Bioinformatic Prediction of an tRNASec Gene Nested inside an Elongation Factor SelB Gene in Alphaproteobacteria

In bacteria, selenocysteine (Sec) is incorporated into proteins via the recoding of a particular codon, the UGA stop codon in most cases. Sec-tRNASec is delivered to the ribosome by the Sec-dedicated elongation factor SelB that also recognizes a Sec-insertion sequence element following the codon on the mRNA. Since the excess of SelB may lead to sequestration of Sec-tRNASec under selenium deficiency or oxidative stress, the expression levels of SelB and tRNASec should be regulated. In this bioinformatic study, I analyzed the Rhizobiales SelB species because they were annotated to have a non-canonical C-terminal extension. I found that the open reading frame (ORF) of diverse Alphaproteobacteria selB genes includes an entire tRNASec sequence (selC) and overlaps with the start codon of the downstream ORF. A remnant tRNASec sequence was found in the Sinorhizobium melilotiselB genes whose products have a shorter C-terminal extension. Similar overlapping traits were found in Gammaproteobacteria and Nitrospirae. I hypothesized that once the tRNASec moiety is folded and processed, the expression of the full-length SelB may be repressed. This is the first report on a nested tRNA gene inside a protein ORF in bacteria.

The Genome Sequence of M228, a Chinese Isolate of Pseudomonas syringae pv. actinidiae, Illustrates Insertion Sequence Element Mobility

We present here the complete genome sequence of M228, a Chinese biovar 3 strain of Pseudomonas syringae pv. actinidiae, a bacterial pathogen of kiwifruit.

Congenerics

The evolution of Bordetella pertussis from B. bronchiseptica (or a B. bronchiseptica-like ancestor) occurred primarily through gene loss and genome rearrangement, mediated largely through the expansion in the copy number of insertion sequence element repeats in the B. pertussis genome. B. pertussis is attributed as the main causative agent of whooping cough. However, B. parapertussis and B. holmesii also cause disease that is very similar to that caused by B. pertussis (here termed pertussis-like disease). The evolution of B. parapertussis and B. holmesii displays striking similarities to that of B. pertussis and thus this chapter explores what might be gained from comparative studies of B. pertussis, B. parapertussis, and B. holmesii with regard to the understanding of whooping cough.

Genomic Characterization of Colistin Heteroresistance in Klebsiella pneumoniae during a Nosocomial Outbreak

ABSTRACTKlebsiella pneumoniaeis emerging as an important nosocomial pathogen due to its rapidly increasing multidrug resistance, which has led to a renewed interest in polymyxin antibiotics, such as colistin, as antibiotics of last resort. However, heteroresistance (i.e., the presence of a subpopulation of resistant bacteria in an otherwise susceptible culture) may hamper the effectiveness of colistin treatment in patients. In a previous study, we showed that colistin resistance among extended-spectrum-beta-lactamase (ESBL)-producingK. pneumoniaeisolates emerged after the introduction of selective digestive tract decontamination (SDD) in an intensive care unit (ICU). In this study, we investigated heteroresistance to colistin among ESBL-producingK. pneumoniaeisolates by using population analysis profiles (PAPs). We used whole-genome sequencing (WGS) to identify the mutations that were associated with the emergence of colistin resistance in theseK. pneumoniaeisolates. We found five heteroresistant subpopulations, with colistin MICs ranging from 8 to 64 mg/liter, which were derived from five clonally related, colistin-susceptible clinical isolates. WGS revealed the presence of mutations in thelpxM,mgrB,phoQ, andyciMgenes in colistin-resistantK. pneumoniaeisolates. In two strains,mgrBwas inactivated by an IS3-like or ISKpn14insertion sequence element. Complementation intranswith the wild-typemgrBgene resulted in these strains reverting to colistin susceptibility. The MICs for colistin-susceptible strains increased 2- to 4-fold in the presence of the mutatedphoQ,lpxM, andyciMalleles. In conclusion, the present study indicates that heteroresistantK. pneumoniaesubpopulations may be selected for upon exposure to colistin. Mutations inmgrBandphoQhave previously been associated with colistin resistance, but we provide experimental evidence for roles of mutations in theyciMandlpxMgenes in the emergence of colistin resistance inK. pneumoniae.