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Article Abstract
ERK activity oscillates between sustained activation during oocyte formation and transient inactivation during oocyte maturation, fertilization, and early embryogenesis. Consequences of ectopic ERK activity upon oocyte maturation and in early embryogenesis are unknown. We show, in Caenorhabditis elegans, that ectopic ERK activity upon oocyte maturation (metaphase I oocytes) results in embryos with abnormalities in nuclear divisions leading to embryonic death. We uncover that ERK directly phosphorylates Polo-like kinase I (PLK-1), on Serine 404, to inhibit nuclear envelope breakdown (NEBD) in early embryogenesis. The RAS/ERK/PLK-1 pathway poisons zygotic NEBD and inhibits the merging of parental genomes, underlining the importance of turning off ERK prior to embryogenesis. Given the conserved nature of both ERK signaling to oocyte development and PLK1 to embryonic divisions, this work has implications for women undergoing in vitro fertilization (IVF) where ectopic ERK activation during superovulation through hormonal stimulation may diminish oocyte quality and influence zygotic development.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11874628 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2024.115157 | DOI Listing |
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