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. 2016 Mar 4;12(3):e1005868. doi: 10.1371/journal.pgen.1005868

Fig 7. Cpr2 and Ste3 play redundant roles in intiating RNAi during SIS.

Fig 7

(A) Schematic of the genotype of a diploid in which the STE3α gene was deleted. (B) Two independent ste3α/STE3a mutants remain diploid based on FACS analysis of propidium iodide stained cells. Strains used: XW207 and XW208. (C) When sporulated, the progeny from both ste3αΔ/STE3a mutant strains XW207 and XW208 show defects in SIS, with only 21% and 22% silencing, respectively, compared to ~50% in the wild type. Strains used: XW207 and XW208. (D) Schematic of the MAPK cascade triggered by Ste3 and Cpr2. (E) The MATa JF289 strain was crossed with a MATα ste3αΔ strain that contained the CPR2 gene under the control of the constitutively active GPD1 promoter. (F) Analysis of progeny from the cross in (E) showed overexpression of CPR2 suppresses the SIS silencing defect of the ste3α mutant. Strains used: XW209 and XW210.