Adrenocorticotropic Hormone and Cyclic Adenosine Monophosphate are Involved in the Control of Shark Bioluminescence

Among Etmopteridae and Dalatiidae, luminous species use hormonal control to regulate bioluminescence. Melatonin (MT) triggers light emission and, conversely, alpha melanocyte‐stimulating hormone (α‐MSH) actively reduces ongoing luminescence. Prolactin (PRL) acts differentially, triggering light emission in Etmopteridae and inhibiting it in Dalatiidae. Interestingly, these hormones are also known as regulators of skin pigment movements in vertebrates. One other hormone, the adrenocorticotropic hormone (ACTH), also members of the skin pigmentation regulators, is here pharmacologically tested on the light emission. Results show that ACTH inhibits luminescence in both families. Moreover, as MT and α‐MSH/ACTH receptors are members of the G‐protein coupled receptor (GPCR) family, we investigated the effect of hormonal treatments on the cAMP level of photophores through specific cAMP assays. Our results highlight the involvement of ACTH and cAMP in the control of light emission in sharks and suggest a functional similarity between skin pigment migration and luminescence control, this latter being mediated by pigment movements in the light organ‐associated iris‐like structure cells. Luminous sharks use hormonal control to regulate bioluminescence: melatonin triggers light emission and α‐melanocyte‐stimulating hormone reduces ongoing luminescence. Interestingly, these hormones are known as regulators of skin pigment movements in vertebrates. Another hormone, the adrenocorticotropic hormone (ACTH), also members of the skin pigmentation regulators, is here tested on the light emission; moreover, the effect of hormonal treatments on the light organ cAMP concentrations was also investigated. Results show that (1) ACTH has an inhibitory effect and (2) cAMP modulation occurs during luminescence. This research reveals analogy between skin pigment migration and luminescence control in two shark families.