FIG 1.

Model for competence and transformation of V. fischeri. Major regulatory pathways and other factors predicted, based on studies of V. cholerae, to control competence and transformation of V. fischeri are shown. In the top left (blue), quorum sensing regulators are shown. At low cell density, two kinases, LuxQ and AinR, function as kinases, promoting phosphorylation, via LuxU, of the response regulator LuxO, which, in turn, activates transcription of the gene for small RNA Qrr1. Qrr1 activity results in decreased levels of LitR (orange), a positive regulator of competence that promotes light production; in V. cholerae, the LitR homolog HapR controls transcription of dns, which encodes a nuclease that interferes with DNA uptake. At high cell densities, autoinducers made by LuxS and AinS switch the activity of LuxQ and AinR to phosphatases, thereby decreasing Qrr1 levels and increasing LitR levels and light production (yellow). Another major regulator of competence is TfoX (middle, in green). In V. cholerae, TfoX is controlled at the level of translation by the sRNA TfoR, which, in turn, is controlled by chitin-sensing regulators ChiS and TfoS. In V. fischeri, competence is readily induced by overproduction of TfoX, even in the absence of chitin. Another important regulator appears to be the cytidine-responsive regulator CytR (right, in brown), which activates competence via an unknown mechanism. The role of TfoY, if any, in competence remains unknown. At the bottom (in gray and white), a few of the structural genes known to be important for competence in V. cholerae are shown; gray coloring indicates factors assessed in this study.