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.
CITATION STYLE
Mei, W., Lee, K. W., Marlow, F. L., Miller, A. L., & Mullins, M. C. (2009). hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish. Development, 136(17), 3007–3017. https://doi.org/10.1242/dev.037879
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