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Stimulation of immunity-linked genes by membrane disruption is linked to Golgi function and the ARF-1 GTPase

ABSTRACT: Stimulation of immunity-linked genes by membrane disruption is linked to Golgi function and the ARF-1 GTPase

PROVIDER: PRJNA1013344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25918306.fastq.gz	Fastqsanger.gz
	SRR25918307.fastq.gz	Fastqsanger.gz
	SRR25918308.fastq.gz	Fastqsanger.gz
	SRR25918309.fastq.gz	Fastqsanger.gz

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Stimulation of immunity-linked genes by membrane disruption is linked to Golgi function and the ARF-1 GTPase

Project description:Immunity-linked genes (ILGs) are activated by pathogens but also may respond to imbalances in lipids. Why pathogen attack and metabolic changes both impact ILG activation is unclear. We find that ILGs are activated when membrane phosphatidylcholine ratios change in secretory organelles in C. elegans. RNAi targeting of the ADP-ribosylation factor ARF-1, which disrupts the Golgi, also activates ILG expression, suggesting that activation of this membrane stress response could occur outside the ER. Our data argue that ILG upregulation is a coordinated response to changes in trafficking resulting from intrinsic cues (changes in membrane lipids) or extrinsic stimulation (increased secretion during immune response). Indeed, a focused RNAi screen of ILGs uncovered defects in secretion of two GFP reporters as well as accumulation of a pathogen-responsive CUB-domain fusion protein. These results also suggests that genes shared between the classical pathogen responses and lipid stress may act to counteract stress on secretory function.

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Immunity-linked genes are stimulated by a membrane stress pathway linked to Golgi function and the ARF-1 GTPase.

Project description:Infection response and other immunity-linked genes (ILGs) were first named in Caenorhabditis elegans-based expression after pathogen challenge, but many are also up-regulated when lipid metabolism is perturbed. Why pathogen attack and metabolic changes both increase ILGs is unclear. We find that ILGs are activated when phosphatidylcholine (PC) levels change in membranes of secretory organelles in C. elegans. RNAi targeting of the ADP-ribosylation factor arf-1, which disrupts the Golgi and secretory function, also activates ILGs. Low PC limits ARF-1 function, suggesting a mechanism for ILG activation via lipid metabolism, as part of a membrane stress response acting outside the ER. RNAi of selected ILGs uncovered defects in the secretion of two GFP reporters and the accumulation of a pathogen-responsive complement C1r/C1s, Uegf, Bmp1 (CUB) domain fusion protein. Our data argue that up-regulation of some ILGs is a coordinated response to changes in trafficking and may act to counteract stress on secretory function.

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