Abstract
MOF was first identified in Drosophila melanogaster as an important component of the dosage compensation complex. As a member of MYST family of histone acetyltransferase, MOF specifically deposits the acetyl groups to histone H4 lysine 16. Throughout evolution, MOF and its mammalian ortholog have retained highly conserved substrate specificity and similar enzymatic activities. MOF plays important roles in dosage compensation, ESC self-renewal, DNA damage and repair, cell survival, and gene expression regulation. Dysregulation of MOF has been implicated in tumor formation and progression of many types of human cancers. This review will discuss the structure and activity of mammalian hMOF as well as its function in H4K16 acetylation, DNA damage response, stem cell pluripotency, and carcinogenesis.
Highlights
In eukaryotes, the vast amount of genetic material must fit within a relatively small nucleus
Dysregulation of MOF has been implicated in tumor formation and progression of many types of human cancers
MOF is a component of two different protein complexes and requires protein partners to control its histone acetyltransferase (HAT) activity and substrate specificity
Summary
The vast amount of genetic material must fit within a relatively small nucleus. The binding of MSL complex to the male X chromosome is accompanied by increased acetylation of histone H4 lysine 16 (H4K16) as well as a 2-fold transcription activation of X-linked genes [8,11]. MOF plays a fundamental role in male specific gene dosage compensation via acetylation of histone H4K16. The human ortholog of Drosophila MOF (hMOF) exhibits highly conserved substrate specificity and enzymatic activity [5,12]. Both MSL and NSL complexes are found in mammalian cells, which are responsible for acetylation of H4K16 in the nucleosome [5]. HMOF and histone H4K16 acetylation play important roles in DNA damage response, cell cycle regulation, and gene expression. This review will discuss the structure of mammalian hMOF as well as its role in H4K16 acetylation, DNA damage response, stem cell pluripotency, and carcinogenesis
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