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Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds
Published on: August 25, 2013
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Staurosporines decrease ORMDL proteins and enhance sphingomyelin synthesis resulting in depletion of plasmalemmal
Masashi Maekawa1, Minhyoung Lee1,2, Kuiru Wei1
1Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada.
Scientific Reports
|November 3, 2016
Summary
Low-dose staurosporine increases sphingomyelin synthesis, which is essential for maintaining phosphatidylserine and cholesterol distribution in the plasma membrane. This highlights a crucial link between sphingomyelin levels and membrane lipid organization.
Area of Science:
- Cell Biology
- Biochemistry
- Membrane Biology
Background:
- Phosphatidylserine (PS) accumulation in the inner plasma membrane leaflet is vital for eukaryotic cells.
- Sublethal staurosporine disrupts PS localization and K-Ras signaling.
Purpose of the Study:
- To investigate the impact of low-dose staurosporine on membrane lipid composition.
- To elucidate the role of sphingomyelin in regulating phosphatidylserine and cholesterol distribution.
Main Methods:
- Mass-spectrometry and metabolic tracer analysis were employed.
- The regulation of serine-palmitoyltransferase by ORMDL proteins was examined.
Main Results:
- Low-dose staurosporine treatment increased sphingomyelin mass and synthesis rate.
- Staurosporine decreased the abundance of ORMDL proteins, key regulators of sphingolipid synthesis.
- Inhibiting ceramide synthesis blocked the displacement of PS and cholesterol from the inner plasma membrane leaflet.
Conclusions:
- Optimal sphingomyelin levels are required for proper phosphatidylserine and cholesterol distribution in the plasma membrane.
- A complex interplay exists between phosphatidylserine and sphingomyelin trafficking in the plasma membrane.
