The TIP30 Protein Complex, Arachidonic Acid and Coenzyme A Are Required for Vesicle Membrane Fusion

Zhang, Chengliang; Li, Aimin; Gao, Shu‐Qin; Zhang, Xinchun; Xiao, Hua

doi:10.1371/journal.pone.0021233

Cited by 24 publications

(20 citation statements)

References 32 publications

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“…28 It is noteworthy that the rate of colocalization between SH3GLB1 and CHRN as well as between MAP1LC3A and CHRN was significantly decreased in the trim63 −/ − under control conditions. This is in agreement with earlier data that connected SH3GLB1 to endocytic processing rather than autophagy assistance, [51][52][53] and also suggests that TRIM63 controls a pool of autophagic carriers under unchallenged conditions.…”

Section: Discussionsupporting

confidence: 93%

Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

et al. 2013

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Section: Discussionsupporting

confidence: 93%

Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

et al. 2013

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“…Such lipid‐mediated regulations of membrane rearrangements are only beginning to be explored. Sterols ( and references therein), phosphoinositides ( and references therein), PA and DAG ( and references therein) are among few lipids that have regulatory role in membrane fusion and fission.…”

Section: The Role Of Pa In Membrane Fusion and Membrane Fissionmentioning

confidence: 99%

“…Phosphatidic acid, LPA and DAG are involved in many membrane fusion and membrane fission events, such as fission of Golgi membranes , fission during endocytic transport , vacuole fission and fusion , mitochondrial dynamics , exocytosis , vesicle‐vesicle fusion , myoblast fusion , osteoclast fusion , membrane fusion during sporulation , membrane fusion during fertilization . Fusion of PA‐containing vesicles was studied in Refs .…”

Section: The Role Of Pa In Membrane Fusion and Membrane Fissionmentioning

confidence: 99%

Phosphatidic acid in membrane rearrangements

et al. 2019

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Phosphatidic acid (PA) is the simplest cellular glycerophospholipid characterized by unique biophysical properties: a small headgroup; negative charge; and a phosphomonoester group. Upon interaction with lysine or arginine, PA charge increases from −1 to −2 and this change stabilizes protein–lipid interactions. The biochemical properties of PA also allow interactions with lipids in several subcellular compartments. Based on this feature, PA is involved in the regulation and amplification of many cellular signalling pathways and functions, as well as in membrane rearrangements. Thereby, PA can influence membrane fusion and fission through four main mechanisms: it is a substrate for enzymes producing lipids (lysophosphatidic acid and diacylglycerol) that are involved in fission or fusion; it contributes to membrane rearrangements by generating negative membrane curvature; it interacts with proteins required for membrane fusion and fission; and it activates enzymes whose products are involved in membrane rearrangements. Here, we discuss the biophysical properties of PA in the context of the above four roles of PA in membrane fusion and fission.

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“…We searched for potential Golgi factor(s) that is known to modify membrane lipid composition and regulate mitophagy. One such a candidate identified is Endophilin B1 (EndoB1, also known as Bif-1), which was reported to possess an intrinsic PA-binding activity 41 and is require for mitophagy 41, 42 . We found that EndoB1 was concentrated on the OPTN-positive vesicles under basal conditions.…”

Section: Resultsmentioning

confidence: 99%

Parkin coordinates mitochondrial lipid remodeling to execute mitophagy

Lin

Jin

Kapur

et al. 2020

Preprint

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19Mitochondrial failure caused by Parkin mutations contributes to Parkinson's disease. Parkin 20 binds, ubiquitinates, and targets impaired mitochondria for autophagic destruction. Robust 21 mitophagy involves peri-nuclear concentration of Parkin-tagged mitochondria, followed by 22 dissemination of juxtanuclear mitochondrial aggregates, and efficient sequestration of 23 individualized mitochondria by autophagosomes. Here, we report that the execution of complex 24 mitophagic events requires active mitochondrial lipid remodeling. Parkin recruits phospholipase 25 D2 to the depolarized mitochondria and generate phosphatidic acid (PA). Mitochondrial PA is 26 subsequently converted to diacylglycerol (DAG) by Lipin-1 phosphatase-a process that further 27 requires mitochondrial ubiquitination and ubiquitin-binding autophagic receptors, NDP52 and 28Optineurin. We show that Optineurin transports, via Golgi-derived vesicles, a PA-binding factor 29 EndoB1 to ubiquitinated mitochondria, thereby facilitating DAG production. Mitochondrial 30 DAG activates both F-actin assembly to drive mitochondrial individualization, and 31 autophagosome biogenesis to efficiently restrict impaired mitochondria. Thus Parkin, autophagic 32 receptors and the Golgi complex orchestrate mitochondrial lipid remodeling to execute robust 33 mitophagy. 34 35 36 37 38 39 3 17, 18 . Instead, p62 acts to coalesce ubiquitinated mitochondria into large aggregates at the 59 perinuclear region-a dramatic event yet without a clearly defined function 17, 18 . Recent evidence 60 4 further indicates that autophagosomes are actually synthesized "de novo" at or around 61 mitochondria tagged for destruction 15, 19, 20 . How Parkin and different autophagic receptors 62 coordinate local autophagosome biogenesis around condemned mitochondria to efficiently 63 execute mitophagy remains to be fully elucidated. 64 Intriguingly, when subject to massive uncoupling by CCCP, the large mitochondrial 65 populations tagged by Parkin are recognized and actively concentrated by microtubule-based 66 motors and form large perinuclear aggregates or inclusions 12, 21 . Perinuclear mitochondrial 67 inclusions have also been observed in neurons from PD patients 22, 23 , indicating that this process 68 is physiologically relevant. Juxtanuclear mitochondrial aggregates, or termed mito-aggresomes, 69 are subsequently dispersed into smaller units prior to their sequestration by autophagosomes 70 (mitophagosomes) and eventual degradation 11 . Electron microscopy has revealed that some 71 perinuclear mitochondria concentrated by Parkin and PINK1 are fused 21 . These findings imply 72 that dissemination of perinuclear mitochondrial aggregates would require active "de-73 aggregation" and "fission" of mitochondria. Thus, the disposal of impaired mitochondria 74 involves elaborate temporal and spatial regulation orchestrated by Parkin. How Parkin 75 coordinates these events to achieve robust mitophagy is not well understood. 76In this report, we present evidence that the recruitment of Parkin t...

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The TIP30 Protein Complex, Arachidonic Acid and Coenzyme A Are Required for Vesicle Membrane Fusion

Cited by 24 publications

References 32 publications

Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors

Phosphatidic acid in membrane rearrangements

Parkin coordinates mitochondrial lipid remodeling to execute mitophagy

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