Research in our laboratory revolves around the epigenetic circuitry underlying the regulation of gene expression by environmental cues, both during development and disease. The current focus of the laboratory is to understand the mechanisms that epigenetically modulate gene expression during the interaction of the host cell with microbes. Our work has identified

(i) mycobacterial proteins that help pathogenic mycobacteria hijack the host cellular machinery through their interaction with the host epigenome;

(ii) a novel surrogate function of a host epigenetic modifier in the host defense mechanism against mycobacterial infection. These findings have allowed us to study the role of epigenetic mechanisms in the evolution of microbe-host interaction.

• Yaseen I, Choudhury M, Sritharan M, Khosla S (2018) Histone methyltransferase SUV39H1 participates in host defense by methylating mycobacterial histone-like protein HupB. EMBO Journal 37:183-200.
• Dev RR, Ganji R, Singh SP, Mahalingam S, Banerjee S, Khosla S. (2017) Cytosine methylation by DNMT2 facilitates stability and survival of HIV-1 RNA in the host cell during infection. Biochemical Journal 474: 2009-2026.
• Sharma G, Sowpati DT, Singh P, Khan MZ, Ganji R, Upadhyay S, Banerjee S, Nandicoori VK, Khosla S. (2016) Genome-wide non-CpG methylation of the host genome during M. tuberculosis infection. Scientific Reports 6: 25006.
• Khosla S, Sharma G and Yaseen I (2016). Learning epigenetic regulation from mycobacteria. Microbial Cell 3: 92-94.
• Yaseen I, Kaur P, Nandicoori VK, Khosla S. (2015) Mycobacteria modulate host epigenetic machinery by Rv1988 methylation of a non-tail arginine of histone H3. Nature Communications 6:8922.
• Sharma G, Upadhyay S, Srilalitha M, Nandicoori VK, Khosla S. (2015) The interaction of mycobacterial protein Rv2966c with host chromatin is mediated through non-CpG methylation and histone H3/H4 binding. Nucleic Acids Research 43:3922-3937.