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Structure of DNA

98 questions found

Practice Questions

98. A mutation alters the conserved Shine-Dalgarno sequence upstream of a bacterial structural gene. When this mutated polycistronic mRNA interacts with prokaryotic translation machinery, the immediate molecular outcome is the

A. Failure of the small (30S) ribosomal subunit to correctly align with the start codon
B. Accelerated transcription of downstream regulatory genes
C. Spontaneous excision of the mutated sequence by the spliceosome
D. Direct methylation of the structural gene's promoter region

The Shine-Dalgarno sequence base-pairs with the 16S rRNA of the 30S subunit, aligning the bacterial ribosome with the start codon to initiate translation.

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99. A chemical mutagen modifies an adenine base within a gene via deamination, converting it into hypoxanthine. During subsequent rounds of DNA replication, hypoxanthine preferentially pairs with cytosine instead of thymine, resulting in a permanent

A. Transition mutation from an A-T pair to a G-C pair
B. Transversion mutation from an A-T pair to a T-A pair
C. Frameshift mutation via single-nucleotide deletion
D. Nonsense mutation that halts transcription

Hypoxanthine pairs with cytosine, meaning the original template A-T pair becomes a G-C pair after a few rounds of replication, causing a transition mutation.

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Triple-stranded H-DNA forms when a third single strand winds into the major groove of a duplex, binding via alternative Hoogsteen hydrogen bonds.

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Huntington's disease is a classic trinucleotide repeat disorder where a CAG expansion in the HTT gene produces a toxic, polyglutamine-expanded huntingtin protein.

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89. The introduction of a chemical agent that intercalates flat aromatic rings directly between adjacent base pairs along the DNA double helix disrupts its geometry by increasing the vertical distance between base pairs from 0.34 nm to 0.68 nm. This alteration will directly induce

A. A nonsense mutation via base conversion
B. A frameshift mutation during subsequent DNA replication
C. The automatic removal of all upstream promoter sequences
D. The conversion of the B-DNA template into a single-stranded cistron

Intercalating agents distort the helix by stretching the backbone, which tricks DNA polymerase into inserting or omitting bases, causing frameshift mutations.

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90. An in vitro transcription assay utilizes a mutated RNA polymerase that cannot recognize or respond to the prokaryotic intrinsic termination signal. When this enzyme transcribes a gene containing a classic rho-independent terminator, the resulting molecular outcome will be

A. The production of an exceptionally short, truncated RNA molecule
B. The synthesis of an abnormally elongated RNA transcript due to read-through
C. The immediate conversion of the template DNA into a left-handed Z-conformation
D. The covalent attachment of the enzyme to the structural promoter

Without a functional termination response, the polymerase runs past the end of the gene, creating a long, un-terminated read-through transcript.

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91. The treatment of a eukaryotic cell line with a specific drug blocks the activity of the enzyme histone deacetylase (HDAC). Biochemically, this inhibition maintains high levels of histone acetylation across the genome, forcing structural genes to remain inside

A. Densely packed heterochromatin, silencing gene expression
B. Open, accessible euchromatin, promoting transcription
C. A single-stranded RNA state that bypasses translation
D. A left-handed Z-DNA configuration that excludes polymerases

Inhibiting HDAC keeps histones acetylated, neutralizing their positive charges and keeping chromatin open (euchromatin) to boost transcription.

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XP is caused by defects in the NER pathway, which is responsible for cutting out UV-induced pyrimidine dimers and bulky DNA distortions.

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93. A segment of double-stranded DNA is analyzed and found to have a melting temperature (Tm​) of 85∘C, while a second fragment of identical length melts at 72∘C. The physical explanation for the higher Tm​ of the first fragment is

A. A higher density of negative charges along its outer phosphate rails
B. A higher proportion of Guanine-Cytosine (G-C) base pairs
C. The presence of long non-coding intron loops within its sequence
D. Its unique organization into nucleosome core filaments

G-C pairs are bound by three hydrogen bonds, meaning G-C rich fragments require higher temperatures to denature than A-T rich sequences of the same length.

