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Protein kinase G (PknG), a thioredoxin-fold–containing eukaryotic-like serine/threonine protein kinase, is a virulence factor in Mycobacterium tuberculosis, required for inhibition of phagolysosomal fusion. Here, we unraveled novel functional facets of PknG during latency-like conditions. We found that PknG mediates persistence under stressful conditions like hypoxia and abets drug tolerance.
Protein Kinase G (PknG), a thioredoxin-fold containing eukaryotic like serine/threonine protein kinase (STPK), is a virulence factor in the Mycobacterium tuberculosis, required for inhibition of phago-lysosomal fusion. Here, we unravelled novel functional facets of PknG during latency like conditions. We find that PknG mediates persistence under stressful conditions like hypoxia and abets drug tolerance.
In prior work, we identified four putative PG degrading amidases in the genome of Mycobacterium tuberculosis and M. smegmatis, which were designated as Ami1 (Rv3717, MSMEG_6281), Ami2 (Rv3915- CwlM, MSMEG_6935), Ami3 (Rv3811, MSMEG_6406), and Ami4 (Rv3594, MSMEG_5315)34. Ami1 and Ami2 belong to the amidase_3 domain family, while Ami3 and Ami4 belong to the amidase_2 domain family of cell wall hydrolysing amidases.
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