Sphingolipid long chain base phosphates can regulate apoptotic-like programmed cell death in plants
► Evidence sphingolipid long chain base phosphates regulate cell death in plants. ► Sphingosine-1-phosphate can attenuate cell death in Arabidopsis thaliana. ► A ‘sphingolipid rheostat’ may be involved in controlling cell fate in plants . Sphingolipids are ubiquitous components of eukaryotic cells a...
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Veröffentlicht in: | Biochemical and biophysical research communications 2011-07, Vol.410 (3), p.574-580 |
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Sprache: | eng |
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Zusammenfassung: | ► Evidence sphingolipid long chain base phosphates regulate cell death in plants. ► Sphingosine-1-phosphate can attenuate cell death in
Arabidopsis thaliana. ► A ‘sphingolipid rheostat’ may be involved in controlling cell fate in plants
.
Sphingolipids are ubiquitous components of eukaryotic cells and sphingolipid metabolites, such as the long chain base phosphate (LCB-P), sphingosine 1 phosphate (S1P) and ceramide (Cer) are important regulators of apoptosis in animal cells. This study evaluated the role of LCB-Ps in regulating apoptotic-like programmed cell death (AL-PCD) in plant cells using commercially available S1P as a tool.
Arabidopsis cell cultures were exposed to a diverse array of cell death-inducing treatments (including Cer) in the presence of S1P. Rates of AL-PCD and cell survival were recorded using vital stains and morphological markers of AL-PCD. Internal LCB-P levels were altered in suspension cultured cells using inhibitors of sphingosine kinase and changes in rates of death in response to heat stress were evaluated. S1P reduced AL-PCD and promoted cell survival in cells subjected to a range of stresses. Treatments with inhibitors of sphingosine kinase lowered the temperature which induced maximal AL-PCD in cell cultures. The data supports the existence of a sphingolipid rheostat involved in controlling cell fate in
Arabidopsis cells and that sphingolipid regulation of cell death may be a shared feature of both animal apoptosis and plant AL-PCD. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2011.06.028 |