CaMKII prevents spontaneous acrosomal exocytosis in sperm through induction of actin polymerization

Ortal Shabtay, Haim Breitbart

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

In order to interact with the egg and undergo acrosomal exocytosis or the acrosome reaction (AR), mammalian spermatozoa must undergo a series of biochemical changes in the female reproductive tract, collectively called capacitation. We showed that F-actin is formed during sperm capacitation and fast depolymerization occurs prior to the AR. We hypothesized that F-actin protects the sperm from undergoing spontaneous-AR (sAR) which decreases fertilization rate. We show that activation of the actin-severing protein gelsolin induces a significant increase in sAR. Moreover, inhibition of CaMKII or PLD during sperm capacitation, caused an increase in sAR and inhibition of F-actin formation. Spermine, which leads to PLD activation, was able to reverse the effects of CaMKII inhibition on sAR-increase and F-actin-decrease. Furthermore, the increase in sAR and the decrease in F-actin caused by the inactivation of the PLD-pathway, were reversed by activation of CaMKII using H2O2 or by inhibiting protein phosphatase 1 which enhance the phosphorylation and oxidation states of CaMKII. These results indicate that two distinct pathways lead to F-actin formation in the sperm capacitation process which prevents the occurrence of sAR.

Original languageEnglish
Pages (from-to)64-74
Number of pages11
JournalDevelopmental Biology
Volume415
Issue number1
DOIs
StatePublished - 1 Jul 2016

Bibliographical note

Publisher Copyright:
© 2016 Elsevier Inc.

Funding

This study was supported by IHEL Foundation. This research was supported by the IHEL Foundation to H. B.

FundersFunder number
Ihel Foundation
Ihel Foundation

    Keywords

    • Acrosome reaction
    • Actin
    • CaMKII
    • PLD
    • ROS
    • Spermatozoa

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