S.O.S. response in molecular biology and arms race in biology

Krishna: Cells face hostile atmospheres very frequently.

For instance bacteria can face hostile environments, including antimicrobial exposure like antibiotics. The SOS response can play a significant role in the generation of persister cells, population-wide tolerance, and shielding. The SOS pathway is an inducible DNA damage repair system that is also pivotal for bacterial adaptation, pathogenesis, and diversification. In addition to the two key SOS regulators, LexA and RecA, some other stressors and stress responses can control SOS factors.

SOS repair refers to the DNA repair system, which uses RecA regulatory protein to inhibit the repressor's activity and activate the SOS inducer genes to recover the DNA damage. It stands for “Save Our Soul”.

Bacteria are exposed to DNA-damaging agents and other environmental and intracellular factors, including cigarette smoke, that trigger the SOS response at a number of sites within the host. The Escherichia coli TisB/IstR module is as yet the only known SOS-regulated toxin–antitoxin module involved in persister formation. Nevertheless, the SOS response plays a key role in the formation of biofilms that are highly recalcitrant to antimicrobials and can be abundant in persisters. Furthermore, the dynamic biofilm environment generates DNA-damaging factors that trigger the SOS response within the biofilm, fueling bacterial adaptation and diversification.

The SOS response is a response to DNA damage in which the cell cycle is arrested and DNA repair and mutagenesis is induced. The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor (LexA) of SOS response genes thereby inducing the response. It is an error-prone repair system that contributes significantly to DNA changes observed in a wide range of species (1).

Image source: Researchgate

Footnotes:

1. SOS response 

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Q: What is biological and evolutionary arms race?

Krishna: Biological arms races are commonplace in nature. Cheetahs, for example, have evolved a sleek body form that lends itself to rapid running, enabling them to feast upon similarly speedy gazelles, the fastest of which may evade predation. On the molecular level, immune cells produce proteins to conquer pathogens, which may in turn evolve mutations to evade detection.

An evolutionary arms race is an ongoing struggle between competing sets of co-evolving genes, phenotypic and behavioural traits, or species, that develop escalating adaptations and counter-adaptations against each other, resembling an arms race.

The co-evolving gene sets may be in different species, as in an evolutionary arms race between a predator species and its prey, or a parasite and its host. Alternatively, the arms race can occur between members of the same species or between different species. 

Though less well known, other games of one-upmanship unfold within the genome. In a new study, biologists  show, for the first time, evidence of a two-sided genomic arms race involving stretches of repetitive DNA called satellites. "Opposing" the rapidly evolving satellites in the arms race are similarly fast-evolving proteins that bind those satellites.

While satellite DNA does not encode genes, it can contribute to essential biological functions, such as formation of molecular machines that process and maintain chromosomes. When satellite repeats are improperly regulated, impairments to these crucial processes can result. Such disruptions are hallmarks of cancer and infertility.

Using two closely related species of fruit flies, researchers probed this arms race by purposefully introducing a species mismatch, pitting, for example, one species' satellite DNA against the other species' satellite-binding protein. Severe impairments to fertility were a result, underscoring evolution's delicate balance, even at the level of a single genome (2).

Footnotes:

2.  Mia T. Levine, Cross-species incompatibility between a DNA satellite and the Drosophila Spartan homolog poisons germline genome integrity, Current Biology (2022). DOI: 10.1016/j.cub.2022.05.009. www.cell.com/current-biology/f … 0960-9822(22)00768-0