Phosphatidylinositol (PI) is a constituent of biomembranes and a precursor of all phosphoinositides (PIPs), which participate in various types of signal transduction. A prominent characteristic of PI is that its sn-2 position is highly enriched in polyunsaturated fatty acids (PUFAs), such as arachidonic acid or eicosapentaenoic acid (EPA). We previously identified the hitherto unannotated enzyme
mboa-7, as an acyltransferase that incorporates PUFAs into the sn-2 position of PI, and showed that
mboa-7 mutants had a reduced EPA content in PI. However, the biological significance of PUFA-containing PI remains unknown, in part due to the absence of overt phenotypes in
mboa-7 mutants. To investigate which PIPs signaling pathway is affected by the reduction of PUFA in PI, we performed an RNAi enhancer screen against PI kinases and phosphatases using
mboa-7 mutants. We found that severe growth defects were caused in
mboa-7 mutants by knockdown of
vps-34, a catalytic subunit of class III PI 3-kinase that produces PI 3-phosphate (PI3P) from PI. In both
vps-34 RNAi-treated wild-type worms and
mboa-7 mutants, the size of PI3P-positive early endosomes was significantly decreased. An RNAi enhancer screen against PI3P-related genes revealed that, like knockdown of
vps-34, knockdown of autophagy-related genes caused severe growth defects in
mboa-7 mutants. Finally, we showed that autophagic clearance of protein aggregates is impaired in
mboa-7 mutants. Taken together, these results indicate the significance of the polyunsaturated fatty acyl moiety of PI in PI3P signaling.