Context-specific interaction of the lipid regulator DIP-2 with phospholipid synthesis in axon regeneration and maintenance.
Abstract
Neurons maintain their morphology over prolonged periods of adult life with limited regeneration after injury. C. elegans DIP-2 is a conserved regulator of lipid metabolism that affects axon maintenance and regeneration after injury. Here, we investigated genetic interactions of dip-2 with mutants in genes involved in lipid biosynthesis and identified roles of phospholipids in axon regrowth and maintenance. CEPT-2 and EPT-1 are enzymes catalyzing the final steps in the de novo phospholipid synthesis (Kennedy) pathway. Loss of function mutants of cept-2 or ept-1 show reduced axon regrowth and failure to maintain axon morphology. We demonstrate that CEPT-2 is cell-autonomously required to prevent age-related axonal defects. Interestingly, loss of function in dip-2 led to suppression of the axon regrowth phenotype observed in either cept-2 or ept-2 mutants, suggesting that DIP-2 acts to counterbalance phospholipid synthesis. Our findings reveal the genetic regulation of lipid metabolism to be critical for axon maintenance under injury and during aging.
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Research summary
The paper claims that the lipid regulator DIP-2 is critical for axon maintenance and regeneration by interacting with phospholipid synthesis pathways. This research is relevant as it explores the genetic regulation of lipid metabolism in relation to neuronal maintenance and regeneration, which are key factors in understanding aging and age-related decline in neuronal function.
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