Practice Questions

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

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

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

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

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

Z-DNA is a left-handed helical variant with a zigzag sugar-phosphate backbone, favored by repeating purine-pyrimidine steps, high salt, or methylation.

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

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

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

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