Differential regulation of the heat shock factor 1 and DAF-16 by neuronal nhl-1 in the nematode C. elegans

• Autor(a) principal: Volovik, Yuli
• Data de Publicação: 2014
• Outros Autores: Moll, Lorna, Marques, Filipa Carvalhal, Maman, Moria, Bejerano-Sagie, Michal, Cohen, Ehud
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/102608; https://doi.org/10.1016/j.celrep.2014.11.028
• topic: Animals; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Chemoreceptor Cells; Forkhead Transcription Factors; Nerve Tissue Proteins; Signal Transduction; Somatomedins; Stress, Physiological; Transcription Factors

In the nematode Caenorhabditis elegans, insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) reduction hyperactivates the transcription factors DAF-16 and heat shock factor 1 (HSF-1), creating long-lived, stress-resistant worms that are protected from proteotoxicity. How DAF-16 executes its distinct functions in response to IIS reduction is largely obscure. Here, we report that NHL-1, a member of the TRIM-NHL protein family, acts in chemosensory neurons to promote stress resistance in distal tissues by DAF-16 activation but is dispensable for the activation of HSF-1. The expression of nhl-1 is regulated by the IIS, defining a neuronal regulatory circuit that controls the organismal stress response. The knockdown of nhl-1 protects nematodes that express the Alzheimer-disease-associated Aβ peptide from proteotoxicity but has no effect on lifespan. Our findings indicate that DAF-16- and HSF-1-regulated heat-responsive mechanisms are differentially controlled by neurons and show that one neuronal protein can be involved in the activation of different stress responses in remote tissues.