The COMPASS Family of Histone H3K4 Methylases: Mechanisms of Regulation in Development and Disease Pathogenesis

By A. Shilatifard. Annual Review of Biochemistry, 2012

1,044 citations recorded by the source corpus.

The Saccharomyces cerevisiae Set1/COMPASS was the first histone H3 lysine 4 (H3K4) methylase identified over ten years ago. Since then, it has been demonstrated that Set1/COMPASS and its enzymatic product, H3K4 methylation, is highly conserved across the evolutionary tree. Although there is only one COMPASS in yeast, human cells bear at least six COMPASS family members each capable of methylating H3K4 with non-redundant functions. In yeast, the monoubiquitination of histone H2B by Rad6/Bre1 is required for proper H3K4 and H3K79 trimethylations. This histone crosstalk and its machinery are also highly conserved from yeast to human. In this review, the process of histone H2B monoubiquitination-dependent and independent histone H3K4 methylation as a mark of active transcription, enhancer signatures, and developmentally poised genes will be discussed. The misregulation of histone H2B monoubiquitination and H3K4 methylation results in the pathogenesis of human diseases including cancer. Recent findings in this regard will also be examined.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a556a82a7a6c82072dc93cdb5afd673fd167c8d9

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In Molecular Biology

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Citations in the corpus

• The RNA polymerase II CTD coordinates transcription and RNA processing. (2012, background): “MLL1/MLL2 are required for proper Hox gene expression, and translocation mutations of MLL are associated with the pathogenesis of leukemia (for review, see Shilatifard 2012).”
• H3K4me3 breadth is linked to cell identity and transcriptional consistency (2014, background): “Perturbations in H3K4me3modifying complexes lead to cancer in mammals (Shilatifard, 2012)and lifespan changes in invertebrates (Greer et al.”
• Histone Marks in the 'Driver's Seat': Functional Roles in Steering the Transcription Cycle. (2017, background): “H3K4me3 is written by a variety of methyltransferases, including the mixed lineage leukemia (MLL) and SET domain containing 1A & B (SETD1A/B) complexes (reviewed in [20,21]).”
• Analysis of nascent RNA identifies a unified architecture of initiation regions at mammalian promoters and enhancers (2014, neutral): “Consistent with this observation, H3K4me3 has been detected at some active enhancers 11, 46 , and can be deposited in a transcription-dependent manner 11, 47 .”
• A double take on bivalent promoters. (2013, background): “The SET1A/B complexes are responsible for the bulk of H3K4me3, while the MLL complexes likely assume more gene-specific roles (Shilatifard 2012).”
• Modification of enhancer chromatin: what, how and why? (2013, background): “For example, H4K16ac was shown to disrupt 30 nm fiber formation and impede ability of chromatin to form cross-fiber interactions (Shogren-Knaak et al., 2006).”