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Cell Regul 1991 May 01;25:391-402. doi: 10.1091/mbc.2.5.391.
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Okadaic acid suppresses calcium regulation of mitosis onset in sea urchin embryos.

Patel R , Whitaker M .

We show that a phosphatase inhibitor, okadaic acid, induces premature and persistent mitosis during the first cell cycle in sea urchin embryos. Okadaic acid-induced mitosis requires protein synthesis, suggesting that it activates the protein synthesis-requiring mitotic H1 kinase. By microinjecting the calcium chelators BAPTA and EGTA and by measuring Cai using fura-2, an indicator dye, we show that okadaic acid-induced mitosis is independent of the calcium signal that usually triggers mitosis onset in sea urchin embryos. Disabling the calmodulin kinase II that is thought to respond to the mitotic Cai signal using a peptide inhibitor fails to prevent mitosis in response to okadaic acid. These data suggest that okadaic acid bypasses calcium regulation of mitosis by inducing constitutive phosphorylation of a site on the H1 kinase that is normally under the control of the calmodulin-regulated kinase.

PubMed ID: 1654128
PMC ID: PMC361809
Article link: Cell Regul
Grant support: [+]

Genes referenced: LOC100887844 LOC115919910

References [+] :
Arion, M-phase-specific protein kinase from mitotic sea urchin eggs: cyclic activation depends on protein synthesis and phosphorylation but does not require DNA or RNA synthesis. 1989, Pubmed, Echinobase