hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish
- Mei, W., Lee, K.W., Marlow, F.L., Miller, A.L., and Mullins, M.C.
- Development (Cambridge, England) 136(17): 3007-3017 (Journal)
- Registered Authors
- Lee, Karen W., Marlow, Florence, Mei, Wenyan, Miller, Andrew L., Mullins, Mary C.
- hnRNP I, brom bones, IP3, Ca2+, Egg activation, Zebrafish, Cortical granule exocytosis, Maternal effect
- MeSH Terms
- Amino Acid Sequence
- Calcium Signaling/physiology*
- Endoplasmic Reticulum/metabolism
- Heterogeneous-Nuclear Ribonucleoproteins/genetics
- Heterogeneous-Nuclear Ribonucleoproteins/metabolism*
- Inositol 1,4,5-Trisphosphate/metabolism
- Molecular Sequence Data
- Sequence Alignment
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 19666827 Full text @ Development
Mei, W., Lee, K.W., Marlow, F.L., Miller, A.L., and Mullins, M.C. (2009) hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish. Development (Cambridge, England). 136(17):3007-3017.
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 Ca(2+) in the egg cytosol at fertilization. This Ca(2+) rise is crucial for all subsequent egg activation steps, such as cortical granule exocytosis, which modifies the vitelline membrane to prevent polyspermy. The cytosolic Ca(2+) rise is primarily initiated by inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release from the endoplasmic reticulum. The genes involved in regulating the IP(3)-mediated Ca(2+) release during egg activation remain largely unknown. Here we report on a zebrafish maternal-effect mutant, brom bones, which is defective in the cytosolic Ca(2+) 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 Ca(2+) or the Ca(2+)-release messenger IP(3), suggesting that brom bones is a regulator of IP(3)-mediated Ca(2+) 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 IP(3)-mediated Ca(2+) release at egg activation.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes