Abstract
SETMAR is a protein lysine methyltransferase that is involved in several DNA processes, including DNA repair via the non-homologous end joining (NHEJ) pathway, regulation of gene expression, illegitimate DNA integration, and DNA decatenation. However, SETMAR is an atypical protein lysine methyltransferase since in anthropoid primates, the SET domain is fused to an inactive DNA transposase. The presence of the DNA transposase domain confers to SETMAR a DNA binding activity towards the remnants of its transposable element, which has resulted in the emergence of a gene regulatory function. Both the SET and the DNA transposase domains are involved in the different cellular roles of SETMAR, indicating the presence of novel and specific functions in anthropoid primates. In addition, SETMAR is dysregulated in different types of cancer, indicating a potential pathological role. While some light has been shed on SETMAR functions, more research and new tools are needed to better understand the cellular activities of SETMAR and to investigate the therapeutic potential of SETMAR.
Highlights
In eukaryotes, DNA is wrapped around proteins called histone to form the chromatin, a nucleoprotein structure
A key factor in chromatin regulation is the addition, removal, and reading of post-translational modifications (PTMs) that can be deposited on the tails of histones, especially H3 and H4
The expression of SETMAR has been found to be regulated by SOX11 [23], a transcription factor involved in development, including neurogenesis and skeletogenesis, and disease, such as neurodevelopmental disorders, osteoarthiritis, and cancers [47]
Summary
DNA is wrapped around proteins called histone to form the chromatin, a nucleoprotein structure. The histone code hypothesis implies that specific patterns of histone PTMs are associated and involved in specific DNA processes. Dimethylation of H3K36 (H3K36me2) is associated with regulation of gene expression and DNA damage repair [6]. H3K36me is catalyzed by several histone methyltransferases, including ASH1L, NSD1-3, SETD3, SETMAR, and SMYD2 [7]. The human SETMAR has been associated with numerous cellular processes, including DNA damage repair via the non-homologous end joining (NHEJ) pathway, illegitimate DNA integration, restart of stalled replication forks, chromosomal decatenation, suppression of chromosomal translocations, and regulation of gene expression [12,13,14,15,16,17,18,19,20,21]. SETMAR is dysregulated in several cancers, such as glioblastoma, leukemia, hematologic neoplasms, breast and colon cancer, and mantle cell lymphoma [16,22,23,24,25,26,27,28,29,30]
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