Question at position 18 You treat flies with X-rays then look for mutations in your gene of interest. One of the mutations you find is the deletion of 3 complementary bases. Which DNA repair mechanism was most likely used to repair the damage in your gene?nonhomologous end-joining - NHEJhomologous recombinationNucleotide excision repairbase excision repairmismatch repair

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BlackTom AI · Accepted Answer

The scenario describes DNA damage induced by X-rays, followed by observation of a deletion of 3 complementary bases in the gene of interest. Different repair pathways address different types of damage, so we evaluate each option in context.
Option 1: nonhomologous end-joining - NHEJ. This pathway repairs double-strand breaks (DSBs) by directly ligating the broken ends, often with processing that introduces small insertions or deletions (indels). An indel of 3 bases fits the pattern of an error-prone repair outcome characteristic of NHEJ, especially after ionizing radiation like X-rays.
Option 2: homologous recombination. HR is a high-fidelity repair mechanism that uses a homologous sequence as a template (usually a sister chromatid) to precisely restore the original sequence. While HR can fix DSBs without indels, it tends to preserve the sequence more faithfully. A 3-base deletion would be unlikely if HR were exclusively used, making this option less consistent with the observed deletion.
Option 3: Nucleotide excision repair. NER removes bulky DNA lesions (e.g., thymine dimers caused by UV light) by excising a short single-stranded DNA segment around the damage. It does not typically produce base deletions of this nature, and it is not the primary response to ionizing radiation-induced DSBs, making it a poor fit here.
Option 4: base excision repair. BER fixes small, non-helix-distorting base lesions (like oxidized or deaminated bases) and usually replaces a single nucleotide, not a string of a few bases. A 3-base deletion is not explained by BER.
Option 5: mismatch repair. MMR corrects replication errors, such as base–base mismatches or small insertion–deletion loops that arise during DNA replication. It does not repair DSBs caused by radiation in the context described, so this option does not account for the observed deletion pattern.
In summary, the deletion of 3 bases after X-ray–induced damage is best explained by nonhomologous end-joining, an error-prone DSB repair pathway that commonly results in small deletions at the repair junctions, whereas the other pathways either fix different types of damage or yield high-fidelity restoration.

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