title: Corazonin neurons function in sexually dimorphic circuitry that shape behavioral responses to stress in Drosophila.
abstract: All organisms are confronted with dynamic environmental changes that challenge homeostasis, which is the operational definition of stress. Stress produces adaptive behavioral and physiological responses, which, in the Metazoa, are mediated through the actions of various hormones. Based on its associated phenotypes and its expression profiles, a candidate stress hormone in Drosophila is the corazonin neuropeptide. We evaluated the potential roles of corazonin in mediating stress-related changes in target behaviors and physiologies through genetic alteration of corazonin neuronal excitability. Ablation of corazonin neurons confers resistance to metabolic, osmotic, and oxidative stress, as measured by survival. Silencing and activation of corazonin neurons lead to differential lifespan under stress, and these effects showed a strong dependence on sex. Additionally, altered corazonin neuron physiology leads to fundamental differences in locomotor activity, and these effects were also sex-dependent. The dynamics of altered locomotor behavior accompanying stress was likewise altered in flies with altered corazonin neuronal function. We report that corazonin transcript expression is altered under starvation and osmotic stress, and that triglyceride and dopamine levels are equally impacted in corazonin neuronal alterations and these phenotypes similarly show significant sexual dimorphisms. Notably, these sexual dimorphisms map to corazonin neurons. These results underscore the importance of central peptidergic processing within the context of stress and place corazonin signaling as a critical feature of neuroendocrine events that shape stress responses and may underlie the inherent sexual dimorphic differences in stress responses.
authors.affiliation: Department of Biology, Wake Forest University, Winston-Salem, North Carolina, United States of America.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Colin A
authors.initials: CA
authors.lastname: Bretz
authors.forename: Shane A
authors.initials: SA
authors.lastname: Hawksworth
authors.forename: Jay
authors.initials: J
authors.lastname: Hirsh
authors.forename: Erik C
authors.initials: EC
authors.lastname: Johnson
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D002470:Cell Survival; D004298:Dopamine / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D005260:Female; D015870:Gene Expression; D007150:Immunohistochemistry; D008136:Longevity; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009474:Neurons / Q000378:metabolism / Q000502:physiology*; D009479:Neuropeptides / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012737:Sex Factors; D013312:Stress, Physiological; D014280:Triglycerides / Q000378:metabolism
chemical_list: C489221:Crz protein, Drosophila; D029721:Drosophila Proteins; D009479:Neuropeptides; D014280:Triglycerides; D004298:Dopamine