyrimidine catabolism. A deficiency in DPD can lead to severe toxicity when treating patients with the chemotherapy drug **5-Fluorouracil (5-FU)**.
Question 10: Which of the following compounds is an analogue of hypoxanthine?
- A. Arabinoside C
- B. Allopurinol (Correct Answer)
- C. Ribose phosphate
- D. 5-phosphoribosylpyrophosphate (PRPP)
Explanation: **Explanation:** **Allopurinol** is a structural analogue of **hypoxanthine**, a naturally occurring purine base. This structural similarity is the basis for its clinical use in treating gout. Allopurinol acts as a **suicide inhibitor** of the enzyme **Xanthine Oxidase**. Under normal conditions, xanthine oxidase converts hypoxanthine to xanthine and xanthine to uric acid. Allopurinol competes for the active site and is converted into oxypurinol (alloxanthine), which binds irreversibly to the enzyme, thereby reducing uric acid production and increasing levels of more soluble precursors (hypoxanthine and xanthine). **Analysis of Incorrect Options:** * **Arabinoside C (Cytarabine):** This is a pyrimidine analogue (specifically a cytosine analogue) used primarily as a chemotherapy agent in leukemias. It interferes with DNA synthesis. * **Ribose phosphate:** This is a phosphorylated five-carbon sugar that serves as a structural component of nucleotides, not a nitrogenous base analogue. * **5-phosphoribosylpyrophosphate (PRPP):** This is an activated form of ribose-5-phosphate. It is a key substrate in both the *de novo* and salvage pathways of purine and pyrimidine synthesis, but it is not a base analogue. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Allopurinol is a classic example of **competitive inhibition** (initially) and **suicide inhibition** (by its metabolite oxypurinol). * **Drug Interaction:** Because xanthine oxidase also metabolizes **6-Mercaptopurine (6-MP)** and **Azathioprine**, co-administration with Allopurinol leads to toxic levels of these drugs. The dose of 6-MP must be reduced by 75%. * **Lesch-Nyhan Syndrome:** Allopurinol is used to manage hyperuricemia in these patients, though it does not improve neurological symptoms.
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