Learning epigenetic regulation from mycobacteria
Authors:Sanjeev Khosla1, Garima Sharma1,2 and Imtiyaz Yaseen1,2
doi: 10.15698/mic2016.02.480
Volume 3, pp. 92 to 94, published 18/01/2016.
1 Centre for DNA Fingerprinting and Diagnostics (CDFD), Hyderabad, India.
2 Graduate Studies, Manipal University, Manipal, India.
Keywords:
Rv1988, Mycobacterium tuberculosis, histone arginine methylation, DNA methylation, epigenetics, Rv2966c, H3R42.
Corresponding Author(s):
Conflict of interest statement:
A patent application, based on the results described in the original research paper, has been filed by the Centre for DNA Fingerprinting and Diagnostics (CDFD), in which S.K. and I.Y. are listed as inventors. The remaining authors declare no competing financial interests.
Please cite this article as:
Sanjeev Khosla, Garima Sharma and Imtiyaz Yaseen (2016). Learning epigenetic regulation from mycobacteria. Microbial Cell 3(2): 92-94. doi: 10.15698/mic2016.02.480
© 2016 Khosla et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
In a eukaryotic cell, the transcriptional fate of a gene is determined by the profile of the epigenetic modifications it is associated with and the conformation it adopts within the chromatin. Therefore, the function that a cell performs is dictated by the sum total of the chromatin organization and the associated epigenetic modifications of each individual gene in the genome (epigenome). As the function of a cell during development and differentiation is determined by its microenvironment, any factor that can alter this microenvironment should be able to alter the epigenome of a cell. In the study published in Nature Communications (Yaseen [2015] Nature Communications 6:8922 doi: 10.1038/ncomms9922), we show that pathogenic Mycobacterium tuberculosis has evolved strategies to exploit this pliability of the host epigenome for its own survival. We describe the identification of a methyltransferase from M. tuberculosis that functions to modulate the host epigenome by methylating a novel, non-canonical arginine, H3R42 in histone H3. In another study, we showed that the mycobacterial protein Rv2966c methylates cytosines present in non-CpG context within host genomic DNA upon infection. Proteins with ability to directly methylate host histones H3 at a novel lysine residue (H3K14) has also been identified from Legionella pnemophilia (RomA). All these studies indicate the use of non-canonical epigenetic mechanisms by pathogenic bacteria to hijack the host transcriptional machinery.