Figure 4—figure supplement 1. | Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence

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Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence

Figure 4—figure supplement 1.

Affiliation details

Joslin Diabetes Center, United States; Harvard Medical School, United States; Boston University, United States
Figure 4—figure supplement 1.
Download figureOpen in new tabFigure 4—figure supplement 1. SKN-1-dependence of the increased proteasome activity in GSC(−) animals.

(A) GSC absence reduces relative proteasome subunit gene mRNA abundance, detected by RNA-seq. (B, C) The skn-1(zu135) mutation suppresses the increase in 26S proteasome activity seen in day-1 adult glp-1(ts) animals. (D, E) skn-1 RNAi administered from the egg stage suppresses proteasome activity in day-1 adult glp-1(ts) animals. (F, G) skn-1 RNAi administered post-developmentally, starting at day-1 adulthood, significantly reduces proteasome activity in day-5 adult glp-1(ts) animals. (B, D, F) Kinetic curves of chymotrypsin-like proteasome activity. (C, E, G) Graphs of proteasome activity slopes. Data are represented as mean ± SEM. n = 3; p < 0.001***.

DOI: http://dx.doi.org/10.7554/eLife.07836.010