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Editorial
. 2013 Aug 15;12(16):2528-9.
doi: 10.4161/cc.25839. Epub 2013 Jul 29.

Regulating PLK1 dynamics by Cullin3/KLHL22-mediated ubiquitylation

Editorial

Regulating PLK1 dynamics by Cullin3/KLHL22-mediated ubiquitylation

Jochen Beck et al. Cell Cycle. .
No abstract available

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Figures

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Figure 1. Model of PLK1 regulation by CUL3/KLHL22 mediated ubiquitylation (A) During prometaphase, PLK1 is recruited to kinetochores via PDB-mediated interactions with PLK1 kinetochore receptors, and there is highly dynamic exchange of kinetochore-bound PLK1 with the free cytoplasmic pool. Upon chromosome biorientation during metaphase, CUL3/KLHL22 accumulates at the mitotic spindle, where it potentially ubiquitylates the free pool of PLK1 in the PBD at K492, thus preventing its recruitment to kinetochore-associated interactors, resulting in PLK1 removal from kinetochores. Alternatively, the structural changes in centromere and kinetochore regions during metaphase may allow CUL3/KLHL22 to access kinetochore-bound PLK1, promoting its release and preventing its re-recruitment. (B) After removal of PLK1 from metaphase kinetochores, PLK1 may first be sequestered by a centrosome-associated UBP. At anaphase onset, PLK1 might be deubiquitylated by an unknown DUB, which could be activated by Cyclin B degradation. Without ubiquitin conjugated to its PBD, PLK1 can now establish new interactions, e.g., with PRC1, thus targeting PLK1 to the central spindle. Similarly, we propose that CUL3/KLHL21-ubiquitylated Aurora B is transferred from centromeres and anchored to the central spindle via the action of an ubiquitin-binding protein associated with central spindle microtubules.

Comment on

  • Ubiquitylation-dependent localization of PLK1 in mitosis.
    Beck J, Maerki S, Posch M, Metzger T, Persaud A, Scheel H, Hofmann K, Rotin D, Pedrioli P, Swedlow JR, Peter M, Sumara I. Beck J, et al. Nat Cell Biol. 2013 Apr;15(4):430-9. doi: 10.1038/ncb2695. Epub 2013 Mar 3. Nat Cell Biol. 2013. PMID: 23455478 Free PMC article.

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