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The 21-nucleotide let-7 RNA regulates developmental timing in Caenorhabditis elegans
It is shown that let-7 is a heterochronic switch gene that encodes a temporally regulated 21-nucleotide RNA that is complementary to elements in the 3′ untranslated regions of the heteroch chronic genes lin-14, lin-28, Lin-41, lin -42 and daf-12, indicating that expression of these genes may be directly controlled by let- 7.
Posttranscriptional regulation of the heterochronic gene lin-14 by lin-4 mediates temporal pattern formation in C. elegans
daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans.
Life-span regulation by insulin-like metabolic control is analogous to mammalian longevity enhancement induced by caloric restriction, suggesting a general link between metabolism, diapause, and longevity.
Genes and Mechanisms Related to RNA Interference Regulate Expression of the Small Temporal RNAs that Control C. elegans Developmental Timing
A uniform system for microRNA annotation.
Guidelines are presented for the identification and annotation of new miRNAs from diverse organisms, particularly so that mi RNAs can be reliably distinguished from other RNAs such as small interfering RNAs.
The Fork head transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C. elegans
It is shown that null mutations in Daf-16 suppress the effects of mutations in daf-2 or age-1; lack of dAF-16 bypasses the need for this insulin receptor-like signalling pathway.
Conservation of the sequence and temporal expression of let-7 heterochronic regulatory RNA
Two small RNAs regulate the timing of Caenorhabditis elegans development and may control late temporal transitions during development across animal phylogeny.
The lin-41 RBCC gene acts in the C. elegans heterochronic pathway between the let-7 regulatory RNA and the LIN-29 transcription factor.
Regulation of DAF-2 receptor signaling by human insulin and ins-1, a member of the unusually large and diverse C. elegans insulin gene family.
Structural predictions and likely C-peptide cleavage sites typical of mammalian insulins suggest thatins-1 is most closely related to insulin, and overexpression of ins-1 causes partially penetrant arrest at the dauer stage and enhances dauer arrest in weak daf-2 mutants, suggesting that INS-1 and human insulin antagonize DAF-2 insulin-like signaling.
Caenorhabditis elegans Akt/PKB transduces insulin receptor-like signals from AGE-1 PI3 kinase to the DAF-16 transcription factor.
It is shown that two C. elegans Akt/PKB homologs transduce insulin receptor-like signals that inhibit dauer arrest and that AKT-1 andAKT-2 signaling are indispensable for insulin receptors-like signaling in the nervous system and in tissues that are remodeled during dauer formation.