Candida albicans ( C. albicans) is an opportunistic pathogen in humans and possesses a white-opaque heritable switching system. Wor1 is a master regulator of white-opaque switching and is essential for opaque cell formation in C. albicans. However, the regulatory network of Wor1 in white-opaque switching is still vague. In this study, we obtain a series of Wor1-interacting proteins using LexA-Wor1 as bait. Among these proteins, function unknown now 30 (Fun30) interacts with Wor1 in vitro and in vivo. Fun30 expression is upregulated in opaque cells at the transcriptional and protein levels. Loss of FUN30 attenuates white-to-opaque switching, while ectopic expression of FUN30 significantly increases white-to-opaque switching in an ATPase activity-dependent manner. Furthermore, FUN30 upregulation is dependent on CO 2; loss of FLO8, a key CO 2-sensing transcriptional regulator, abolishes FUN30 upregulation. Interestingly, deletion of FUN30 affects the WOR1 expression regulation feedback loop. Thus, our results indicate that the chromatin remodeller Fun30 interacts with Wor1 and is required for WOR1 expression and opaque cell formation.
Keywords: Fun30; Wor1; chromatin remodeller; white-opaque switching.