Control of Emi2 activity and stability through Mos-mediated recruitment of PP2A.
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Before fertilization, vertebrate eggs are arrested in meiosis II by cytostatic factor (CSF), which holds the anaphase-promoting complex (APC) in an inactive state. It was recently reported that Mos, an integral component of CSF, acts in part by promoting the Rsk-mediated phosphorylation of the APC inhibitor Emi2/Erp1. We report here that Rsk phosphorylation of Emi2 promotes its interaction with the protein phosphatase PP2A. Emi2 residues adjacent to the Rsk phosphorylation site were important for PP2A binding. An Emi2 mutant that retained Rsk phosphorylation but lacked PP2A binding could not be modulated by Mos. PP2A bound to Emi2 acted on two distinct clusters of sites phosphorylated by Cdc2, one responsible for modulating its stability during CSF arrest and one that controls binding to the APC. These findings provide a molecular mechanism for Mos action in promoting CSF arrest and also define an unusual mechanism, whereby protein phosphorylation recruits a phosphatase for dephosphorylation of distinct sites phosphorylated by another kinase.
SubjectAmino Acid Sequence
Molecular Sequence Data
Proto-Oncogene Proteins c-mos
Ribosomal Protein S6 Kinases
Published Version (Please cite this version)10.1073/pnas.0707537104
Publication InfoFreel, CD; Guo, Y; Hansen, DV; Jackson, PK; Kornbluth, S; Tang, W; ... Wu, JQ (2007). Control of Emi2 activity and stability through Mos-mediated recruitment of PP2A. Proc Natl Acad Sci U S A, 104(42). pp. 16564-16569. 10.1073/pnas.0707537104. Retrieved from https://hdl.handle.net/10161/8391.
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Jo Rae Wright University Professor
Our lab studies the regulation of complex cellular processes, including cell cycle progression and programmed cell death (apoptosis). These tightly orchestrated processes are critical for appropriate cell proliferation and cell death, and when they go awry can result in cancer and degenerative disorders. Within these larger fields, we have focused on understanding the cellular mechanisms that prevent the onset of mitosis prior to the completion of DNA replication, the process