Janus Kinase Mutations in Mice Lacking PU.1 and Spi-B Drive B Cell Leukemia through Reactive Oxygen Species-Induced DNA Damage.

Precursor B cell acute lymphoblastic leukemia (B-ALL) is caused by genetic lesions in developing B cells that function as drivers for the accumulation of additional mutations in an evolutionary selection process. We investigated secondary drivers of leukemogenesis in a mouse model of B-ALL driven by PU.1/Spi-B deletion (Mb1-CreΔPB).

The Rcs regulon in Proteus mirabilis: implications for motility, biofilm formation, and virulence.

The overall role of the Rcs phosphorelay in Proteus mirabilis is largely unknown. Previous work had demonstrated that the Rcs phosphorelay represses the flhDC operon and activates the minCDE cell division inhibition system. To identify additional cellular functions regulated by the Rcs phosphorelay, an analysis of RNA-seq data was undertaken.

Regulation of the Min Cell Division Inhibition Complex by the Rcs Phosphorelay in Proteus mirabilis.

Unlabelled: A key regulator of swarming in Proteus mirabilis is the Rcs phosphorelay, which represses flhDC, encoding the master flagellar regulator FlhD4C2. Mutants in rcsB, the response regulator in the Rcs phosphorelay, hyperswarm on solid agar and differentiate into swarmer cells in liquid, demonstrating that this system also influences the expression of genes central to differentiation. To gain a further understanding of RcsB-regulated genes involved in swarmer cell differentiation, transcriptome sequencing (RNA-Seq) was used to examine the RcsB regulon.

Expression of the DisA amino acid decarboxylase from Proteus mirabilis inhibits motility and class 2 flagellar gene expression in Escherichia coli.

In Proteus mirabilis, a putative phenylalanine decarboxylase (DisA) acts in a regulatory pathway to inhibit class 2 flagellar gene expression and motility. In this study, we demonstrate that DisA expression in Escherichia coli blocked motility and resulted in a 50-fold decrease in the expression of class 2 (fliA) and class 3 (fliC) flagellar genes. However, the expression of flhDC encoding the class 1 activator of the flagellar cascade was unchanged by DisA expression at both the transcriptional and translational levels.

Novel mechanism for fluoroquinolone resistance in Acinetobacter baumannii.

An EZ::TNTnp transposon insertion in an open reading frame of unknown function (ncr) in Acinetobacter baumannii resulted in an 8-fold increase in ciprofloxacin resistance (Cip(r)). Transposon insertions in an ncr mutant that reduced Cip(r) back to wild type mapped to three genes encoding subunits of the RecCBD exonuclease. The ncr mutation increased transcription of the recCBD genes, and overexpression of the recCBD genes in a wild-type background resulted in a 4-fold increase in Cip(r).