We often say that 'competent cells bind and take up DNA', but we don't really know whether binding of DNA to the cell surface is a distinct step from uptake of the DNA into the periplasm. If it is, we also don't know whether binding is specific for uptake sequences. And if it is, we'd want to then find out whether uptake was also specific for uptake sequences. I've been reading a 2002 paper about DNA binding and uptake specificity in Neisseria, because I'm considering including this question as an aim of our NIH proposal, but I just realized that I should first decide why this is (or isn't) an important question.
Years ago I had a grad student working on a related question, and part of our motivation was the issue of whether sequence specificity is intrinsic to the process of DNA uptake, as is predicted by our hypothesis that it's a way to help get stiff inflexible DNAs across the outer membrane. If instead the specificity is caused by a protein external to the uptake machinery, this would be consistent with hypotheses positing a benefit of screening DNA for relatedness before letting it into the cell.
The practical obstacle to answering this question is that we have no good assay for DNA binding (and of course also no mutants that can still bind DNA but can't take it up). At present, DNA binding must be measured indirectly, by giving cells radioactively labeled DNA and comparing cell-associated cpm with and without pretreatment with DNase, which removes DNA that has bound to cells but not been taken inside them.
The Neisseria paper (Aas et al, 2002) took advantage of the pilT gene, which H. influenzae and its relatives don't have. They showed that wildtype Neisseria cells associate with DNA, and that this does not require the DUS uptake sequence. Wildtype cells take up most of the DUS-containing DNA they bind - after a 30 minute incubation about 70% of the cell-associated DNA is DNase I-resistant - but take up less than 1% of DNA lacking a DUS.
PilT retracts the type 4 pili filaments thought to bind DNA into the cell (mutants that don't make pili don't associate with DNA), and they predicted that cells lacking PilT would bind DNA to their surface but be unable to bring it in. But very little DNA associated with their pilT mutants even when no DNase I was used. So the non-specific DNA binding seen on wildtype cells requires not just the machinery thought to assemble pili but also the protein thought to disassemble them.
Cells lacking the major pilus protein (pilin) encoded by pilE don't have visible pili and they didn't bind DNA or take up DNA, but cells lacking the minor pilin-like protein encoded by comP do have visible pili and they bound DNA normally, but they didn't take any of it up even if it had DUSs. Overexpressing the normally-scarce ComP protein increased by 20-fold the amount of DNA bound and taken up, and proportionately increased the transformation frequency. This increased uptake was specific for DNA containing a DUS, although a modest increase was also seen for DNA that lacked DUS.
Overexpressing ComP also caused increased and DUS-dependent DNA uptake by cells carrying a knockout of pilT, although the effect was small - these cells took up only about 5% as much DNA as wildtype cells with normal ComP expression.
What does all this mean? Because they couldn't show that ComP binds DNA, the authors concluded that it probably acts indirectly, by activating or stabilizing another component that does the DNA binding. They also thought that ComP may normally act as a minor component of pili composed mainly of PilE. They also suggested that pilus retraction by PilT may not be the main force pulling DNA into the cell; instead the DNA may be quickly handed over to a periplasmic receptor that does the bulk of the pulling-in.
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