Premium
The MyT1 family recruits histone deacetylase to regulate neural transcription
Author(s) -
Romm E.,
Kim J. G.,
Kim N. W.,
Nagle J.,
Hudson L. D.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.1_2.x
Subject(s) - biology , zinc finger , genetics , transcription factor , corepressor , microbiology and biotechnology , histone , histone deacetylase , gene , repressor
The MyT1 gene family is comprised of three zinc finger genes (MyT1, MyT1‐Like/MyT1L and NZF3) of the structurally unique CCHC class that are expressed predominantly in the developing central nervous system. To understand the molecular mechanism by which this family promotes neural differentiation, we searched for interaction partners. In both a yeast and a mammalian two hybrid system, MyT1 and MyT1L interacted with Sin3B, a protein, which can mediate transcriptional repression by binding to histone deacetylase (HDAC). MyT1‐Sin3B complexes could also be coimmunoprecipitated from transfected mammalian cells. The interacting domain includes three amphipathic alpha‐helices and is highly conserved among MyT1 family members. MyT1 and MyT1L can partner with both Sin3B isoforms, the full length form that includes the HDAC‐binding domain and an alternatively spliced short form (Sin3BSF) that lacks this domain and would consequently antagonize Sin3B‐mediated corepression. MyT1 has two zinc finger clusters, and one of these DNA‐binding domains recognizes a broad consensus site (GGTGGGGa/g a/g a/g) suggestive of a wide range of potential gene targets for this transcription factor. We present a model in which the MyT1 family of zinc finger proteins, when tethered to the DNA binding site of a neural promoter, can recruit the corepressor Sin3B. Depending on the relative availability of Sin3B isoforms, the MyT1 gene family may favor the silencing or activation of selected genes during neural development.