The BosR Is Back!

TL;DR

This paper explores BosR, a protein in the Lyme disease bacterium that regulates gene expression in different host environments.

Contribution

The paper highlights BosR's novel RNA-binding role and its regulation of genes independent of RpoS in Borrelia burgdorferi.

Findings

BosR regulates gene expression through an RpoS-independent mechanism in Borrelia burgdorferi.

BosR functions as an RNA-binding protein with RNA chaperone activity, affecting post-transcriptional regulation.

BosR is crucial for the bacterium's adaptation between tick and vertebrate hosts.

Abstract

BosR is a novel nucleic acid‐binding protein in the ferric uptake regulator (FUR) family that regulates gene expression in the Lyme disease spirochete Borrelia (Borreliella) burgdorferi. This issue of Molecular Microbiology contains a comprehensive transcriptomic study that keenly defines the regulatory swath of BosR in the vertebrate host of
B. burgdorferi
. Despite homology to Fur‐like and PurR‐like orthologs, BosR has traditionally been linked to regulation of RpoS, the alternative sigma factor that controls the regulon required for establishing a vertebrate infection. However, BosR regulates other genes through an RpoS‐independent mechanism, which is elegantly elaborated in Grassmann et al., along with clearly demonstrating that BosR does not participate in the defense against oxidative and nitrosative stress in the vertebrate. However, the recently recognized role of BosR as an RNA‐binding protein with RNA chaperone activity that regulates gene expression in a post‐transcriptional fashion is not wholly appreciated, which clouds the results on determining the DNA‐binding site in vivo. Regardless, this seminal study enshrines BosR as a major regulator of gene expression in
B. burgdorferi
and delineates a multitude of BosR‐regulated cellular functions in the spirochete related to its ability to navigate between its tick vector and vertebrate host in nature as well as to persist in these two disparate environments.