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Identification of the Extracytoplasmic Function sigma Factor sigma(P) Regulon in Bacillus thuringiensis
Journal article   Open access   Peer reviewed

Identification of the Extracytoplasmic Function sigma Factor sigma(P) Regulon in Bacillus thuringiensis

Theresa D. Ho, Kelsie M. Nauta, Emma K. Luhmann, Lilliana Radoshevich and Craig D. Ellermeier
mSphere, Vol.7(1), e00967-21
02/23/2022
DOI: 10.1128/msphere.00967-21
PMCID: PMC8791391
PMID: 35080471
url
https://doi.org/10.1128/msphere.00967-21View
Published (Version of record) Open Access

Abstract

Antimicrobial resistance is major concern for public health. beta-Lactams remain an important treatment option for many diseases. However, the spread of beta-lactam resistance continues to rise. Bacillus thuringiensis and other members of the Bacillus cereus family are resistant to many beta-lactams. Resistance is dependent upon the extracytoplasmic function sigma factor sigma(P). We used label-free quantitative proteomics to identify proteins whose expression was dependent upon sigma(P). We compared the protein profiles of strains which either lacked sigma(P) or overexpressed sigma(P). We identified 8 members of the sigma(P) regulon which included four beta-lactamases as well as three penicillin-binding proteins (PBPs). Using transcriptional reporters, we confirmed that these genes are induced by beta-lactams in a sigma(P)-dependent manner. These genes were deleted individually or in various combinations to determine their role in resistance to a subset of beta-lactams, including ampicillin, methicillin, cephalexin, and cephalothin. We found that different combinations of beta-lactamases and PBPs are involved in resistance to different beta-lactams. Our data show that B. thuringiensis utilizes a suite of enzymes to protect itself from beta-lactam antibiotics. IMPORTANCE Antimicrobial resistance is major concern for public health. beta-Lactams remain an important treatment option for many diseases. However, the spread of beta-lactam resistance continues to rise. Many pathogens acquire antibiotic resistance from environmental bacteria. Thus, understanding beta-lactam resistance in environmental strains may provide insights into additional mechanisms of antibiotic resistance. Here, we describe how a single regulatory system, sigma(P), in B. thuringiensis controls expression of multiple genes involved in resistance to beta-lactams. Our findings indicate that some of these genes are partially redundant. Our data also suggest that the large number of genes controlled by sigma(P) results in increased resistance to a wider range of beta-lactam classes than any single gene could provide.
Microbiology Life Sciences & Biomedicine Science & Technology

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