Abstract
A DNA sequence is the hard copy of the human genome and it is a driving force in determining the physiological processes in an organism. Concurrently, the chemical modification of the genome and its related histone proteins is dynamically involved in regulating physiological processes and diseases, which overall constitutes the epigenome network. Among the various forms of epigenetic modifications, DNA methylation at the C-5 position of cytosine in the cytosine–guanine (CpG) dinucleotide is one of the most well studied epigenetic modifications. DNA methyltransferases (DNMTs) are a family of enzymes involved in generating and maintaining CpG methylation across the genome. In mammalian systems, DNA methylation is performed by DNMT1 and DNMT3s (DNMT3A and 3B). DNMT1 is predominantly involved in the maintenance of DNA methylation during cell division, while DNMT3s are involved in establishing de novo cytosine methylation and maintenance in both embryonic and somatic cells. In general, all DNMTs require accessory proteins, such as ubiquitin-like containing plant homeodomain (PHD) and really interesting new gene (RING) finger domain 1 (UHRF1) or DNMT3-like (DNMT3L), for their biological function. This review mainly focuses on the role of DNMT3B and its isoforms in de novo methylation and maintenance of DNA methylation, especially with respect to their role as an accessory protein.
Highlights
With the improvement in DNA-sequencing technologies, genetic alterations were initially recognized as the main contributors of the initiation and progression of diseases including cancer [1,2,3,4]
DNMT3A and DNMT3B are mainly expressed in undifferentiated cells, where they are essential for the formation and subsequent maintenance of DNA methylation marks [15,76,78,79]
DNMT1 is a key enzyme for maintenance of DNA methylation, the double knockout of Dnmt3a and Dnmt3b in mouse embryonic cells resulted in a gradual loss of DNA methylation over time, indicating the involvement of Dnmt3a/Dnmt3b in maintaining DNA methylation profiles during embryonic development (Figure 1) [76,77]
Summary
With the improvement in DNA-sequencing technologies, genetic alterations were initially recognized as the main contributors of the initiation and progression of diseases including cancer [1,2,3,4]. The epigenome of an organism represents the collection of cellular processes that alter gene regulation, which are not attributed to the DNA sequence alone. This information is represented by histone modification, histone variants, nucleosome occupancy, expression of non-coding regulatory RNAs, and DNA methylation. These modifications dynamically regulate gene expression to maintain physiological processes, cellular function, and organismal development [5,7,9,10,11,12,13,14,15,16,17,18,19]
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