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Colenso, C.

Publications and source records attributed to Colenso, C..

2 recordsLinked to original sources

Structure and dynamics of Burkholderia pseudomallei OXA-57, a distinctive low-efficiency class D β-lactamase with carbapenem-hydrolyzing activity

The Gram-negative bacterium Burkholderia pseudomallei causes the severe disease melioidosis. {beta}-Lactams, including carbapenems, are the primary treatment, but are susceptible to chromosomal {beta}-lactamases, including the class D enzyme OXA-57. Here we show recombinant OXA-57 is active towards penicillins and first-generation cephalosporins, slowly hydrolyzes carbapenems including imipenem and meropenem, but is inactive towards oxyimino-cephalosporins (e.g., ceftazidime). Unlike many OXA enzymes, OXA-57 is sensitive to the mechanism-based inhibitor clavulanic acid, but less so to the diazabicyclooctane avibactam and not to the cyclic boronate vaborbactam. Crystal structures of covalent OXA-57:avibactam and OXA-57:meropenem complexes reveal limited hydrogen- bonding interactions with bound ligands. In molecular dynamics simulations, bound meropenem is mobile, while the water necessary for deacylation has only limited active site access. These observations are consistent with the low level of meropenem turnover, supporting proposals that OXA {beta}-lactamases generally possess limited carbapenemase activity, and highlight the potential importance of OXA-57 in B. pseudomallei {beta}-lactam resistance. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=109 SRC="FIGDIR/small/630153v1_ufig1.gif" ALT="Figure 1000"> View larger version (24K): org.highwire.dtl.DTLVardef@d635d7org.highwire.dtl.DTLVardef@168d67borg.highwire.dtl.DTLVardef@1d95733org.highwire.dtl.DTLVardef@1ebeabb_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

Evolutionary analyses unveil the molecular mechanism of fast inactivation in calcium-permeable TRP channels

Fundamental for calcium homeostasis in vertebrates, TRPV5 and TRPV6 are calcium-selective ion channels belonging to the Transient Receptor Potential (TRP) gene family. Detailed phylogenetic analysis suggests that duplications from which TRPV5 and TRPV6 originated occurred independently in the ancestors of mammals, sauropsids, amphibians, and chondrichthyans. Coincident with the conquest of land and the physiological changes needed to maintain calcium homeostasis, our expression analyses suggest a change in the expression pattern from gills to kidney. Within amniotes, we identified a traceable sequence signature of three amino acids at the amino-terminal intracellular region that correlates well with both of the duplication events and the phenotype of fast inactivation observed in TRPV6 channels. Electrophysiological recordings and mutagenesis suggest that calcium-induced fast inactivation is an evolutionary innovation that emerged independently from each duplication event. Simulations of molecular dynamics suggest that calcium-induced channel rearrangements are important modulatory regions of TRP channels.

evolutionary biology↗