How does a TFs function depend on the promoter it regulates? We know that a TF can have different effects on different promoters. For example, consider this: CpxR regulates LdtC,YccA, EfeU at a similar location. Yet two of them are activated, one repressed tinyurl.com/3hr9njnd
There's more in the paper, but heres an overarching fig. All the paper data (and some existing data) collapsed to the same basic, universal behavior. We never see evidence of the relationships that would come from "destabilizing" type interactions. Everything looks stabilizing.
For me, this reshapes how I think about regulation. Every TF we look at has this useful behavior of buffering physiological &/or genetic perturbations to promoter activity. Although we expected many TFs would actively amplify perturbations, they don't. tinyurl.com/3hr9njnd
So we built a bunch of promoters and tested how these candidate stabilizers (and not stabilizers) regulate them. The ones we thought were stabilizers all pretty much have this tell-tale relationship (stronger promoters, lower fold-change)
The ones where we could not say for certain (kappa close to 1), showed varied (less clear) relationships. It's a good time to note that kappa ~ 1 doesn't mean it CAN'T be a stabilizer, only that we don't see evidence of stabilization (which can be for more than one reason).
So we measured 204 TFs at ~12 binding positions on the promoter and looked for signs of a specific mechanism of regulation by plotting their FC when regulating one pos. vs another; "stabilizing" interactions are inferred when we see curvature (kappa not equal to 1).
