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Removal or masking of phosphatidylinositol(4,5)bisphosphate from the outer mitochondrial membrane causes mitochondrial fragmentation.

ABSTRACT: Mitochondria are central players in programmed cell death and autophagy. While phosphoinositides are well established regulators of membrane traffic, cellular signalling and the destiny of certain organelles, their presence and role for mitochondria remain elusive. In this study we show that removal of PtdIns(4,5)P? by phosphatases or masking the lipid with PH domains leads to fission of mitochondria and increased autophagy. Induction of general autophagy by amino acid starvation also coincides with the loss of mitochondrial PtdIns(4,5)P?, suggesting an important role for this lipid in the processes that govern mitophagy. Our findings reveal that PKC? can rescue the removal or masking of PtdIns(4,5)P?, indicating that the inositol lipid is upstream of PKC.

SUBMITTER: Rosivatz E

PROVIDER: S-EPMC3032883 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature

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Removal or masking of phosphatidylinositol(4,5)bisphosphate from the outer mitochondrial membrane causes mitochondrial fragmentation.

Rosivatz Erika E Woscholski Rudiger R

Cellular signalling 20101030 2

Mitochondria are central players in programmed cell death and autophagy. While phosphoinositides are well established regulators of membrane traffic, cellular signalling and the destiny of certain organelles, their presence and role for mitochondria remain elusive. In this study we show that removal of PtdIns(4,5)P₂ by phosphatases or masking the lipid with PH domains leads to fission of mitochondria and increased autophagy. Induction of general autophagy by amino acid starvation also coincides ...[more]

PMID: 21044681

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