L1 starvation assay was adapted from a previously described protocol (3). Worms strains were grown and maintained at 20 °C as described (29). This result is consistent with the observation that miR-71 is specifically required for revery play login the starvation-induced stress response (Fig. S5). For example, we observed a robust retarded mutant phenotype in the vulval lineage but did not see obvious defects in seam cell differentiation or alae formation. It seems plausible that miRNAs that control developmental timing are also involved in regulating the metabolic rate through repressing the InsR pathway activity.

However, it remains unclear how, and to what extent, miRNAs coordinate animal survival and development in response to stresses. However, the mechanisms that coordinate the long-term survival, overall developmental arrest, and reinitiation remain to be investigated. However, when newly hatched L1 worms encounter an environment with no food, developmental programs arrest and the worm enters L1 diapause. When late, first larval stage (L1) worms sense unfavorable conditions, they enter an alternative and long-lived larval stage called dauer larvae (or dauer diapause). The nematode Caenorhabditis elegans responds to starvation by entering developmental arrest at multiple stages of its life cycle (1). Extreme climate events such as droughts and heatwaves are intensifying under climate change, yet their combined effects on plant recovery remain unclear.

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Moreover, the expression of hbl-1 is repressed by let-7 family miRNAs at L3 during normal development, and the hyperactivity of hbl-1 caused by failure of miRNA regulation leads to retarded development (26). The reporter construct, the control plasmid, and a transformation marker plasmid were coinjected into worms to generate the extrachromosomal arrays for analysis. Elegans and Caenorhabditis briggsae, leading us to focus further analyses on these two genes. We further examined the functional relationship between miR-71 and DAF-16, a FOXO transcription factor acting critically and negatively downstream of AGE-1/PI3K in the InsR pathway.

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(B) Survival rate of single and double mutants to indicate the functional relationship between ain-1 and age-1. The two ain-1 loss-of-function alleles displayed significant reductions in L1 starvation survival rate. We further found that this survival rate reduction of ain-1 mutants was overcome by ectopic expression of the AIN-2 protein in the intestine but not in the muscle (Fig. 1A and Fig. S1A). We found that ain-1 but not ain-2 mutants displayed a significant reduction in L1 starvation survival rate compared with that of wild type (Fig. 1 A and D).

This is consistent with hbl-1 being one of the downstream targets of miR-71, although this modest effect alone is not expected to account for the vulval developmental phenotype in mir-71 mutant. In starved L1 worms, we detected only a slight increase in the mRNA level of hbl-1 in mir-71 mutants compared with that in wild type (∼10%), which may not be biologically significant. In contrast, the mir-71(lf) mutant worms recovering on hbl-1(RNAi) displayed precocious VPC divisions similar to that seen in wild type (Fig. 4E). Consistent with the observation described above, the 4-d–starved mir-71(lf) mutants recovering on the RNAi control plates displayed the highly penetrant retarded defect in VPC division. If this were true, the starved mir-71(lf); daf-16(lf) double-mutant worms should show a slow growth phenotype similar to that of daf-16(lf) worms, but no specific VPC timing defect. (H) Fluorescence and DIC images showing that a lin-42 3′UTR reporter was repressed in mir-71(+) worms (2/2 transgenic lines) and prominently derepressed in mir-71(−) worms (2/2 transgenic lines).

{Furthermore, a recent study suggests that the expression of certain miRNAs is differentially regulated by starvation-induced dauer diapause (15). Consistent with these ideas, several recent lines of evidence suggest that miRNA let-7 and the heterochronic genes lin-42 and hbl-1 are required to regulate the starvation-induced dauer diapause (10–12) and that a number of miRNAs including lin-4 and mir-71 are involved in regulating life span (13, 14). Furthermore, worms that are long-lived due to dietary restriction or decreased mitochondrial respiratory rates are short-lived during L1 diapause, suggesting that the mechanisms controlling L1 starvation survival are different at least in some aspects from those controlling aging (3).}