Emi2 inhibition of the Anaphase-promoting Complex/Cyclosome absolutely requires Emi2 binding via the C-Terminal RL Tail

Emi2 (also called Erp1) inhibits the anaphase-promoting complex/cyclosome (APC/C) and thereby causes metaphase II arrest in unfertilized vertebrate eggs. Both the D-box and the zinc-binding region (ZBR) of Emi2 have been implicated in APC/C inhibition. However, it is not well known how Emi2 interact...

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Hauptverfasser: Ohe, Munemichi (VerfasserIn) , Inoue, Daigo (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: January 20, 2010
In: Molecular biology of the cell
Year: 2010, Jahrgang: 21, Heft: 6, Pages: 905-913
ISSN:1939-4586
DOI:10.1091/mbc.E09-11-0974
Online-Zugang:Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1091/mbc.E09-11-0974
Verlag, kostenfrei, Volltext: http://www.molbiolcell.org/content/21/6/905
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Verfasserangaben:Munemichi Ohe, Yoshiko Kawamura, Hiroyuki Ueno, Daigo Inoue, Yoshinori Kanemori, Chiharu Senoo, Michitaka Isoda, Nobushige Nakajo, and Noriyuki Sagata

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520 |a Emi2 (also called Erp1) inhibits the anaphase-promoting complex/cyclosome (APC/C) and thereby causes metaphase II arrest in unfertilized vertebrate eggs. Both the D-box and the zinc-binding region (ZBR) of Emi2 have been implicated in APC/C inhibition. However, it is not well known how Emi2 interacts with and hence inhibits the APC/C. Here we show that Emi2 binds the APC/C via the C-terminal tail, termed here the RL tail. When expressed in Xenopus oocytes and egg extracts, Emi2 lacking the RL tail fails to interact with and inhibit the APC/C. The RL tail itself can directly bind to the APC/C, and, when added to egg extracts, either an excess of RL tail peptides or anti-RL tail peptide antibody can dissociate endogenous Emi2 from the APC/C, thus allowing APC/C activation. Furthermore, and importantly, the RL tail-mediated binding apparently promotes the inhibitory interactions of the D-box and the ZBR (of Emi2) with the APC/C. Finally, Emi1, a somatic paralog of Emi2, also has a functionally similar RL tail. We propose that the RL tail of Emi1/Emi2 serves as a docking site for the APC/C, thereby promoting the interaction and inhibition of the APC/C by the D-box and the ZBR. 
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