A single rare σ70 variant establishes a unique gene expression pattern in the E. coli pathobiont LF82.

LF82, an adherent-invasive Escherichia coli (AIEC) pathobiont, is associated with Crohn's disease, an inflammatory bowel disease of unknown etiology. Although AIEC phenotypes differ from those of 'commensal' or pathogenic E. coli, work has failed to identify genetic features accounting for these differences.

Unlocking Drug Resistance in Multiple Myeloma: Adipocytes as Modulators of Treatment Response.

Multiple myeloma (MM) is an incurable hematological malignancy characterized by the clonal proliferation of malignant plasma cells. Despite the development of a diverse array of targeted drug therapies over the last decade, patients often relapse and develop refractory disease due to multidrug resistance. Obesity is a growing public health threat and a risk factor for multiple myeloma, although the mechanisms by which obesity contributes to MM growth and progression have not been fully elucidated.

The pathobiont LF82 encodes a unique variant of σ that results in specific gene expression changes and altered phenotypes.

LF82, an adherent invasive pathobiont, is associated with ileal Crohn's disease, an inflammatory bowel disease of unknown etiology. Although LF82 contains no virulence genes, it carries several genetic differences, including single nucleotide polymorphisms (SNPs), that distinguish it from nonpathogenic . We have identified and investigated an extremely rare SNP that is within the highly conserved gene, encoding σ, the primary sigma factor for RNA polymerase.

Conformational change of the response regulator BvgA accompanies its activation of the virulence gene .

The BvgAS two-component system regulates virulence gene expression in . Although precise three-dimensional structural information is not available for the response regulator BvgA, its sequence conservation with NarL and previous studies have indicated that it is composed of 3 domains: an -terminal domain (NTD) containing the phosphorylation site, a linker, and a DNA-binding C-terminal domain (CTD). Previous work has determined how BvgA dimers interact with the promoter (P ) of , the gene encoding the virulence adhesin filamentous hemagglutinin.