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. 2017 Apr 19;206(2):939–952. doi: 10.1534/genetics.117.202515

Figure 5.

Figure 5

Epistatic relationships among stress pathway components. (A) skr-1/2 RNA interference (RNAi) is epistatic to alh-6. The alh-6(k1018) mutants constitutively activate the gst-4::gfp reporter gene that is most obvious in bodywall muscles. Knockdown of the nearly identical Skp-related genes skr-1 and skr-2 by RNAi results in a severe reduction of the gst-4::gfp signal in the alh-6(k1018) mutant background, placing skr-1/2 downstream of alh-6 in the stress response pathway. (B) wdr-23 RNAi is epistatic to xrep-4. The xrep-4(k1024) mutants are unable to induce the gst-4::gfp translational fusion reporter gene expression in response to exogenous toxins such as acrylamide. However, knockdown of wdr-23 by RNAi in the xrep-4(k1024) mutant background strongly induces gst-4::gfp reporter gene expression, placing WDR-23 activity downstream of XREP-4. (C) The skn-1(gof) allele is epistatic to xrep-4. The skn-1(k1023) mutation is a dominant gain-of-function allele that results in constitutively active gst-4::gfp expression, even in the absence of stress. That phenotype is unchanged when skn-1(k1023) mutant animals are exposed to xrep-4 RNAi, placing skn-1 downstream of XREP-4.