QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online August 7, 2009
doi: 10.1242/10.1242/dev.037879

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Mei, W. Articles by Mullins, M. C. PubMed PubMed Citation Articles by Mei, W. Articles by Mullins, M. C. Social Bookmarking                         What's this?

hnRNP I is required to generate the Ca²⁺ signal that causes egg activation in zebrafish

Wenyan Mei^1,2, Karen W. Lee^3,*, Florence L. Marlow¹, Andrew L. Miller³ and Mary C. Mullins^1,

¹ Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
² The Research Institute at Nationwide Children's Hospital, Center for Cell and Developmental Biology, 700 Children's Drive, Columbus, OH 43205, USA.
³ Department of Biology, HKUST, Clear Water Bay, Kowloon, Hong Kong.

Author for correspondence (mullins{at}mail.med.upenn.edu)

Accepted 2 July 2009

Egg activation is an important cellular event required to prevent polyspermy and initiate development of the zygote. Egg activation in all animals examined is elicited by a rise in free Ca²⁺ in the egg cytosol at fertilization. This Ca²⁺ rise is crucial for all subsequent egg activation steps, such as cortical granule exocytosis, which modifies the vitelline membrane to prevent polyspermy. The cytosolic Ca²⁺ rise is primarily initiated by inositol 1,4,5-trisphosphate (IP₃)-mediated Ca²⁺ release from the endoplasmic reticulum. The genes involved in regulating the IP₃-mediated Ca²⁺ release during egg activation remain largely unknown. Here we report on a zebrafish maternal-effect mutant, brom bones, which is defective in the cytosolic Ca²⁺ rise and subsequent egg activation events, including cortical granule exocytosis and cytoplasmic segregation. We show that the egg activation defects in brom bones can be rescued by providing Ca²⁺ or the Ca²⁺-release messenger IP₃, suggesting that brom bones is a regulator of IP₃-mediated Ca²⁺ release at fertilization. Interestingly, brom bones mutant embryos also display defects in dorsoventral axis formation accompanied by a disorganized cortical microtubule network, which is known to be crucial for dorsal axis formation. We provide evidence that the impaired microtubule organization is associated with non-exocytosed cortical granules from the earlier egg activation defect. Positional cloning of the brom bones gene reveals that a premature stop codon in the gene encoding hnRNP I (referred to here as hnrnp I) underlies the abnormalities. Our studies therefore reveal an important new role of hnrnp I in regulating the fundamental process of IP₃-mediated Ca²⁺ release at egg activation.

Key words: hnRNP I, brom bones, IP₃, Ca²⁺, Egg activation, Zebrafish, Cortical granule exocytosis, Maternal effect

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?