9.A.21 The DNA Uptake Competence (ComC) Family
&9;ComC of Acinetobacter sp. strain BD413 functions together with a pilin-like competence factor, ComP, probably together with other putative competence factors, ComB, ComE and ComF. ComP and ComC are essential for binding and uptake of DNA in Acinetobacter. ComB, E, F, and P all resemble prepilins of type IV pili and to pilin-like components of protein translocation systems. ComC resembles type IV pilus biogenesis factors. Homologues of type IV pilus subunits are involved in natural transformation in a variety of bacteria, but it is not known if type IV pili or a similar structure is involved in DNA uptake. ComP may be present in both the cytoplasm and the outer membrane of Acinetobacter.
Homologues of ComC are found in Pseudomonas aeruginosa, Xylella fastidiosa and species of Neisseria. In Neisseria, PilC may be involved in class II pilus formation, natural transformation and adhesion to epithelial cells. In both Gram-positive and Gram-negative bacteria, DNA uptake is believed to be a two step process (Krüger and Stingl, 2011).
Pseudomonas aeruginosa infects every type of host that has been examined by deploying multiple virulence factors. Previous studies of virulence regulation have largely focused on chemical cues, but P. aeruginosa may also respond to mechanical cues. It activates virulence in response to attachment to a range of chemically distinct surfaces, suggesting that it responds to mechanical properties of its substrates. Surface-activated virulence requires quorum sensing, but activating quorum sensing does not induce virulence without surface attachment. The activation of virulence by surfaces requires the surface-exposed protein PilY1, which has a domain homologous to a eukaryotic mechanosensor. Specific mutation of the putative PilY1 mechanosensory domain is sufficient to induce virulence in non-surface-attached cells, suggesting that PilY1 mediates surface mechanotransduction. Triggering virulence only when cells are both at high density and attached to a surface—two host-nonspecific cues—explains how P. aeruginosa precisely regulates virulence while maintaining broad host specificity.
The reactions believed to be catalyzed by ComC homologues are:
(1) DNA (out) à DNA (in)
(2) Protein (in) à Protein (out)