Literature DB >> 31029705

Coordinated Cell Death in Isogenic Bacterial Populations: Sacrificing Some for the Benefit of Many?

Philipp F Popp1, Thorsten Mascher2.   

Abstract

Antibiotics are classically perceived as biological weapons that bacteria produce to hold their ground against competing species in their natural habitat. But in the context of multicellular differentiation processes, antimicrobial compounds sometimes also play a role in intraspecies competition, resulting in the death of a sub-population of genetically identical siblings for the benefit of the population. Such a strategy is based on the diversification and hence phenotypic heterogeneity of an isogenic bacterial population. This review article will address three such phenomena. In Bacillus subtilis, cannibalism is a differentiation strategy that enhances biofilm formation, prolongs or potentially even prevents full commitment to endospore formation under starvation conditions, and protects cells within the biofilm against competing species. The nutrients released by lysed cells can be used by the toxin producers, thereby delaying the full activation of the master regulator of sporulation. A related strategy is associated with the initiation of competence development under nutrient excess in Streptococcus pneumoniae. This process, termed fratricide, causes allolysis in a sub-population and is thought to enhance genetic diversity within the species. In Myxococcus xanthus, a large fraction of the population undergoes programmed cell death during the formation of fruiting bodies. This sacrifice ensures the survival of the sporulating sub-population by providing nutrients and hence energy to complete this differentiation process. The biological relevance and underlying regulatory mechanisms of these three processes will be discussed in order to extract common features of such strategies. Moreover, open questions and future challenges will be addressed.
Copyright © 2019. Published by Elsevier Ltd.

Entities:  

Keywords:  autolysis; cannibalism; fratricide; phenotypic heterogeneity; programmed cell death

Mesh:

Year:  2019        PMID: 31029705     DOI: 10.1016/j.jmb.2019.04.024

Source DB:  PubMed          Journal:  J Mol Biol        ISSN: 0022-2836            Impact factor:   5.469


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