Sumoylation of Wor1 by a novel SUMO E3 ligase controls cell fate in XXXX .

@entity1 @entity3158 @entity5132 @entity376 @entity62
UNASSIGNED: @entity5132 is the most common @entity1 fungal pathogen, yet is a normal commensal resident of the @entity1 gut. @entity3158 levels in the gut are much higher than in air, and it is known that elevated @entity3158 concentration promotes @entity5132 cells to undergo a phenotypic switch from white to opaque phase. Wor1, the master regulator of opaque cell formation, is required for both the white-to-opaque transition and opaque maintenance. To elucidate the regulatory mechanism of Wor1, we set out to identify Wor1-interacting proteins using a yeast two-hybrid screen. A SUMO E3 ligase named Wos1 (Wor1 SUMO-ligase 1) was identified to interact with Wor1 and regulate Wor1 sumoylation. WOS1 expression is up-regulated in response to high @entity3158 , and the induction by @entity3158 is dependent on the transcription factor Flo8. Under high @entity3158 conditions, Wos1 is required for the white-to-opaque switch and acts downstream of Flo8. At atmospheric @entity3158 levels, over-expression of Wos1 enhances Wor1 sumoylation and promotes the white-to-opaque switch. Wor1 is found to be sumoylated at @entity376 385, and loss of this mark by point mutation leads to a defect in @entity3158 -mediated opaque cell induction. Together our genetic and biological data show that Wos1-mediated Wor1 sumoylation contributes to the regulation of @entity3158 -induced @entity62 as well as heritable maintenance of the opaque cell type.
