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

<p>(A) Schematic of the genotype of a diploid in which the <i>STE3</i>α gene was deleted. (B) Two independent <i>ste3</i>α/<i>STE3</i><b>a</b> mutants remain diploid based on FACS analysis of propidium iodide stained cells. Strains used: XW207 and XW208. (C) When sporulated, the progeny from both <i>ste3</i>αΔ/<i>STE3</i><b>a</b> 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 <i>MAT</i><b>a</b> JF289 strain was crossed with a <i>MAT</i>α <i>ste3</i>αΔ strain that contained the <i>CPR2</i> gene under the control of the constitutively active <i>GPD1</i> promoter. (F) Analysis of progeny from the cross in (E) showed overexpression of <i>CPR2</i> suppresses the SIS silencing defect of the <i>ste3</i>α mutant. Strains used: XW209 and XW210.