info:eu-repo/semantics/publishedVersion
An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
Fecha
2018Registro en:
An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans; XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; Cordoba; Argentina; 2018; 343-343
CONICET Digital
CONICET
Autor
Veuthey, Tania Vanesa
Giunti, Sebastián
Masson, Camila
de Rosa, Maria Jose
Rayes, Diego Hernán
Resumen
Multicellular organisms coordinate the systemic response to stress. We have shown that in C. elegans the acute-stress response activates neurons that release tyramine (TA), the invertebrate analog of adrenaline/noradrenaline. TA stimulates the DAF-2/Insulin/IGF-1 pathway and precludes the nuclear translocation of the DAF-16/FOXO transcription factor through the activation of an adrenergic-like receptor TYRA-3 in the intestine. In contrast, environmental long-term stressors reduce TA release allowing the induction of FOXO-dependent cytoprotective genes. However, how the insuline and tyraminergic pathway are linked is unknown. We here found that genetic silencing of an insulin like-peptide (ILP) (INS-3) increases the resistance to thermal and oxidative stress, reaching levels similar to tdc-1 (incapable of synthetizing TA) and tyra-3 null mutants. Moreover, unlike wild type animals, exogenous TA does not impair oxidative or thermal stress resistance. In addition, double null mutants between TA- deficient and ILPs null mutants (tdc-1 or tyra-3 with ins-3 or 7) showed levels of stress resistance similar to those found in INS-3 single null mutants, suggesting genetic interaction. Intestinal expression of INS-3 rescues the resistance phenotype of INS-3 null mutants to wild-type levels. We proposed that TA released form the nervous system promotes intestinal release of ILPs, which activate DAF-2 in other cells, inhibiting the systemic stress response mediated by DAF-16/FOXO.