Biodegradation of phenoxyacetic acid in soil by Pseudomonas putida PP0301(pR0103), a constitutive degrader of 2, 4–dichlorophenoxyacetate

The efficacy of using genetically engineered microbes (GEMs) to degrade recalcitrant environmental toxicants was demonstrated by the application of Pseudomonas putida PP0301(pR0103) to an Oregon agricultural soil amended with 500 u.g/g of a model xenobiotic, phenoxyacetic acid (PAA). P. putida PP0301(pR0103) is a constitutive degrader of 2, 4–dichlorophenoxyacetate (2, 4–D) and is also active on the non–inducing substrate, PAA. PAA is the parental compound of 2, 4–dichlorophenoxyacetic acid (2, 4–D) and whilst the indigenous soil microbiota degraded 500 ng/g 2, 4–D to less than 10 J–g/g, PAA degradation was insignificant during a 40–day period. No significant degradation of PAA occurred in soil inoculated with the parental strain P. putida PP0301 or the inducible 2, 4–D degrader P. putida PP0301(pR0101). Moreover, co–amendment of soil with 2, 4–D and PAA induced the microbiota to degrade 2, 4–D; PAA was not degraded. P. putida PP0301–(pR0103) mineralized 500–Μg/g PAA to trace levels within 13 days and relieved phytotoxicity of PAA to Raphanus sativus (radish) seeds with 100% germination in the presence of the GEM and 7% germination in its absence. In unamended soil, survival of the plasmid–free parental strain P. putida PP0301 was similar to the survival of the GEM strain P. putida PP0301(pR0103). However, in PAA amended soil, survival of the parent strain was over 10 000–fold lower (< 3 colony forming units per gram of soil) than survival of the GEM strain after 39 days.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75471/1/j.1365-294X.1992.tb00160.x.pd

Intimate adhesion of Neisseria meningitidis to human epithelial cells is under the control of the crgA gene, a novel LysR-type transcriptional regulator

PilC1, a pilus-associated protein in Neisseria menin– gitidis, is a key element in initial meningococcal adhesion to target cells. A promoter element (CREN, contact regulatory element of Neisseria) is responsible for the transient induction of this gene upon cell contact. crgA (contact-regulated gene A) encodes a transcriptional regulator whose expression is also induced upon cell contact from a promoter region similar to the CREN of pilC1. CrgA shows significant sequence homologies to LysR-type transcriptional regulators. Its inactivation in meningococci provokes a dramatic reduction in bacterial adhesion to epithelial cells. Moreover, this mutant is unable to undergo intimate adhesion to epithelial cells or to provoke effacing of microvilli on infected cells. Purified CrgA is able to bind to pilC1 and crgA promoters, and CrgA seems to repress the expression of pilC1 and crgA. Our results support a dynamic model of bacteria–cell interaction involving a network of regulators acting in cascade. CrgA could be an intermediate regulator in such a network