Nucleic Acid Biochemistry Practice Questions

Q: How does the diphtheria toxin inhibit protein synthesis?

Inactivates EF-2. ***Inactivates EF-2*** - The **diphtheria toxin** is an A-B toxin, where the A subunit acts as an enzyme. - The A subunit **ADP-ribosylates** and thereby inactivates **elongation factor-2 (EF-2)**, which is essential for eukaryotic protein synthesis. *Inhibits RNA polymerase* - **RNA polymerase inhibition** would prevent **transcription**, the synthesis of RNA from a DNA template. - The diphtheria toxin specifically targets **translation (protein synthesis)**, not transcription. *Interferes with tRNA* - **tRNA (transfer RNA)** is critical for carrying specific amino acids to the ribosome during protein synthesis. - While tRNA is involved in protein synthesis, the diphtheria toxin's primary mechanism is not direct interference with tRNA itself, but rather with an elongation factor. *Blocks ribosome binding* - Blocking **ribosome binding** would prevent the initiation of protein synthesis. - The diphtheria toxin allows for initial ribosome binding but then halts the **elongation phase** of protein synthesis by targeting EF-2.

Q: A patient presents with hyperuricemia and gout. Which enzyme's overactivity is most likely associated?

PRPP synthetase. ***PRPP synthetase*** - **Overactivity** of **PRPP synthetase** leads to increased production of **5-phosphoribosyl-1-pyrophosphate (PRPP)**, a key substrate for *de novo* purine synthesis. - This increased purine synthesis results in an **overproduction of uric acid**, causing **hyperuricemia** and **gout**. *HGPRT* - **Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)** deficiency, not overactivity, is associated with hyperuricemia and gout, as seen in **Lesch-Nyhan syndrome**. - Its normal function is in the **salvage pathway**, recycling purine bases; deficiency leads to increased *de novo* purine synthesis. *Xanthine oxidase* - **Xanthine oxidase** is involved in the catabolism of purines, converting **hypoxanthine to xanthine** and then **xanthine to uric acid**. - While inhibition of this enzyme (e.g., by allopurinol) is a treatment for gout, its **overactivity alone is not typically the primary cause** of hereditary hyperuricemia; rather, altered purine metabolism leading to excess substrates for xanthine oxidase is the issue. *Adenosine deaminase* - Deficiency of **adenosine deaminase (ADA)** is primarily associated with **severe combined immunodeficiency (SCID)**, due to the accumulation of toxic metabolites that impair lymphocyte development. - It is not directly linked to the pathogenesis of **hyperuricemia** or **gout**.

Q: Which enzyme deficiency is associated with Lesch-Nyhan syndrome, which is characterized by self-mutilation and hyperuricemia?

Hypoxanthine-guanine phosphoribosyltransferase. ***Hypoxanthine-guanine phosphoribosyltransferase*** - Deficiency of **hypoxanthine-guanine phosphoribosyltransferase (HGPRT)** leads to an inability to salvage purines, resulting in their degradation to **uric acid**. - This overproduction of uric acid causes **hyperuricemia** and characteristic neurological symptoms, including **self-mutilation**, choreoathetosis, and cognitive dysfunction, defining Lesch-Nyhan syndrome. *Adenosine deaminase* - Deficiency in **adenosine deaminase (ADA)** leads to the accumulation of **adenosine** and **deoxyadenosine**, which are toxic to lymphocytes. - This causes severe combined immunodeficiency **(SCID)**, not Lesch-Nyhan syndrome. *Xanthine oxidase* - **Xanthine oxidase** is involved in the catabolism of purines, converting hypoxanthine to xanthine and then to uric acid. - Its deficiency leads to **xanthinuria**, characterized by low uric acid levels and **xanthine kidney stones**, which is distinct from Lesch-Nyhan syndrome. *Phosphoribosyl pyrophosphate synthetase* - **Phosphoribosyl pyrophosphate (PRPP) synthetase** is involved in the *de novo* purine synthesis pathway. - Overactivity (not deficiency) of this enzyme can lead to increased purine production and **hyperuricemia**, but a deficiency typically impairs purine synthesis and does not present with Lesch-Nyhan features.

Q: Which enzyme deficiency is associated with increased levels of orotic acid and megaloblastic anemia?

