Fig. 10: Multi-pronged mechanism of Rv2067c induces necrosis in macrophages to enhance Mtb’s survival. | Nature Communications

Fig. 10: Multi-pronged mechanism of Rv2067c induces necrosis in macrophages to enhance Mtb’s survival.

From: The Mycobacterium tuberculosis methyltransferase Rv2067c manipulates host epigenetic programming to promote its own survival

Fig. 10

Mtb secretes MTase Rv2067c into the host macrophages, which trimethylates free H3 at lysine 79. Rv2067c mediated H3K79me3 mark enhances the expression of genes such as NLRC3, SESTRIN3 and TMTC1, enabling the bacteria to counter the host defense. Rv2067c also steers the cell toward RIPK3-mediated necrosis by downregulating DOT1L to impact the expression of pro-inflammatory cytokines such as TNF-α and IL-6. A concomitant upregulation of anti-apoptotic markers is observed. Green and red arrows show upregulation and downregulation of genes, respectively.

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