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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:The regulation of metabolism is vital to any organism and can be achieved by transcriptionally activating or repressing metabolic genes. Although many examples of transcriptional metabolic rewiring have been reported, a systems-level study of how metabolism is rewired in response to metabolic perturbations is lacking in any animal. Here we apply Worm Perturb-Seq (WPS)-a high-throughput method combining whole-animal RNA-interference and RNA-sequencing to around 900 metabolic genes in the nematode Caenorhabditis elegans. We derive a metabolic gene regulatory network (mGRN) in which 385 perturbations are connected to 9,414 genes by more than 110,000 interactions. The mGRN has a highly modular structure in which 22 perturbation clusters connect to 44 gene expression programs. The mGRN reveals different modes of transcriptional rewiring from simple reaction and pathway compensation to rerouting and more complex network coordination. Using metabolic network modelling, we identify a design principle of transcriptional rewiring that we name the compensation-repression (CR) model. The CR model explains most transcriptional responses in metabolic genes and reveals a high level of compensation and repression in five core metabolic functions related to energy and biomass. We provide preliminary evidence that the CR model may also explain transcriptional metabolic rewiring in human cells.

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