To test whether the activity of the InsR pathway was down-regulated by miR-71, we first examined the endogenous expression of components of the InsR pathway in mir-71(lf). (C) The poor survival rate of daf-16(mu86, null) was enhanced by mir-71(lf). To identify individual miRNAs that play prominent roles in L1 diapause, we screened 72 available mutant strains of individual miRNAs and miRNA families (87 miRNAs in total) using the L1 starvation assay. (D) A representative chart of the L1 starvation survival rates of different miRNA mutants.
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Furthermore, the observed derepression of individual genes by mir-71(lf) seemed too weak to account for the phenotype, consistent with the idea that a prominent phenotype of an miRNA mutation is caused by the collective effect of changing expression in many revery play login genes, an important property of miRNA-mediated gene regulation. (F) Fluorescence and DIC images showing that an hbl-1 3′UTR reporter was repressed in mir-71(+) worms and slightly derepressed in mir-71(lf) mutants. (E) DIC images showing that hbl-1(RNAi) caused precocious VPC divisions in late L2/early L3 in both wild-type and mir-71(lf) worms recovered from 4 d of L1 starvation. Note that the daf-16(lf) worms recovering from 3 d of L1 starvation displayed a ∼12-h delay in overall development and that the mir-71(lf); daf-16(lf) double mutants displayed an ∼24-h delay. (C) Bar graph showing that the delayed VPC timing defects of mir-71(lf) worms was suppressed by an unc-31(lf) mutation and partially suppressed by an age-1(rf) mutation.