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Crosstalk between protein kinases A and C regulates sea urchin sperm motility

Published online by Cambridge University Press:  02 December 2021

Arlet Loza-Huerta
Affiliation:
Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Apdo. Postal 510-3, Cuernavaca, Morelos, México62210
Hiram Pacheco-Castillo
Affiliation:
Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Apdo. Postal 510-3, Cuernavaca, Morelos, México62210
Alberto Darszon
Affiliation:
Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Apdo. Postal 510-3, Cuernavaca, Morelos, México62210
Carmen Beltrán*
Affiliation:
Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Apdo. Postal 510-3, Cuernavaca, Morelos, México62210
*
Author for correspondence: Carmen Beltrán. Instituto de Biotecnología-Universidad Nacional Autónoma de México. Av. Universidad # 2001. Cuernavaca, Morelos, CP.62210, México. E-mail: [email protected]

Summary

Fertilization, a crucial event for species preservation, in sea urchins, as in many other organisms, requires sperm motility regulation. In Strongylocentrotus purpuratus sea urchins, speract, a sperm chemoattractant component released to seawater from the outer egg layer, attracts sperm after binding to its receptor in the sperm flagellum. Previous experiments performed in demembranated sperm indicated that motility regulation in these cells involved protein phosphorylation mainly due to the cAMP-dependent protein kinase (PKA). However, little information is known about the involvement of protein kinase C (PKC) in this process. In this work, using intact S. purpuratus sea urchin sperm, we show that: (i) the levels of both phosphorylated PKA (PKA substrates) and PKC (PKC substrates) substrates change between immotile, motile and speract-stimulated sperm, and (ii) the non-competitive PKA (H89) and PKC (chelerythrine) inhibitors diminish the circular velocity of sperm and alter the phosphorylation levels of PKA substrates and PKC substrates, while the competitive inhibitors Rp-cAMP and bisindolylmaleimide (BIM) do not. Altogether, our results show that both PKA and PKC participate in sperm motility regulation through a crosstalk in the signalling pathway. These results contribute to a better understanding of the mechanisms that govern motility in sea urchin sperm.

Type
Research Article
Copyright
© The Author(s), 2021. Published by Cambridge University Press

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