A positive perspective on DNA methylation: regulatory functions of DNA methylation outside of host defense in Gram-positive bacteria

Abstract

The presence of post-replicative DNA methylation is pervasive among both prokaryotic and eukaryotic organisms. In bacteria, the study of DNA methylation has largely been in the context of restriction-modification systems, where DNA methylation serves to safeguard the chromosome against restriction endonuclease cleavage intended for invading DNA. There has been a growing recognition that the methyltransferase component of restriction-modification systems can also regulate gene expression, with important contributions to virulence factor gene expression in bacterial pathogens. Outside of restriction-modification systems, DNA methylation from orphan methyltransferases, which lack cognate restriction endonucleases, has been shown to regulate important processes, including DNA replication, DNA mismatch repair, and the regulation of gene expression. The majority of research and review articles have been focused on DNA methylation in the context of Gram-negative bacteria, with emphasis toward Escherichia coli, Caulobacter crescentus, and related Proteobacteria. Here we summarize the epigenetic functions of DNA methylation outside of host defense in Gram-positive bacteria, with a focus on the regulatory effects of both phase variable methyltransferases and DNA methyltransferases from traditional restriction-modification systems.

Keywords:

• Restriction-modification
• Bacillus subtilis
• Gram-positive
• gene expression
• epigenetics

Acknowledgements

We wish to thank all of the scientists in the field for their dedication to understanding the regulatory functions of bacterial MTases. We would also like to acknowledge the thoughtful reviewer comments that were used to improved this manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The present research was financially supported by a National Science Foundation grant MCB 1714539 to LAS. TMN was supported in part by a National Science Foundation predoctoral fellowship [#DEG 1256260] and NLF was supported in part by a National Science Foundation postdoctoral fellowship [#2010735].