Cell autonomous and cell non-autonomous pathways contribute to organismal responses to protein synthesis inhibition.

<p><i>A</i>. Germ cell proliferation is restricted in response to protein synthesis inhibition (N = 9–20). <i>B</i>-<i>D</i>. As compared to control RNAi (<i>B</i>), hypodermal-specific RNAi targeting <i>egl-45</i> (<i>C</i>) or <i>rps-11</i> (<i>D</i>) is sufficient to drive developmental arrest; pre-L4 (blue) to L4 (red), to adult (green), and reproductive adult (purple). Note that "pre-L4" is almost exclusively L2 stage past 24hrs, based on germline and molting data (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007520#sec010" target="_blank">Methods</a> for details) (N = 279–335 from 2 biological replicates). <i>E</i>-<i>G</i>. Hypodermal-specific protein synthesis inhibition arrests germ cell proliferation (<i>E</i>) (N = 21–22 from 2 biological replicates), organism level resistance to oxidative (<i>F</i>) and thermal (<i>G</i>) stress as compared to control RNAi-treated L2 stage animals (the bars in each stress resistance graph represent a unique set of biological replicates (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007520#pgen.1007520.s010" target="_blank">S1 Table</a>) relative to its own independent control cohort, N = 178–403 from 2–3 biological replicates). * p<0.025, ** p<0.005, **** p<0.00005 (<i>A</i>, <i>E</i>: One-way ANOVA; <i>F</i>-<i>G</i>: Fisher's exact test). See also <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007520#pgen.1007520.s010" target="_blank">S1 Table</a>.