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Identification of novel protein‐protein interactions pertinent to regulation of mammalian hampin/MSL1 and histone acetylase MYST1/MOF
Author(s) -
Dmitriev Ruslan I,
Korneenko Tatyana V,
Pestov Nikolay B,
Modyanov Nikolay N,
Shakhparonov Mikhail I
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a283-c
Subject(s) - tetratricopeptide , biology , rna splicing , rna polymerase ii , interactome , transcription factor , two hybrid screening , microbiology and biotechnology , splicing factor , transcription (linguistics) , genetics , rna , gene , promoter , gene expression , linguistics , philosophy
Mammalian protein hampin is a homolog of drosophila MSL1. Despite their poor sequence homology, functions of both proteins are conserved in that they both associate with histone acetylase MYST1/MOF. In order to identify new regulatory mechanisms of the hampin/MSL11‐MYST1/MOF complex, we attempted to find new interacting proteins using cDNA library screening using yeast two‐hybrid system. Screening of a whole mouse embryo library against hampin yielded several clones of MYST1 and also four novel proteins: two tetratricopeptide repeat proteins (TTC4 and KIAA0103), NOP17 and a zinc finger transcription factor GC BP. Sequential screening of these proteins revealed that KIAA0103 binds to oncosuppressor RASSF1C and splicing factor PRP3, RASSF1C binds to ring finger protein 10, and MYST1 binds to NELF‐C, a component of negative transcription elongation complex. Interactions hampin‐TTC4, hampin‐MYST1 and MYST1‐NELF‐C were confirmed by pull‐down experiments of bacterially expressed proteins. Our results together with published data allowed reconstruction of a fragment of mammalian interactome that includes hampin and to hypothesize that H4 K16 acetyltransferase activity of MYST/MOF may be linked to regulation of transcription by RNA polymerase II, RNA splicing, DNA repair, and oncosuppression. Supported by Russian Foundation for Basic Resarch and National Institutes of Health.