000285025 001__ 285025 000285025 005__ 20260205153026.0 000285025 0247_ $$2doi$$a10.1016/j.isci.2025.114422 000285025 0247_ $$2pmid$$apmid:41641102 000285025 0247_ $$2pmc$$apmc:PMC12865584 000285025 037__ $$aDZNE-2026-00150 000285025 041__ $$aEnglish 000285025 082__ $$a050 000285025 1001_ $$0P:(DE-2719)9002963$$aNiedworok, Patrizia$$b0$$eFirst author$$udzne 000285025 245__ $$aBCL-11 enables adaptive stress responses to environmental challenges. 000285025 260__ $$aSt. Louis$$bElsevier$$c2026 000285025 3367_ $$2DRIVER$$aarticle 000285025 3367_ $$2DataCite$$aOutput Types/Journal article 000285025 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1770301651_11293 000285025 3367_ $$2BibTeX$$aARTICLE 000285025 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000285025 3367_ $$00$$2EndNote$$aJournal Article 000285025 520__ $$aInsulin/IGF-1 signaling (IIS) is a master regulator of metabolism, stress resilience, and cell homeostasis in multicellular organisms. In the nematode Caenorhabditis elegans, DAF-2 regulates dauer diapause, animal growth, and lifespan extension in a DAF-16/FOXO-dependent manner. Here we investigated IIS in animals expressing pathogenic variants of BCL-11, an evolutionarily conserved transcription factor that has been implicated in human neurodevelopmental disorders. We found that hypomorphic bcl-11 mutations have a limited impact on C. elegans growth and survival under standard growth conditions. On the contrary, BCL-11 deficiency compromises the cytoprotective properties of daf-2 signaling upon animal exposure to stress. During embryonic development, daf-16 loss of function rescues egg hatching defects in daf-2;bcl-11 mutants, suggesting a transcriptional interplay between BCL-11 and DAF-16 in IIS-deficient animals. 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