Phosphatidylinositol 5 phosphate 4 kinase regulates phosphatidylinositol 3,4 bisphosphate levels in vivo
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In Drosophila , loss of phosphatidylinositol 5 phosphate 4 kinase (PIP4K) results in a reduction in larval salivary gland cell size. Previous studies have shown that this reduction in cell size is not correlated with the levels of phosphatidylinositol 5 phosphate (PI5P), the canonical substrate of PIP4K but to the levels of phosphatidylinositol 3 phosphate (PI3P) a substrate that is used less effectively by the PIP4K enzyme in vitro . The phosphorylation of PI3P by PIP4K generates phosphatidylinositol 3,4 bisphosphate [PI(3,4)P 2 ]. Using a biosensor for PI(3,4)P 2 , surprisingly, we find that depletion of PIP4K leads to an elevation of intracellular PI(3,4)P 2 punctae in salivary gland cells. This elevation in PI(3,4)P 2 punctae was not dependent on the catalytic activity of dPIP4K. Rather, we found that the elevation of PI(3,4)P 2 was dependent on the catalytic activity of Class II phosphatidylinositol 3 kinase (Class II PI3K). Thus, the PIP4K protein regulates an intracellular pool of PI(3,4)P 2 via Class II PI3K activity in Drosophila cells.
