A single transcriptional regulator is crucial for the adaptation of Staphylococcus aureus to diverse niches
Vogl, C.; Mikula, L. C.; Marbach, H.; Mayer-Weihrauch, K.; Herndler, S.; Breitschopf, L.; Pickering, A.; Jobson, M.-E.; Cabal, A. R.; Dinhopl, N.; Loncaric, I.; Ruppitsch, W.; Shaw, L. N.; Keane, O. M.; Fitzgerald, R.; Ehling-Schulz, M.; Heilbronner, S.; Grunert, T.
Show abstract
The adaptation of versatile multi-host pathogens to various hosts and various niches within hosts is often still poorly understood. The alternative Sigma factor B (SigB) is the master regulator of the general stress response of most gram-positive bacteria, which is a classic case of adaptive plasticity. In Staphylococcus aureus, SigB appears co-opted to function as a switch between intracellular and extracellular niches. During bovine mastitis, low SigB-activity confers an advantage in the milk-rich extracellular niche of the bovine udder. We show that narrowly adapted SigB-deficient strains evolved repeatedly from phenotypically plastic SigB-wildtype strains during persistent mastitis. This genetic assimilation appears driven by the cost of phenotypic plasticity: long time lags in adapting to milk and slow growth. Surprisingly, we observe that mutations causing SigB-deficiency allow even human isolates to grow in milk. While host adaptation often proceeds by mobile genetic elements exchanged between strains, we show how a master regulator in the core genome can drive niche adaptation.
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