Premium
The phosphatidylinositol transfer protein PITP‐1 facilitates fast recovery of eating behavior after hypoxia in the nematode Caenorhabditis elegans
Author(s) -
Abergel Zohar,
Shaked Maayan,
Shukla Virendra,
Wu ZhengXing,
Gross Einav
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202000704r
Subject(s) - caenorhabditis elegans , hypoxia (environmental) , nematode , microbiology and biotechnology , chemistry , biology , ecology , biochemistry , oxygen , organic chemistry , gene
Among the fascinating adaptations to limiting oxygen conditions (hypoxia) is the suppression of food intake and weight loss. In humans, this phenomenon is called high‐altitude anorexia and is observed in people suffering from acute mountain syndrome. The high‐altitude anorexia appears to be conserved in evolution and has been seen in species across the animal kingdom. However, the mechanism underlying the recovery of eating behavior after hypoxia is still not known. Here, we show that the phosphatidylinositol transfer protein PITP‐1 is essential for the fast recovery of eating behavior after hypoxia in the nematode Caenorhabditis elegans . Unlike the neuroglobin GLB‐5 that accelerates the recovery of eating behavior through its function in the oxygen (O 2 )‐sensing neurons, PITP‐1 appears to act downstream, in neurons that express the mod‐1 serotonin receptor. Indeed, pitp‐1 mutants display wild‐type‐like O 2 ‐evoked‐calcium responses in the URX O 2 ‐sensing neuron. Intriguingly, loss‐of‐function of protein kinase C 1 (PKC‐1) rescues pitp‐1 mutants’ recovery after hypoxia. Increased diacylglycerol (DAG), which activates PKC‐1, attenuates the recovery of wild‐type worms. Together, these data suggest that PITP‐1 enables rapid recovery of eating behavior after hypoxia by limiting DAG’s availability, thereby limiting PKC activity in mod‐1 ‐expressing neurons.