Table 4.

Aging alters expression of genes involved in G2 arrest folowing oxidative stress and induces genes involved in double strand break repair at the replication fork

Gene	Fold change	Function
STK2	↓5.6	Required for progression through G2. Loss of STK2 prevents progression through the G2 block to mitosis.
MCM8	↑ 3.5	Prevents accumulation of replication intermediates; localizes to replication forks
GEMENIN	↑ 2.1	Prevents re-replication in cells arrested in G2
MAD2	↑ 1.9	Inhibits mitosis in presence of misaligned chromosomes.
BRCA2	↑ 1.7	Stabilizes blocked replication forks.
TIMELESS	↑ 1.7 *	Involved at replication fork: coordinates replication with genotoxic stress
PRIMASE1	↑ 1.5 *	Stabilizes lagging strand synthesis; important in replication fork stability and DSB repair.
BLM	↑ 1.5	RecQ helicase: recombination helicase. Repairs damaged replication forks; required for fork restart.
HAT1	↑1.5*	Acetyltransferase involved in DSB repair, both NHEJ and HR.
RAD21	↑ 1.5	Involved in sister chromatid alignment; DSB repair; component of cohesin
MSH3	↑ 1.5	Involved in MMR; also involved in crossover recombination
BRCA1	↑ 1.4 *	Involved in DSB repair; localizes to replication forks in response to replication stress.
MLH1	↑ 1.4*	Involved in MMR; also involved in crossover recombination
MSH6	↑ 1.4	Involved in MMR; also involved in crossover recombination
MSH2	↑ 1.4	Involved in MMR; also involved in crossover recombination
RPA	↑1.4	Single strand binding protein; critical in DSB repair. Prevents chromosome breaks and aneuploidy.
RAD52	↑ 1.3 *	Critical initiator of DSB repair; recruits Rad51 onto RPA-bound single strand DNA.

Fold change represents the difference in response to oxidative stress between old and young animals (ΔOld:ΔYoung) unless annotated by (*) which indicates a statistically significant change seen in old, treated animals only (ΔOld). All differences are significant at p<0.005.