Sending out an SOS - the bacterial DNA damage response

Abstract

The term "SOS response" was first coined by Radman in 1974, in an intellectual effort to put together the data suggestive of a concerted gene expression program in cells undergoing DNA damage. A large amount of information about this cellular response has been collected over the following decades. In this review, we will focus on a few of the relevant aspects about the SOS response: its mechanism of control and the stressors which activate it, the diversity of regulated genes in different species, its role in mutagenesis and evolution including the development of antimicrobial resistance, and its relationship with mobile genetic elements.

Dynamic microfluidic single-cell screening identifies pheno-tuning compounds to potentiate tuberculosis therapy

“…Upgrading this platform may also involve increasing the number of conditions that can be simultaneously tested in a more compact and robust device. Despite these manufacturing hindrances, we accomplished a first screening, and identified four initial PTC hits that induced more homogeneous activation of RecA, as a proxy of the SOS response 21 .…”

“…RecA, a key enzyme for DNA damage repair in the SOS response 21 , is unevenly expressed in clonal mycobacterial cells in the absence of stress, as transient pulses occurring in more than half of the population 17 . RecA-pulsing cells are also more likely to die upon treatment with DNA-damaging agents, such as fluoroquinolones and mitomycin C (MIT).…”

How an overlooked gene in coenzyme a synthesis solved an enzyme mechanism predicament

“…This mobility allows many conformers, but few are properly aligned for cleavage (Schmitzberger et al, 2003). A parallel case is the DNA damage (SOS) response in which an activated form of the RecA protein binds several repressor proteins and accelerates their slow autocatalytic cleavage (Lima‐Noronha et al, 2022). However, PanD differs in that the new N‐terminus is remodeled into a pyruvoyl moiety.…”

Snapshots ofPseudomonas aeruginosaSOS response activation complex reveal structural prerequisites for LexA engagement and cleavage

“…In recent years, anti-evolutive, anti-virulence, anti-biofilm, and quorum quencher strategies have been proposed as new approaches in antimicrobial chemotherapy, as they could counteract the rapid acquisition of antibiotic resistance and weaken the pathogenicity of bacterial infections (Mulani et al, 2019;Merrikh & Kohli, 2020;Culyba et al, 2015;Mühlen & Dersch, 2016). A master regulator involved in the control of cell division, fitness to environmental stressors, prophage activation, biofilm maturation, production of virulence factors, and error-prone DNA replication is represented by the SOS response pathway (Gotoh et al, 2010;Lima-Noronha et al, 2022;Galhardo et al, 2009;Pacheco & Sperandio, 2012). Most importantly, it is the most conserved mechanism of bacterial response to DNA damage induced by the exposure to antimicrobials, UV radiation, and reactive oxygen species.…”

“…A master regulator involved in the control of cell division, fitness to environmental stressors, prophage activation, biofilm maturation, production of virulence factors, and error-prone DNA replication is represented by the SOS response pathway (Gotoh et al , 2010; Lima-Noronha et al , 2022; Galhardo et al , 2009; Pacheco & Sperandio, 2012). Most importantly, it is the most conserved mechanism of bacterial response to DNA damage induced by the exposure to antimicrobials, UV radiation, and reactive oxygen species.…”