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Like other members of the Etmopterus genus, Etmopterus molleri is bioluminescent. Bioluminescence in E. molleri is controlled by photophores, which are regulated by hormones. Hormonal control of bioluminescence in E. molleri involves the expression of melatonin, adrenocorticotropic hormone (ACTH), prolactin, α-melanocyte-stimulating hormone on melanocortin receptors, α-MSH receptors, prolactin receptors, and ACTH receptors. Melanocortin receptors, α-MSH receptors, and ACTH receptors belong to a family of G-protein-coupled receptors, which are modulated by cyclic adenosine monophosphate (cAMP).

Similarly to Etmopterus spinax, activation of melanocortin receptors by melatonin initiates luminescence production in the photophores. However, in contrast to E. spinax, light emission in E. molleri requires a higher threshold of prolactin to emit light. This difference may be explained by the observation that overall E. molleri requires a higher threshold of hormone to produce luminescence than E. spinax.

Hormone activity is also modulated by nitric oxide, which reduces the ability of hormones to activate light production in photophores. This finding suggests that nitric oxide may be produced as needed by the organism to reduce the luminescence response when appropriate.

While melatonin in the Etmopteridae family initiates bioluminescence reactions by binding to melanocortin receptors, ACTH inhibits light emission in photophores through binding to ACTH receptors. ACTH modulation by cAMP inhibits light emission in Etmopteridae.

The evolution of melanocortin receptors began prior to evolution of the Chordata phylum. Conservation of melanonocortin receptors from invertebrates to vertebrates expanded to include new functions over evolutionary history. In E. spinax, melanocortin receptors serve a variety of functions beyond controlling luminescence in photophores.