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. 2020 Nov 5;11:592615. doi: 10.3389/fmicb.2020.592615

FIGURE 7.

FIGURE 7

Model of Mn-dependent CcpA repression. (A) Depiction of a segment of the glycolysis and gluconeogenesis pathway in S. sanguinis from KEGG (Kanehisa and Goto, 2000). Red circles indicate potentially Mn-cofactored enzymes. Gene expression for each post-EDTA time point compared to T–20 is indicated by the colored boxes. Significant changes (P < 0.05) are indicated by red (increased) or blue (decreased). TPM values at T–20 are colored as indicated, with values ≥ 1,000 fully saturated (green). (B) Model of Mn-dependent CcpA repression based on CCR in Firmicutes as described by Gorke and Stulke (2008). In the top panel, normal Mn levels in BHI result in low FBP, which leads to less phosphorylation of HPr to HPr(Ser-P) by HPr kinase/phosphorylase (HPrK). With low FBP and HPr(Ser-P), CcpA exists mainly in its free state, unbound to cre sites in the DNA. This results in little to no repression of the CcpA regulon. The bottom panel depicts Mn depletion, where reduced activity of fructose-1,6-bisphosphatase and fructose-bisphosphate aldolase leads to an accumulation of FBP. This induces the phosphorylation of HPr so that it is primarily in the HPr(Ser-P) state. Increased FBP levels also enhance binding of CcpA to HPr(Ser-P) and to DNA. This results in augmented repression of the CcpA regulon.