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Bacterial sugar utilization gives rise to distinct single-cell behaviours.

ABSTRACT: Inducible utilization pathways reflect widespread microbial strategies to uptake and consume sugars from the environment. Despite their broad importance and extensive characterization, little is known how these pathways naturally respond to their inducing sugar in individual cells. Here, we performed single-cell analyses to probe the behaviour of representative pathways in the model bacterium Escherichia coli. We observed diverse single-cell behaviours, including uniform responses (d-lactose, d-galactose, N-acetylglucosamine, N-acetylneuraminic acid), 'all-or-none' responses (d-xylose, l-rhamnose) and complex combinations thereof (l-arabinose, d-gluconate). Mathematical modelling and probing of genetically modified pathways revealed that the simple framework underlying these pathways - inducible transport and inducible catabolism - could give rise to most of these behaviours. Sugar catabolism was also an important feature, as disruption of catabolism eliminated tunable induction as well as enhanced memory of previous conditions. For instance, disruption of catabolism in pathways that respond to endogenously synthesized sugars led to full pathway induction even in the absence of exogenous sugar. Our findings demonstrate the remarkable flexibility of this simple biological framework, with direct implications for environmental adaptation and the engineering of synthetic utilization pathways as titratable expression systems and for metabolic engineering.

SUBMITTER: Afroz T

PROVIDER: S-EPMC4160389 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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Bacterial sugar utilization gives rise to distinct single-cell behaviours.

Afroz Taliman T Biliouris Konstantinos K Kaznessis Yiannis Y Beisel Chase L CL

Molecular microbiology 20140716 6

Inducible utilization pathways reflect widespread microbial strategies to uptake and consume sugars from the environment. Despite their broad importance and extensive characterization, little is known how these pathways naturally respond to their inducing sugar in individual cells. Here, we performed single-cell analyses to probe the behaviour of representative pathways in the model bacterium Escherichia coli. We observed diverse single-cell behaviours, including uniform responses (d-lactose, d- ...[more]

PMID: 24976172

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Project description:Severe liver diseases are characterized by expansion of liver progenitor cells (LPC), which correlates with disease severity. However, the origin and role of LPC in liver physiology and in hepatic injury remains a contentious topic. We found that ductular reaction cells in human cirrhotic livers express hepatocyte nuclear factor 1 homeobox B (HNF1?). However, HNF1? expression was not present in newly generated epithelial cell adhesion molecule (EpCAM)-positive hepatocytes. In order to investigate the role of HNF1?-expressing cells we used a tamoxifen-inducible Hnf1?CreER/R26R(Yfp/LacZ) mouse to lineage-trace Hnf1?(+) biliary duct cells and to assess their contribution to LPC expansion and hepatocyte generation. Lineage tracing demonstrated no contribution of HNF1?(+) cells to hepatocytes during liver homeostasis in healthy mice or after loss of liver mass. After acute acetaminophen or carbon tetrachloride injury no contribution of HNF1?(+) cells to hepatocyte was detected. We next assessed the contribution of Hnf1?(+) -derived cells following two liver injury models with LPC expansion, a diethoxycarbonyl-1,4-dihydro-collidin (DDC)-diet and a choline-deficient ethionine-supplemented (CDE)-diet. The contribution of Hnf1?(+) cells to liver regeneration was dependent on the liver injury model. While no contribution was observed after DDC-diet treatment, mice fed with a CDE-diet showed a small population of hepatocytes derived from Hnf1?(+) cells that were expanded to 1.86% of total hepatocytes after injury recovery. Genome-wide expression profile of Hnf1?(+) -derived cells from the DDC and CDE models indicated that no contribution of LPC to hepatocytes was associated with LPC expression of genes related to telomere maintenance, inflammation, and chemokine signaling pathways.HNF1?(+) biliary duct cells are the origin of LPC. HNF1?(+) cells do not contribute to hepatocyte turnover in the healthy liver, but after certain liver injury, they can differentiate to hepatocytes contributing to liver regeneration.

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Bacterial sugar utilization gives rise to distinct single-cell behaviours.

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Bacterial sugar utilization gives rise to distinct single-cell behaviours.

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