DNA is the molecule that stores the chemical instructions necessary for life and its stability is therefore of the utmost importance. Despite this, DNA is damaged by both exogenous and endogenous factors at an alarming frequency. The most severe type of DNA damage is a double-strand break (DSB), in which a scission occurs in both strands of the double helix, effectively dividing a single normal chromosome into two pathological chromosomes. Homologous recombination (HR) is a universal DSB repair mechanism that solves this problem by identifying another region of the genome that shares high sequence similarity with the DSB site and using it as a template for repair. Rad51 possess the enzymatic activity that is essential for this repair but several auxiliary factors are required for Rad51 to fulfil its function. It is becoming increasingly clear that many HR factors are subjected to post-translational modification. Here, we review what is known about how these modifications affect HR. We first focus on cases where there is experimental evidence to support a function for the modification, then discuss speculative cases where a function can be inferred. Finally, we contemplate why such modifications might be necessary.
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