We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Conversion of the LIN-1 ETS Protein of Caenorhabditis elegans from a SUMOylated Transcriptional Repressor to a Phosphorylated Transcriptional Activator.
- Authors
Leight, Elizabeth R.; Murphy, John T.; Fantz, Douglas A.; Pepin, Danielle; Schneider, Daniel L.; Ratliff, Thomas M.; Mohammad, Duaa H.; Herman, Michael A.; Kornfeld, Kerry
- Abstract
The LIN-1 ETS transcription factor plays a pivotal role in controlling cell fate decisions during development of the Caenorhabditis elegans vulva. Prior to activation of the RTK/Ras/ERK-signaling pathway, LIN-1 functions as a SUMOylated transcriptional repressor that inhibits vulval cell fate. Here we demonstrate using the yeast two-hybrid system that SUMOylation of LIN-1 mediates interactions with a protein predicted to be involved in transcriptional repression: the RAD-26 Mi-2β/CHD4 component of the nucleosome remodeling and histone deacetylation (NuRD) transcriptional repression complex. Genetic studies indicated that rad-26 functions to inhibit vulval cell fates in worms. Using the yeast two-hybrid system, we showed that the EGL-27/MTA1 component of the NuRD complex binds the carboxy-terminus of LIN-1 independently of LIN-1 SUMOylation. EGL-27 also binds UBC-9, an enzyme involved in SUMOylation, and MEP-1, a zinc-finger protein previously shown to bind LIN-1. Genetic studies indicate that egl-27 inhibits vulval cell fates in worms. These results suggest that LIN-1 recruits multiple proteins that repress transcription via both the SUMOylated amino-terminus and the unSUMOylated carboxy-terminus. Assays in cultured cells showed that the carboxy-terminus of LIN-1 was converted to a potent transcriptional activator in response to active ERK. We propose a model in which LIN-1 recruits multiple transcriptional repressors to inhibit the 1° vulval cell fate, and phosphorylation by ERK converts LIN-1 to a transcriptional activator that promotes the 1° vulval cell fate.
- Subjects
CAENORHABDITIS elegans genetics; TRANSCRIPTION factors; HISTONE deacetylase; PHOSPHORYLATION; CHROMATIN
- Publication
Genetics, 2015, Vol 199, Issue 3, p761
- ISSN
0016-6731
- Publication type
Article
- DOI
10.1534/genetics.114.172668