KCl induces a caspase-independent programmed cell death in the unicellular green chlorophyte Chlamydomonas reinhardtii (Chlorophyceae)

Abstract:

Programmed cell death (PCD) plays an important role in mediating adaptation responses under adverse conditions such as high salinity. To understand the molecular mechanism of adaptation of algal cells to salt, the freshwater alga Chlamydomonas reinhardtii was challenged with 200 mM KCl. In the present study, vegetative cells of C. reinhardtii undergo cell death when exposed to 200 mM KCl, this death being dose-dependent, with 100–800 mM KCl causing 16–64% cell death. Within half an hour of KCl exposure, a ~1.9-fold rise in the intracellular H₂O₂ content followed an increase in antioxidant enzyme (superoxide dismutats, catalase, and ascorbate peroxidase) activities and their transcript levels. Furthermore, apoptotic hallmarks such as disruption of mitochondrial membrane potential, DNA nicks, apoptosis-inducing factor (AIF) release into the cytoplasm, and genomic DNA fragmentation were observed. Interestingly, KCl stress did not stimulate caspase-3-like protease activity. Additionally, cells undergoing PCD showed characteristic shrinkage with an accumulation of lipids and vacuoles, along with degraded chloroplast. These results illustrate that KCl induces reactive oxygen species production that leads to AIF release from mitochondria, causing a caspase-independent cell death in C. reinhardtii.

Key Words::

• Apoptosis-inducing factor
• Caspase-independent pathway
• Chlamydomonas reinhardtii
• KCl stress
• Programmed cell death

ACKNOWLEDGEMENTS

This work was supported by the Department of Atomic Energy, India.