‘Black cat, white cat: whatever catches the mouse is a good cat’ (Chinese proverb). Throughout the 3000 million years that bacteria have been on planet Earth, they have evolved amazing mechanisms for rapid adaptation to every imaginable type of environmental change. To give one extreme example, as little as 50 years after the introduction of the first antibiotics, very few of these drugs remain effective today at combating microbial infections (Davies, 1997). When bacteria are faced with antimicrobials, the only challenge they must overcome is to defeat the toxic effect of the compound through modification, cleavage or pumping the drug out of the cells; these processes generally involve one or just a few proteins. A far more complex environmental threat is that posed by organic chemicals, which have been discharged into many ecosystems through industrial and urban activities. Many of these chemicals are xenobiotic compounds (literally, alien to life), which include types of chemical ligatures (typically covalent C–Cl bonds) that have never been present in significant amounts in the biosphere and against which the housekeeping metabolic pathways of most microbes are generally useless (van der Meer et al ., 1992). Unlike antibiotics, the challenge in this case is the construction of entire biodegradation pathways that endow bacteria with the ability to grow on these otherwise unpalatable chemicals. Such an outcome involves not just one protein, but sometimes dozens, which must adapt to entirely new substrates and intermediates. However, difficult as this might be, the successful assembly of a degradation pathway does not guarantee per se the survival of a particular strain. Bacteria that colonize polluted sites are subject to extremely tough competition from other microbial residents of the same niche. Transcriptional regulation of biodegradative genes and operons thus becomes a critical asset for the success of a newly assembled pathway to …

The gene cluster adjacent to the sequence of rpoN (encoding sigma factor ς⁵⁴) ofPseudomonas putida has been studied with respect to the C source regulation of the Pu promoter of theupper TOL (toluene catabolism) operon. The region includes four open reading frames (ORFs), two of which (named ptsNand ptsO genes) encode proteins similar to components of the phosphoenolpyruvate:sugar phosphotransferase system. Each of the four genes was disrupted with a nonpolar insertion, and the effects in the inhibition caused by glucose on Pu activity were inspected with a lacZ reporter system. Although cells lacking ORF102, ORF284, and ptsO did not display any evident phenotype under the conditions tested, the loss ofptsN, which encodes the IIA^Ntr protein, madePu unresponsive to repression by glucose. TheptsN mutant had rates of glucose/gluconate consumption identical to those of the wild type, thus ruling out indirect effects mediated by the transport of the carbohydrate. A site-directedptsN mutant in which the conserved phospho-acceptor site His⁶⁸ of IIA^Ntr was replaced by an aspartic acid residue made Pu blind to the presence or absence of glucose, thus supporting the notion that phosphorylation of IIA^Ntr mediates the C source inhibition of the promoter. These data substantiate the existence of a molecular pathway for co-regulation of some ς⁵⁴ promoters in which IIA^Ntr is a key protein intermediate.

Skates are cartilaginous fish whose body plan features enlarged wing-like pectoral fins, enabling them to thrive in benthic environments^1,2. However, the molecular underpinnings of this unique trait remain unclear. Here we investigate the origin of this phenotypic innovation by developing the little skateLeucoraja erinaceaas a genomically enabled model. Analysis of a high-quality chromosome-scale genome sequence for the little skate shows that it preserves many ancestral jawed vertebrate features compared with other sequenced genomes, including numerous ancient microchromosomes. Combining genome comparisons with extensive regulatory datasets in developing fins—including gene expression, chromatin occupancy and three-dimensional conformation—we find skate-specific genomic rearrangements that alter the three-dimensional regulatory landscape of genes that are involved in the planar cell polarity pathway. Functional inhibition of planar cell polarity signalling resulted in a reduction in anterior fin size, confirming that this pathway is a major contributor to batoid fin morphology. We also identified a fin-specific enhancer that interacts with severalhoxagenes, consistent with the redeployment ofhoxgene expression in anterior pectoral fins, and confirmed its potential to activate transcription in the anterior fin using zebrafish reporter assays. Our findings underscore the central role of genome reorganization and regulatory variation in the evolution of phenotypes, shedding light on the molecular origin of an enigmatic trait.