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94. A point mutation occurs within the consensus sequence of a 5′ splice donor site of a crucial structural gene. During pre-mRNA processing, this molecular defect will most likely cause the spliceosome to

A. Skip the downstream exon entirely or retain the entire mutated intron
B. Add an exceptionally long poly-A tail to the 5' end of the transcript
C. Convert the mature mRNA back into a double-stranded DNA template
D. Shift the promoter sequence into the coding exon

Mutilating a splice site prevents the spliceosome from recognizing the intron-exon boundary, leading to intron retention or exon skipping during splicing.

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95. A researcher utilizes a chemical toxin that selectively prevents the hydrolysis of pyrophosphate (PPi​) during nucleic acid synthesis. The immediate impact of this drug on gene replication and transcription is the

A. Acceleration of nucleotide polymerization rates
B. Thermodynamic arrest of phosphodiester bond formation
C. Spontaneous conversion of ribose sugars into deoxyribose variants
D. Uncontrolled duplication of upstream promoter sequences

Polymerization relies on the cleavage of pyrophosphate (PPi​→2Pi​) to provide the forward driving force; blocking this halts the reaction.

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NMD is a surveillance mechanism that detects premature stop codons on transcripts and degrades them, preventing the accumulation of toxic, truncated proteins.

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97. An analysis of the spatial orientation of the B-DNA double helix shows that the glycosidic bonds linking the bases to the sugar rings project at unequal angles. This structural asymmetry means that the phosphodiester backbones are

A. Arranged directly opposite each other, forming a perfectly symmetrical cylinder
B. Arranged closer together on one side of the helix than the other, creating distinct grooves
C. Linked covalently across the core via disulfide bridges
D. Restricted to a rigid left-handed zigzag spatial orientation

Because the glycosidic bonds project unevenly, the backbones wind asymmetrically around the axis, creating alternating major and minor grooves.

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82. The molecular weight of a gene is determined directly by the

A. Number of lipid layers surrounding the chromosome
B. Total number of nucleotide base pairs making up its sequence
C. Concentration of amino acids stored in the cell nucleus
D. Number of ribosomes attached to its promoter

The mass of a gene depends on its length; longer nucleotide sequences contain more base pairs, increasing the total molecular weight.

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Thymine is a pyrimidine base specific to DNA, whereas RNA uses uracil as the complementary partner for adenine.

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84. The presence of a negative electrical charge running along the entire outer surface of the DNA double helix is caused by the

A. Alkaline nature of the purine structures
B. Ionized oxygen atoms within the repeating phosphate groups
C. Hydroxyl groups located on the deoxyribose sugars
D. Hydrogen bonds holding the complementary strands together

Each phosphate group in the phosphodiester backbone loses a hydrogen atom at cellular pH, giving the exterior of the DNA a negative charge.

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85. The precise sequence of amino acids in a polypeptide chain is dictated directly by the sequence of

A. Sugars in the cellular polysaccharide matrix
B. Nucleotide triplets within the exons of a structural gene
C. Histone proteins forming the core nucleosomes
D. Fatty acids in the surrounding membrane

The linear sequence of nucleotide codons inside exons determines the exact order of amino acids added during protein translation.

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86. A molecular analysis of a mutant bacterial strain reveals a defect in DNA topoisomerase I. During gene transcription, this enzyme deficiency will result in the

A. Failure of the spliceosome to remove structural introns
B. Accumulation of excessive positive supercoiling ahead of the transcription bubble, stalling transcription
C. Spontaneous conversion of the template strand into an RNA-DNA virus
D. Immediate loss of the poly-A tail from the structural transcripts

Unwinding the helix creates torsional strain and positive supercoils ahead of the moving polymerase; without topoisomerase to relieve this stress, transcription stalls.

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