Affinity maturation and class switch recombination require
targeted DNA lesions within immunoglobulin loci. AID initiates these processes
by deaminating cytidine residues in single-stranded DNA during transcription. A
mutation abolishes the ability of AID to modify cytidines, while leaving
transcription and DNA repair pathways intact.

What is the most direct mechanistic consequence
of this defect for antibody diversification?

Question

Affinity maturation and class switch recombination require
targeted DNA lesions within immunoglobulin loci. AID initiates these processes
by deaminating cytidine residues in single-stranded DNA during transcription. A
mutation abolishes the ability of AID to modify cytidines, while leaving
transcription and DNA repair pathways intact.

What is the most direct mechanistic consequence
of this defect for antibody diversification?

Accepted Answer

Failure
to generate uracil from cytidine, preventing initiation of both somatic
hypermutation and class switch recombination

Answer

Inability
of DNA repair complexes to bind immunoglobulin loci despite intact lesions

Answer

Failure
of transcription-dependent exposure of switch regions to enzymatic attack

Answer

Conversion
of cytidine to guanine, producing aberrant mutational spectra

Crowdly

Affinity maturation and class switch recombination require targeted DNA lesions...

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