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A Persistence Detector for Metabolic Network Rewiring in an Animal

ABSTRACT: A Persistence Detector for Metabolic Network Rewiring in an Animal

PROVIDER: PRJNA508963 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8308160.fastq.gz	Fastqsanger.gz
	SRR8308170.fastq.gz	Fastqsanger.gz
	SRR8308161.fastq.gz	Fastqsanger.gz
	SRR8308171.fastq.gz	Fastqsanger.gz
	SRR8308162.fastq.gz	Fastqsanger.gz

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A Persistence Detector for Metabolic Network Rewiring in an Animal

Project description:Biological systems must possess mechanisms that prevent inappropriate responses to spurious environmental inputs. Caenorhabditis elegans has two breakdown pathways for the short-chain fatty acid propionate: a canonical, vitamin B12-dependent pathway and a propionate-shunt that is used when vitamin B12 levels are low. The shunt pathway is kept off when there is sufficient flux through the canonical pathway, likely to avoid generating shunt-specific toxic intermediates. Here, we discover a transcriptional regulatory circuit that activates shunt gene expression upon propionate buildup. The nuclear hormone receptors NHR-10 and NHR-68 function together as a ‘persistence detector’ in a type 1, coherent feed-forward loop with an AND-logic gate to delay shunt activation upon propionate accumulation, and to avoid spurious shunt activation in response to a non-sustained pulse of propionate. Together, our findings identify the first persistence detector in an animal, which transcriptionally rewires propionate metabolism to maintain homeostasis.

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Project description:Biological systems must possess mechanisms that prevent inappropriate responses to spurious environmental inputs. Caenorhabditis elegans has two breakdown pathways for the short-chain fatty acid propionate: a canonical, vitamin B12-dependent pathway and a propionate shunt that is used when vitamin B12 levels are low. The shunt pathway is kept off when there is sufficient flux through the canonical pathway, likely to avoid generating shunt-specific toxic intermediates. Here, we discovered a transcriptional regulatory circuit that activates shunt gene expression upon propionate buildup. Nuclear hormone receptor 10 (NHR-10) and NHR-68 function together as a "persistence detector" in a type 1, coherent feed-forward loop with an AND-logic gate to delay shunt activation upon propionate accumulation and to avoid spurious shunt activation in response to a non-sustained pulse of propionate. Together, our findings identify a persistence detector in an animal, which transcriptionally rewires propionate metabolism to maintain homeostasis.

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