Aged people get more cancers than young ones due to use of Non-homologous end joining instead of homologous recombination for repairing double strand breaks

Double stranded breaks are the most dangerous form of DNA damage occurring in the genome. Double strand breaks are caused by internal agents like reactive oxygen species and many external agents like radiation.  Replication errors also cause double strand breaks.   Living organisms have two methods for correcting this error: Homologous recombination(HR) found both in bacteria and eukaryotes and non-homologous end joining (NHEJ) found mostly in eukaryotes. HR is a method which corrects the double strand breaks by using the homologous chromosome as the reference (this is the reason for diploid nature of most eukaryotes). Except for gene conversion, it does not cause mutation  to the genes in which the double strand break has occurred (usually broken ends have damaged bases which are removed  and correct bases are added by HR using the homologous chromosome as the template). But NHEJ just joins the broken ends without replacing the damaged bases (as it does not have a template to refer) leading to mutation of the genes in which double strand breaks occurred.

SOMETHING UNUSUAL: RecA of Dinococcus radiodurans binds to double standed DNA first

The D. radiodurans RecA protein (361 amino acids, Mr 38,013) is 57% identical (72% similar) to the E. coli RecA protein (352 amino acids, Mr 37,842). In vitro, the protein promotes all of the key recombino genic activities of RecA-class recombinases. It forms filaments on DNA, hydrolyses ATP and dATP in a DNA-dependent fashion and promotes DNA-strand exchange. However, the D. radiodurans RecA protein has one distinct function. The DNA strand-exchange reactions of the E. coli RecA protein, and all other homologues examined to date, are ordered so that the single-stranded DNA is generally bound first, before the double-stranded DNA is bound.