Fig 5.
skn-1 is required for the viability of the
rpn-10 mutant and controls the expression of proteasome subunits. (A) The
rpn-10 mutant showsactivation of an
rpn-7p::GFP reporter in multiple tissues including the pharynx, intestine, and hypodermis that is confirmed by quantifying the GFPfluorescence in the images (B) (n = 11 for WT and
rpn-10, p <0.001 by t-test.) (C) Treating the
rpn-10 mutant with
skn-1, but not
hsf-1 RNAi results in a developmental arrest phenotype. (D) Analysis of gene expression via Nanostring shows an increase in proteasome subunits in the
rpn-10 mutant compared to wild-type animals. The increase in proteasome subunits depends on
skn-1 but not
elt-2, and the activation of
skn-1 with
wdr-23 RNAi fails to activate subunit expression. (E) In parallel Nanostring studies, the
rpn-10 mutant also shows a small
skn-1 dependent, but not
elt-2 dependent, increase in the expression of the oxidative stress response genes,
gcs-1,
gst-4, and
gst-5. In contrast,
wdr-23 RNAi produces a marked increase in the expression of these genes (mean expression level of
gcs-1-4,326,
gst-4-24,714, and
gst-5-4,982). For details of statistical testing for Panel D and Panel E see S5 Table.