Quiescence Through the Prism of Evolution

Daignan‐Fornier, Bertrand; Laporte, Damien; Sagot, Isabelle

doi:10.3389/fcell.2021.745069

Cited by 9 publications

(7 citation statements)

References 81 publications

(69 reference statements)

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“…S1E), suggests that E. coli employs YfiN to weather inhospitable conditions. A reversible quiescent state is known to favor adaptive evolution from microbes to humans [43][44][45]. Our findings likely extend to all YfiN-encoding bacteria given that the majority of the homologs lack the Ip site.…”

Section: Yfin Exploits the Absence Of Autoinhibitory I Sites To Enabl...mentioning

confidence: 52%

A Second Role for the Second Messenger Cyclic-di-GMP inE. coli: Arresting Cell Growth by Altering Metabolic Flow

Hwang

Harshey

2022

Preprint

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C-di-GMP primarily controls motile to sessile transitions in bacteria. Diguanylate cyclases (DGCs) catalyze the synthesis of c-di-GMP from two GTP molecules. Typically, bacteria encode multiple DGCs that are activated by specific environmental signals. Their catalytic activity is modulated by c-di-GMP binding to autoinhibitory sites (I-sites). YfiN is a conserved inner membrane DGC that lacks these sites. Instead, YfiN activity is directly repressed by periplasmic YfiR, which is inactivated by redox stress. In E. coli, an additional envelope stress causes YfiN to relocate to the mid-cell to inhibit cell division by interacting with the division machinery. Here, we report a third activity for YfiN in E. coli, where cell growth is inhibited without YfiN relocating to the division site. This action of YfiN is only observed when the bacteria are cultured on gluconeogenic carbon sources, and is dependent on absence of the autoinhibitory sites. Restoration of I-site function relieves the growth-arrest phenotype, and disabling this function in a heterologous DGC causes acquisition of this phenotype. Arrested cells are tolerant to a wide range of antibiotics. We show that the likely cause of growth arrest is depletion of cellular GTP from run-away synthesis of c-di-GMP, explaining the dependence of growth arrest on gluconeogenic carbon sources that exhaust more GTP during production of glucose. This is the first report of c-di-GMP-mediated growth arrest by altering metabolic flow.

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Section: Yfin Exploits the Absence Of Autoinhibitory I Sites To Enabl...mentioning

confidence: 52%

A Second Role for the Second Messenger Cyclic-di-GMP inE. coli: Arresting Cell Growth by Altering Metabolic Flow

Hwang

Harshey

2022

Preprint

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show abstract

“…S2E ), suggests that E. coli employs YfiN to weather inhospitable conditions. A reversible quiescent state is known to favor adaptive evolution from microbes to humans ( 50 – 52 ). Our findings likely extend to all YfiN-encoding bacteria given that the majority of the homologs lack the I p site.…”

Section: Discussionmentioning

confidence: 99%

A Second Role for the Second Messenger Cyclic-di-GMP in E. coli: Arresting Cell Growth by Altering Metabolic Flow

Hwang¹,

Harshey²

2023

mBio

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The c-di-GMP signaling network in bacteria not only controls a variety of cellular processes such as motility, biofilms, cell development, and virulence, but does so by a dizzying array of mechanisms. The DGC YfiN singularly represents the versatility of this network in that it not only inhibits motility and promotes biofilms, but also arrests growth in Escherichia coli by relocating to the mid-cell and blocking cell division.

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“…In complex multicellular organisms, the creation of a microenvironment means that proliferation and quiescence are controlled internally and are thus decoupled from external nutrient cues. Here we see the possibility of "being quiescent in a plentiful environment" (Daignan-Fornier et al 2021). The question is what this intake inhibition entails for the evolution of balancing: does balancing per se require this multicellular trait or is this just another form of balancing building on previous ones?…”

Section: Multicellular Diversity and The Inhibition Of Intakementioning

confidence: 97%

Everything in moderation or moderating everything? Nutrient balancing in the context of evolution and cancer metabolism

Sholl

2022

Biol Philos

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While philosophers of science have marginally discussed concepts such as 'nutrient', 'naturalness', 'food', or the 'molecularization' of nutrition, they have yet to seriously engage with the nutrition sciences. In this paper, I offer one way to begin this engagement by investigating conceptual challenges facing the burgeoning field of nutritional ecology and the question of how organisms construct a 'balanced' diet. To provide clarity, I propose the distinction between nutrient balance as a property of foods or dietary patterns and nutrient balancing as an evolved capacity to regulate nutrient intake. This distinction raises conceptual and empirical issues, such as what properties constitute this capacity and whether they are the same in all organisms. Additionally, while scientists use the term 'balancing', its intension and extension need further clarification. Based on the literature, the properties of external nutrient detection, internal sensing of nutrient levels, and organismal regulation could provide a basic recipe for nutrient balancing. Next, using an evolutionary lens, I examine nutrient acquisition in some prokaryotes, slime molds, simple multicellular eukaryotes, and in the quirks of multicellular metabolism to raise questions about the origins and universality of balancing. Finally, I build on this explication of balance and balancing by considering how obesity and cancer might respectively elucidate problems of organismal nutrient imbalances versus disrupted cellular nutrient balancing.

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Quiescence Through the Prism of Evolution

Cited by 9 publications

References 81 publications

A Second Role for the Second Messenger Cyclic-di-GMP inE. coli: Arresting Cell Growth by Altering Metabolic Flow

A Second Role for the Second Messenger Cyclic-di-GMP inE. coli: Arresting Cell Growth by Altering Metabolic Flow

A Second Role for the Second Messenger Cyclic-di-GMP in E. coli: Arresting Cell Growth by Altering Metabolic Flow

Everything in moderation or moderating everything? Nutrient balancing in the context of evolution and cancer metabolism

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