FERNANDINO Juan Ignacio
congresos y reuniones científicas
THE CNS ACTS AS A TRANSDUCER OF STRESS-INDUCED MASCULINIZATION THROUGH CORTICOTROPIN-RELEASING HORMONE B
CASTAÑEDA CORTÉS, D.C.; ARIAS PADILLA, L.F.; LANGLOIS, V.S.; SOMOZA, G.M.; FERNANDINO, J.I.
Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017
Exposure to environmental stressors during early development has important implications for the rescheduling of many cellular and molecular mechanisms. In many fish, environmental stressors like high temperatures (HT) increase cortisol levels that in turn induce gonadal masculinization of genotypic females, overriding genetic factors related to gonadal development. Here, we show for the first time that the CNS is acting as the transducer of environmental stressors-induced gonadal masculinization. The mRNA of Corticotropin-releasing hormone b (crhb) and its receptors (crhr1 and crhr2) were elevated at HT during the critical developmental period when the gonadal primordium was sexually labile. Mutations of both crh receptors by CRISPR/Cas9 in genetic female medaka embryos prevented them to masculinize when exposed to HT. However, some XX individuals exhibited an intersex gonad (testis-ova) with the loss of crhr1 function. The prevention of masculinization in the cas9+sgRNA-crhr1 and -crhr2 injected larvae was likely due to the lack of Acth release from the pituitary gland, which in turn did not induce cortisol production, the downstream effector of the hypothalamic-pituitary interrenal (HPI) axis. Finally, we could rescue HT-induced female-to-male sex reversal in cas9+sgRNA-crhr2 injected embryos by the addition of cortisol. Taken together, these results revealed the importance of the central nervous system (CNS) as the transducer of stress-induced masculinization in genetic females.