UV-irradiation of E. coli induces a two fold increase in ATP pool in the first 20 min. Afterwards, in RecA+ strains ATP level drops quickly below values of non irradiated cells. Mutants of E. coli defective in RecA protein or with either RecA protease activity deficient or protease resistant LexA repressor do not present this decrease, showing that it is due to cleavage of LexA repressor by RecA protease. The ATP increase produced in the first 20 min is dependent on RecBC exonuclease activity and it must be due to substrate level phosphorylation since an uncoupler such as dinitrophenol does not affect it.
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http://dx.doi.org/10.1016/0006-291x(83)91236-6 | DOI Listing |
Sci Rep
September 2024
Biomedical Sciences Department, School of Public Health, State University of New York at Albany, Albany, USA.
The recA gene, encoding Recombinase A (RecA) is one of three Mycobacterium tuberculosis (Mtb) genes encoding an in-frame intervening protein sequence (intein) that must splice out of precursor host protein to produce functional protein. Ongoing debate about whether inteins function solely as selfish genetic elements or benefit their host cells requires understanding of interplay between inteins and their hosts. We measured environmental effects on native RecA intein splicing within Mtb using a combination of western blots and promoter reporter assays.
View Article and Find Full Text PDFJ Biol Chem
September 2024
Department of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, Uttar Pradesh, India; Centre for Environmental Sciences and Engineering, Indian Institute of Technology Kanpur, Kanpur, Uttar Pradesh, India; Mehta Family Centre for Engineering in Medicine, Indian Institute of Technology, Kanpur, Uttar Pradesh, India; Kotak School of Sustainability, Indian Institute of Technology, Kanpur, Uttar Pradesh, India. Electronic address:
Nat Struct Mol Biol
October 2024
Department of Biochemistry and Biophysics, University of Pennsylvania, Philadelphia, PA, USA.
Drug Resist Updat
July 2024
Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Macarena/CSIC/Universidad de Sevilla, Sevilla, Spain, Sevilla, Spain; Departamento de Microbiología, Facultad de Medicina, Universidad de Sevilla, Sevilla, Spain; Centro de Investigación Biomédica en Red en Enfermedades Infecciosas (CIBERINFEC), Instituto de Salud Carlos III, Madrid, Spain.
In recent years, new evidence has shown that the SOS response plays an important role in the response to antimicrobials, with involvement in the generation of clinical resistance. Here we evaluate the impact of heterogeneous expression of the SOS response in clinical isolates of Escherichia coli on response to the fluoroquinolone, ciprofloxacin. In silico analysis of whole genome sequencing data showed remarkable sequence conservation of the SOS response regulators, RecA and LexA.
View Article and Find Full Text PDFFront Microbiol
March 2024
Molecular Biology Division, Bhabha Atomic Research Centre, Mumbai, India.
The co-protease activity in the RecA-ssDNA complex cleaves the autorepressor LexA, resulting in the derepression of a large number of genes under LexA control. This process is called the SOS response, and genes that are expressed in response to DNA damage are called SOS genes. The proteins encoded by the SOS genes are involved in both DNA repair and maintaining the functions of crucial cell division proteins (e.
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