Heat stress: an inducer of programmed cell death in Chlorella saccharophila.

Abstract

Programmed cell death (PCD) has been recognized as a fundamental cellular process conserved in metazoans, plants and yeast. However, the cellular mechanisms leading to PCD have not been fully elucidated in unicellular organisms. Evidence is presented that heat stress induces PCD in Chlorella saccharophila cells. Our results demonstrate that heat shock triggers a PCD pathway occurring with characteristics features such as chromatin condensation, DNA fragmentation, cell shrinkage and detachment of the plasma membrane from the cell wall, and suggest the presence of caspase 3-like activity. The caspase 3 inhibitor Ac-DEVD-CHO gave significant protection against heat shock-induced cell death. Moreover, a reduction in photosynthetic pigment contents associated with alteration of chloroplast morphology and a fairly rapid disappearance of the ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit and the light-harvesting complex of PSII have been observed. The timing of events in the signaling cascade associated with the C. saccharophila heat shock PCD response is discussed. Insights into this field may have general implications for understanding the pathway of cell death in unicellular green algae.

• Authors: Anna Zuppini, Carlo Andreoli, Barbara Baldan
• Journal: Plant & cell physiology (Plant Cell Physiol) Vol. 48 Issue 7 Pg. 1000-9 (Jul 2007) ISSN: 0032-0781 [Print] Japan
• PMID: 17567640 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Caspase Inhibitors
• Oligopeptides
• Reactive Oxygen Species
• acetyl-aspartyl-glutamyl-valyl-aspartal

Topics

• Apoptosis (physiology)
• Caspase Inhibitors
• Cell Survival
• Chlorella (cytology, ultrastructure)
• DNA Fragmentation
• Enzyme Activation
• Heat-Shock Response (physiology)
• Hot Temperature
• Oligopeptides (pharmacology)
• Reactive Oxygen Species
• Time Factors