The TWK-26 potassium channel governs nutrient absorption in the intestine.

Ion channels are necessary for proper water and nutrient absorption in the intestine, which supports cellular metabolism and organismal growth. While a role for Na co-transporters and pumps in intestinal nutrient absorption is well defined, how individual K uniporters function to maintain ion homeostasis is poorly understood. Using , we show that a gain-of-function mutation in , which encodes a two-pore domain K ion channel orthologous to human KCNK3, facilitates nutrient absorption and suppresses the metabolic and developmental defects displayed by impaired intestinal MAP Kinase (MAPK) signaling.

The mutation is a loss-of-function insertion within the locus.

The genes encoding the mitogen-activated protein kinases DRL-1 and FLR-4 are required for growth and lipid homeostasis in . Interestingly, the mutant, which was previously isolated in a forward genetic screen for mutations that confer fluoride resistance, phenocopies the and loss-of-function mutants; however, the genetic identity of is unknown. Through whole genome sequencing, we found that the mutation is an insertion in the locus and disrupts gene function, resulting in dramatic growth defects and impaired vitellogenin production.

Opposing action of the FLR-2 glycoprotein hormone and DRL-1/FLR-4 MAP kinases balance p38-mediated growth and lipid homeostasis in C. elegans.

Animals integrate developmental and nutritional signals before committing crucial resources to growth and reproduction; however, the pathways that perceive and respond to these inputs remain poorly understood. Here, we demonstrate that DRL-1 and FLR-4, which share similarity with mammalian mitogen-activated protein kinases, maintain lipid homeostasis in the C. elegans intestine.