UMP synthase. ***UMP synthase*** - A deficiency in **UMP synthase** (a bifunctional enzyme with orotate phosphoribosyltransferase and OMP decarboxylase activities) leads to the accumulation of its substrate, **orotic acid**. - **Orotic aciduria** impairs pyrimidine synthesis, which in turn affects DNA replication in rapidly dividing cells, leading to **megaloblastic anemia**. *Dihydroorotate dehydrogenase* - This enzyme is involved in an earlier step of **pyrimidine synthesis**, converting dihydroorotate to orotate. - A deficiency would cause **dihydroorotate accumulation**, not orotic acid, and is a different, though related, metabolic disorder. *Ribonucleotide reductase* - **Ribonucleotide reductase** converts ribonucleotides to deoxyribonucleotides, essential for DNA synthesis. - While its inhibition can cause **megaloblastic anemia** (e.g., hydroxyurea), it does not directly lead to **orotic acid accumulation**. *Adenylosuccinate lyase* - This enzyme is involved in **purine synthesis**, converting adenylosuccinate to AMP. - A deficiency would affect purine metabolism and would not cause **orotic acid accumulation** or megaloblastic anemia directly related to pyrimidine synthesis.

Q: In the context of DNA replication, which of the following is NOT a function of the enzyme DNA polymerase?

Initiating synthesis of new DNA strands. ***Initiating synthesis of new DNA strands*** - DNA polymerase **cannot initiate** the synthesis of a DNA strand from scratch; it requires a pre-existing **3'-hydroxyl group**, which is provided by an **RNA primer** synthesized by **primase**. - Its role is to **elongate** a pre-existing polynucleotide chain, not to start a new one. *Proofreading newly synthesized DNA* - DNA polymerase possesses **3' to 5' exonuclease activity**, allowing it to remove incorrectly paired nucleotides during replication. - This **proofreading function** significantly reduces the error rate during DNA synthesis. *Elongating DNA by adding nucleotides* - The primary function of DNA polymerase is to add **deoxyribonucleotides** to the 3' end of a growing DNA strand, synthesizing a new strand complementary to the template. - This process is essential for the accurate **duplication** of genetic material. *Repairing DNA damage during replication* - Beyond basic replication, DNA polymerase enzymes (e.g., **DNA Pol I** in prokaryotes, various polymerases in eukaryotes) are involved in **DNA repair mechanisms**, such as filling gaps created by excision repair. - They can replace damaged or incorrect nucleotides and synthesize the correct sequence during replication and repair processes.

Q: A patient with a history of gout is advised to avoid foods high in purines. Which metabolic product is primarily responsible for this condition?

Uric acid (a product of purine metabolism). ***Uric acid (a product of purine metabolism)*** - **Gout** is caused by the deposition of **uric acid crystals** in joints, leading to inflammation and pain. - **Purines**, found in certain foods, are metabolized into uric acid, thus increasing its levels in the body. *Nitrogen (a component of purines)* - While nitrogen is a **component of purine molecules**, it is not the direct metabolic product responsible for gout. - Nitrogen is present in various biological molecules and is excreted in different forms, primarily as urea, not directly causing gout. *Ammonia (a waste product of protein metabolism)* - **Ammonia** is a highly toxic waste product predominantly from **protein and amino acid metabolism**. - It is converted to **urea in the liver** for safe excretion and is not directly involved in the pathogenesis of gout. *Pyruvate (an end product of glycolysis)* - **Pyruvate** is a crucial intermediate metabolite in **carbohydrate metabolism** (glycolysis). - It plays a central role in energy production but has no direct connection to purine metabolism or gout.

Q: Which of the following statements about tRNA is correct?

The CCA sequence is added post-transcriptionally.. ***The CCA sequence is added post-transcriptionally.*** - The **CCA motif** at the 3' end of tRNA is crucial for amino acid attachment and is added by the enzyme **tRNA nucleotidyltransferase** after transcription. - This **post-transcriptional modification** ensures that the tRNA is fully functional for protein synthesis. *80% of total RNA* - **Ribosomal RNA (rRNA)**, not tRNA, constitutes the majority (approximately 80%) of cellular RNA. - tRNA typically makes up about **15%** of total cellular RNA. *Contains 50-60 nucleotides* - Transfer RNA molecules are relatively small, typically containing between **70 to 90 nucleotides**, not 50-60. - This specific length is important for their characteristic **cloverleaf secondary structure** and L-shaped tertiary structure. *Longest RNA* - **Messenger RNA (mRNA)** molecules are generally the longest type of RNA, varying greatly in length depending on the protein they encode. - tRNA molecules are among the **shortest** RNA molecules.

