Evolution of the corticotropin-releasing hormone signaling system and its role in stress-induced phenotypic plasticity.
Developing animals respond to variation in their habitats by altering their rates of development and/or their morphologies (i.e., they exhibit phenotypic plasticity). In vertebrates, one mechanism by which plasticity is expressed is through activation of the neuroendocrine system, which transduces environmental information into a physiological response. Recent findings of ours with amphibians and of others with mammals show that the primary vertebrate stress neuropeptide, corticotropin-releasing hormone (CRH), is essential for adaptive developmental responses to environmental stress. For instance, CRH-dependent mechanisms cause accelerated metamorphosis in response to pond-drying in some amphibian species, and intrauterine fetal stress syndromes in humans precipitate preterm birth. CRH may be a phylogenetically ancient developmental signaling molecule that allows developing organisms to escape deleterious changes in their larval/fetal habitat. The response to CRH is mediated by at least two different receptor subtypes and may also be modulated by a secreted binding protein.
Denver
R J
RJ
Department of Biology, University of Michigan, Ann Arbor 48109, USA. rdenver@umich.edu
D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000502:physiology*; D005333:Fetus / Q000502:physiology; D006801:Humans; D008675:Metamorphosis, Biological; D010641:Phenotype; D015398:Signal Transduction / Q000502:physiology*; D014714:Vertebrates
D003346:Corticotropin-Releasing Hormone