1. SPP-5 affects larval arrest via insulin signaling pathway in Caenorhabditis elegans.
- Author
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Xie G and Shao Z
- Subjects
- Animals, RNA Interference, Receptor, Insulin metabolism, Receptor, Insulin genetics, Gene Expression Regulation, Developmental, Caenorhabditis elegans genetics, Caenorhabditis elegans metabolism, Caenorhabditis elegans growth & development, Caenorhabditis elegans Proteins metabolism, Caenorhabditis elegans Proteins genetics, Signal Transduction, Insulin metabolism, Larva growth & development, Larva metabolism, Larva genetics
- Abstract
Diapause is an endocrine-mediated metabolic and growth arrest state in response to unfavorable external environments. The nematode Caenorhabditis elegans can enter diapause/arrest during embryonic, larval, or adult stages when subjected to detrimental external environments. Larval stage 1 (L1) arrest happens when animals hatch without food. Previous work has shown that the insulin pathway plays a prominent role in regulating L1 arrest. However, the downstream signal molecular mechanisms and biomarkers are still missing. In this study, we showed that SaPosin-like Protein family member SPP-5 is significantly upregulated during L1 arrest, suggesting that it could act as an L1 arrest biomarker. Using RNA interference we demonstrated that spp-5 knockdown accelerated larval development, while the overexpression resulted in L1 arrest. Consistently, SPP-5 level was significantly up-regulated in the L1 arrest daf-2(e1370) mutants, and spp-5(RNAi) suppressed the daf-2(e1370) induced L1 arrest. These results suggest that SPP-5 can serve as an L1 arrest biomarker and promote the arrest probably via the insulin signaling pathway., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)
- Published
- 2024
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