Nitric oxide signaling in ctenophores

Leonid L Moroz; Krishanu Mukherjee; Daria Y Romanova

doi:10.3389/fnins.2023.1125433

Nitric oxide signaling in ctenophores

Front Neurosci. 2023 Mar 22:17:1125433. doi: 10.3389/fnins.2023.1125433. eCollection 2023.

Authors

Leonid L Moroz^{1

2}, Krishanu Mukherjee², Daria Y Romanova³

Affiliations

¹ Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, United States.
² The Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, FL, United States.
³ Institute of Higher Nervous Activity and Neurophysiology of RAS, Moscow, Russia.

Abstract

Nitric oxide (NO) is one of the most ancient and versatile signal molecules across all domains of life. NO signaling might also play an essential role in the origin of animal organization. Yet, practically nothing is known about the distribution and functions of NO-dependent signaling pathways in representatives of early branching metazoans such as Ctenophora. Here, we explore the presence and organization of NO signaling components using Mnemiopsis and kin as essential reference species. We show that NO synthase (NOS) is present in at least eight ctenophore species, including Euplokamis and Coeloplana, representing the most basal ctenophore lineages. However, NOS could be secondarily lost in many other ctenophores, including Pleurobrachia and Beroe. In Mnemiopsis leidyi, NOS is present both in adult tissues and differentially expressed in later embryonic stages suggesting the involvement of NO in developmental mechanisms. Ctenophores also possess soluble guanylyl cyclases as potential NO receptors with weak but differential expression across tissues. Combined, these data indicate that the canonical NO-cGMP signaling pathways existed in the common ancestor of animals and could be involved in the control of morphogenesis, cilia activities, feeding and different behaviors.

Keywords: Ctenophora; Mnemiopsis; Placozoa; Pleurobrachia; Porifera; guanylate cyclase; nervous system evolution; nitric oxide synthase.

Grants and funding

This work was supported in part by the Human Frontiers Science Program (RGP0060/2017) and the National Science Foundation (1146575, 1557923, 1548121, and 1645219) grants to LM. Research reported in this publication was also supported in part by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health under Award Number R01NS114491 (to LM).