Q: Bond formation between ribose sugar and nitrogen is ?

Glycosidic linkage. ***Glycosidic linkage*** - A **glycosidic bond** forms between the **anomeric carbon** of a carbohydrate (like **ribose**) and another functional group (like the **nitrogenous base**). - Specifically, this bond links the **1' carbon atom** of the ribose sugar to a **nitrogen atom** (N-1 in pyrimidines, N-9 in purines) of the nitrogenous base to form a **nucleoside**. *Phosphodiester linkage* - This bond connects the **5' carbon** of one sugar to the **3' carbon** of another sugar via a **phosphate group**, forming the backbone of **DNA and RNA**. - It involves a **phosphate** and **two ester bonds**, not directly linking sugar to a nitrogenous base. *Phosphoester linkage* - A **phosphoester bond** is formed when a **phosphate group** reacts with a **hydroxyl group** of an alcohol, typically found in molecules like **nucleotides** (e.g., 5'-phosphate of a nucleoside). - This type of bond is part of the **phosphodiester linkage** but does not describe the bond between the sugar and the nitrogenous base. *Acidanhydride linkage* - An **acid anhydride linkage** is formed between **two acid groups** with the elimination of water, such as in **ATP** where two phosphate groups are linked by this high-energy bond. - This type of bond is not involved in the connection between a **ribose sugar** and a **nitrogenous base**.

Question 1

How does the diphtheria toxin inhibit protein synthesis?

Accepted Answer

Inactivates EF-2

Answer

Inhibits RNA polymerase

Answer

Interferes with tRNA

Answer

Blocks ribosome binding

Question 2

A patient presents with hyperuricemia and gout. Which enzyme's overactivity is most likely associated?

Accepted Answer

PRPP synthetase

Answer

HGPRT

Answer

Xanthine oxidase

Answer

Adenosine deaminase

Question 3

Which enzyme deficiency is associated with Lesch-Nyhan syndrome, which is characterized by self-mutilation and hyperuricemia?

Accepted Answer

Hypoxanthine-guanine phosphoribosyltransferase

Answer

Adenosine deaminase

Answer

Xanthine oxidase

Answer

Phosphoribosyl pyrophosphate synthetase

Question 4

Which enzyme deficiency is associated with increased levels of orotic acid and megaloblastic anemia?

Accepted Answer

UMP synthase

Answer

Dihydroorotate dehydrogenase

Answer

Ribonucleotide reductase

Answer

Adenylosuccinate lyase

Question 5

In the context of DNA replication, which of the following is NOT a function of the enzyme DNA polymerase?

Accepted Answer

Initiating synthesis of new DNA strands

Answer

Elongating DNA by adding nucleotides

Answer

Proofreading newly synthesized DNA

Answer

Repairing DNA damage during replication

Question 6

A patient with a history of gout is advised to avoid foods high in purines. Which metabolic product is primarily responsible for this condition?

Accepted Answer

Uric acid (a product of purine metabolism)

Answer

Nitrogen (a component of purines)

Answer

Ammonia (a waste product of protein metabolism)

Answer

Pyruvate (an end product of glycolysis)

Question 7

Which of the following statements regarding mitochondrial DNA is FALSE?

Accepted Answer

All respiratory proteins are synthesized within the mitochondria

Answer

Double stranded

Answer

Inherited from mother

Answer

High mutation rate

Question 8

Which of the following statements about tRNA is correct?

Accepted Answer

The CCA sequence is added post-transcriptionally.

Answer

80% of total RNA

Answer

Contains 50-60 nucleotides

Answer

Longest RNA

Question 9

Bond formation between ribose sugar and nitrogen is ?

Accepted Answer

Glycosidic linkage

Answer

Phosphodiester linkage

Answer

Phosphoester linkage

Answer

Acid anhydride linkage

Question 10

Which of the following statements about purine synthesis is true?

Accepted Answer

IMP is the first nucleotide synthesized during purine synthesis.

Answer

Glutamine PRPP amidotransferase is the rate-limiting enzyme in purine synthesis.

Answer

THFA derivatives are required for the formation of C2 and C8 in the purine ring.

Answer

Glutamine donates the amino group for N1 of the purine ring.

Nucleic Acid Biochemistry — MCQs

Nucleic Acid Biochemistry — MCQs

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