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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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• Instead, many specific physiological functions, such as the starvation-induced stress response, are regulated by a miRNA-target network, often involving multiple miRNAs and a large number of their targets.
• Through the Facility, the Commission raises funds by borrowing on the capital markets (issuing bonds on behalf of the EU).
• (D) Fractions of worms that carry 3′UTR reporter transgene and show no GFP expression GFP(−), weak GFP expression GFP(+/−), and comparable GFP expression to mCherry GFP(+).
• 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.
• The eggs were transferred to plates seeded with HB101 and bleached again 3 d later.
• Our genetic analysis indicated that for both L1 diapause survival and developmental recovery functions, miR-71 regulates expressions of genes in both the insulin receptor-dependent and -independent pathways.

We next examined the relationship between miR-71 and UNC-31, which functions upstream of AGE-1 during L1 diapause by regulating calcium-regulated dense-core vesicle fusion and the release of an insulin-like ligand (3). We identified 10 miRNA mutants that showed reduced survival rates with a stringent standard, as well as a few miRNA mutants with slightly increased survival rates (Table S1, Fig. 1D, and Fig. S1B). 1A because the ain-1 mutations reduce, but do not eliminate, miRISC functions. The overall effect of miRNAs on L1 starvation survival is expected to be significantly stronger than that reflected by the data in Fig.

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