4.8 Article

ULK1 phosphorylates Mad1 to regulate spindle assembly checkpoint

Journal

NUCLEIC ACIDS RESEARCH
Volume 47, Issue 15, Pages 8096-8110

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/nar/gkz602

Keywords

-

Funding

  1. National Key R&D Program of China [2017YFA0503900]
  2. National Natural Science Foundation of China [81472581, 81672712, 81874145, 81621063, 91319302, 31261140372]

Ask authors/readers for more resources

The spindle assembly checkpoint (SAC) ensures the fidelity of chromosome segregation during mitosis. Here, we show that ULK1, a serine/threonine kinase that plays a key role in initiation of autophagy, also has an important function in the activation of SAC. ULK1 phosphorylates the SAC protein Mad1 at Ser546 to recruit Mad1 to kinetochores. Furthermore, Rod/ZW10/Zwilch (RZZ) complex may serve as a receptor for phos-Ser546-Mad1 at kinetochore, since phosphorylation of Mad1 by ULK1 strengthens the interaction between Mad1 and RZZ complex. In addition, deletion of ULK1 increases chromosome instability and cytotoxicity of paclitaxel, resulting in significant impairment of cancer cell growth. These findings highlight the role of ULK1 as a protein kinase controlling the fidelity of chromosome segregation and cell-cycle progression.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.8
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available