Salt causes ion disequilibrium‐induced programmed cell death in yeast and plants

• Published in: The Plant journal : for cell and molecular biology 2002-03, Vol.29 (5), p.649-659
• Main Authors: Huh, Gyung‐Hye, Damsz, Barbara, Matsumoto, Tracie K., Reddy, Muppala P., Rus, Ana M., Ibeas, José I., Narasimhan, Meena L., Bressan, Ray A., Hasegawa, Paul M.
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological - drug effects; Ageing, cell death; Animal and plant ecology; Animal, plant and microbial ecology; Apoptosis - drug effects; Arabidopsis; Arabidopsis - drug effects; Arabidopsis - growth & development; Arabidopsis thaliana; Autoecology; Biological and medical sciences; Cell Nucleus - drug effects; Cell physiology; Cell Survival - drug effects; DNA fragmentation; DNA Fragmentation - drug effects; Dose-Response Relationship, Drug; ENA1 gene; Fundamental and applied biological sciences. Psychology; Humans; ion disequilibrium; Ion Transport - drug effects; Molecular and cellular biology; Mutation; NaCl stress; Plant Development; Plant Roots - drug effects; Plant Roots - growth & development; Plants - drug effects; Plants and fungi; programmed cell death; Proto-Oncogene Proteins c-bcl-2 - genetics; Proto-Oncogene Proteins c-bcl-2 - physiology; Saccharomyces cerevisiae; Sodium Chloride - pharmacology; sos1 gene; Time Factors; Vacuoles - drug effects; yeast; Yeasts - drug effects; Yeasts - growth & development
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1046/j.0960-7412.2001.01247.x

Summary Programmed cell death (PCD) is a fundamental cellular process conserved in metazoans, plants and yeast. Evidence is presented that salt induces PCD in yeast and plants because of an ionic, rather than osmotic, etiology. In yeast, NaCl inhibited growth and caused a time‐dependent reduction in viability that was preceded by DNA fragmentation. NaCl also induced the cytological hallmarks of lysigenous‐type PCD, including nuclear fragmentation, vacuolation and lysis. The human anti‐apoptotic protein Bcl‐2 increased salt tolerance of wild‐type yeast strain and calcineurin‐deficient yeast mutant (cnb1Δ) that is defective for ion homeostasis, but had no effect on the NaCl or sorbitol sensitivity of the osmotic hypersensitive hog1Δ mutant – results that further link PCD in the response to the ion disequilibrium under salt stress. Bcl‐2 suppression of cnb1Δ salt sensitivity was ENA1 (P‐type ATPase gene)‐dependent, due in part to transcriptional activation. Salt‐induced PCD (TUNEL staining and DNA laddering) in primary roots of both Arabidopsis thaliana wild type (Col‐1 gl1) and sos1 (salt overly sensitive) mutant seedlings correlated positively with treatment lethality. Wild‐type plants survived salt stress levels that were lethal to sos1 plants because secondary roots were produced from the shoot/root transition zone. PCD‐mediated elimination of the primary root in response to salt shock appears to be an adaptive mechanism that facilitates the production of roots more able to cope with a saline environment. Both salt‐sensitive mutants of yeast (cnb1Δ) and Arabidopsis (sos1) exhibit substantially more profound PCD symptoms, indicating that salt‐induced PCD is mediated by ion disequilibrium.