PI(4,5)P2 controls plasma membrane PI4P and PS levels via ORP5/8 recruitment to ER–PM contact sites

Sohn, Minji; Korzeniowski, Marek; Zewe, James P.; Wills, Rachel C.; Hammond, Gerald; Humpolíčková, Jana; Vrzal, Lukáš; Chalupská, Dominika; Veverka, Václav; Fairn, Gregory D.; Bouřa, Evžen; Balla, Tamás

doi:10.1083/jcb.201710095

Cited by 165 publications

(238 citation statements)

References 33 publications

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“…A similar regulatory mechanism takes place in mammalian cells. Depletion of ORP5 and ORP8 results in increased PI4P and PI(4,5)P 2 levels (Chung et al, 2015b;Sohn et al, 2016;Ghai et al, 2017;Sohn et al, 2018). Our observations and another recent study (Sohn et al, 2018) suggest that ORP5/8 activity is tuned according to changes in PI(4,5)P 2 levels.…”

Section: Phosphoinositide Metabolism Controls Polarized Cell Growthsupporting

confidence: 67%

“…We wondered if other ORP family members undergo dynamic changes in response to external stimuli, similar to the Osh3 protein. The ORP5 protein localizes to ER-PM contacts where it carries out phosphatidylserine-PI4P exchange reactions (Chung et al, 2015b;Sohn et al, 2016;Sohn et al, 2018).…”

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

“…ORP5 cortical localization is mediated by a PH domain that binds PI(4,5)P 2 in the PM (Ghai et al, 2017;Sohn et al, 2018). Thus, ORP5 localization may be regulated in response to stimuli that trigger phospholipase C (PLC) activation and PI(4,5)P 2 hydrolysis.…”

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

“…As monitored by total internal reflection fluorescence (TIRF) microscopy in HeLa cells, addition of 10 M ionomycin (that lowers PI(4,5)P 2 levels) resulted in the rapid loss of GFP-ORP5 cortical localization ( Fig EV7A). This ORP5 regulatory mechanism may simply work through dynamic fluctuations in PH domain-PI(4,5)P 2 interactions (Ghai et al, 2017;Sohn et al, 2018), as ORP5 does not have a GOLD domain.…”

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

“…But importantly, loss of ORP5/8 is known to result in increased PI4P and PI(4,5)P 2 levels at the PM (Chung et al, 2015b;Sohn et al, 2016;Ghai et al, 2017;Sohn et al, 2018). Thus, attenuation of ORP-mediated phosphoinositide…”

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

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A Cytoplasmic GOLD Protein Controls Cell Polarity

Omnus

Cadou

et al. 2018

Preprint

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Phosphoinositide lipids provide spatial landmarks during polarized secretion.Here, we elucidate a role for phosphatidylinositol 4-phosphate (PI4P) metabolism in the control of cell polarity. In budding yeast, PI4P is enriched at the plasma membrane of growing daughter cells. Upon heat shock however, PI4P rapidly increases at the plasma membrane in mother cells resulting in a more uniform PI4P distribution. Rather than phosphoinositide kinase activation, PI4P hydrolysis is impaired to generate the heat-induced PI4P signal in mother cells. This fine tune control of PI4P metabolism is mediated through attenuation of the Osh3 protein that binds and presents PI4P to a phosphoinositide phosphatase.

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Section: Phosphoinositide Metabolism Controls Polarized Cell Growthsupporting

confidence: 67%

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

Section: Stimulus-induced Regulation Of Orp5 Localizationmentioning

confidence: 99%

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A Cytoplasmic GOLD Protein Controls Cell Polarity

Omnus

Cadou

et al. 2018

Preprint

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Membrane contact sites orchestrate cholesterol homeostasis that is central to vascular aging

Pang

Jin

et al. 2023

WIREs Mechanisms of Disease

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Chronological age causes structural and functional vascular deterioration and is a well‐established risk factor for the development of cardiovascular diseases, leading to more than 40% of all deaths in the elderly. The etiology of vascular aging is complex; a significant impact arises from impaired cholesterol homeostasis. Cholesterol level is balanced through synthesis, uptake, transport, and esterification, the processes executed by multiple organelles. Moreover, organelles responsible for cholesterol homeostasis are spatially and functionally coordinated instead of isolated by forming the membrane contact sites. Membrane contact, mediated by specific protein–protein interaction, pulls opposing organelles together and creates the hybrid place for cholesterol transfer and further signaling. The membrane contact‐dependent cholesterol transfer, together with the vesicular transport, maintains cholesterol homeostasis and has intimate implications in a growing list of diseases, including vascular aging‐related diseases. Here, we summarized the latest advances regarding cholesterol homeostasis by highlighting the membrane contact‐based regulatory mechanism. We also describe the downstream signaling under cholesterol homeostasis perturbations, prominently in cholesterol‐rich conditions, stimulating age‐dependent organelle dysfunction and vascular aging. Finally, we discuss potential cholesterol‐targeting strategies for therapists regarding vascular aging‐related diseases.This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology

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