Sodium Selenide Toxicity Is Mediated by O2-Dependent DNA Breaks
Figure 1
Sodium selenide sensitivity distribution of mutants for genes involved in DNA damage and oxidative stress responses.
In the upper panel, 7 gene categories were defined. Selected genes are given in ranking order. Chk, DNA-damage checkpoint category; HR, homologous recombination; Ox, oxidative stress response; NER, nucleotide excision repair; PRR, post-replicative repair; BER, base excision repair; NHEJ, non-homologous end joining. In the lower panel, the 7 categories are presented with black, dark-gray, light-gray and white bars proportional to the percentages of genes ranking under 30, between positions 31 and 100, between 101 and 250 and over 250, respectively. The numbers (n) of genes retained in each category are shown at the right side. Essential genes of interest (such as RAD53, CDC9, MEC1, TRR1,…) were ignored because of the lack of the corresponding mutants in the collection. Two genes (RAD6 and MEC3) were not included in the above categories because they belonged to those for which we could not obtain more than two sets of data (see Methods S2). Eight genes belonging to more than one of the above 7 metabolic pathways were discarded from the analysis. They include SRS2, RAD50 and XRS2 (HR and NHEJ), DOT1 (HR, PRR and NER), BRE1 (HR and Chk), RAD27 (NHEJ and BER), RAD10 and RAD1 (NHEJ, PRR and NER). Actually, none of these genes ranked below 100 in Table S1. Three of them (SRS2, RAD10, RAD1) were between positions 101 and 250. The other ones ranked over 250. Whether these genes were taken into account or not did not significantly influence the histogram (data not shown).