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Salicylic acid‐mediated potentiation of Hsp70 induction correlates with reduced apoptosis in tobacco protoplasts
Author(s) -
Cronjé Marianne J.,
Weir Iona E.,
Bornman Liza
Publication year - 2004
Publication title -
cytometry part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.316
H-Index - 90
eISSN - 1552-4930
pISSN - 1552-4922
DOI - 10.1002/cyto.a.20036
Subject(s) - apoptosis , dna fragmentation , protoplast , hsp70 , salicylic acid , fragmentation (computing) , nicotiana tabacum , biology , programmed cell death , membrane potential , microbiology and biotechnology , heat shock , phosphatidylserine , flow cytometry , heat shock protein , dna damage , biochemistry , dna , membrane , ecology , phospholipid , gene
Background Elevated temperatures jeopardize plant disease resistance, as mediated by salicylic acid (SA). SA potentiates heat‐induced expression of the 70‐kDa heat shock protein (Hsp70) in tomato cells. In mammalian cells, Hsp70 suppresses apoptosis. We hypothesized that potentiation of heat‐induced Hsp70 by SA contributes to a reduction in apoptosis in tobacco protoplasts. Methods Tobacco protoplasts ( Nicotiana tabacum ) were exposed to SA (70 μM) at normal temperatures or in combination with heat shock. Hsp70/Hsc70 accumulation and phosphatidylserine (PS) exposure, DNA fragmentation, as well as loss of mitochondrial membrane potential were quantified by flow cytometry. Results and Conclusions SA at normal temperatures did not influence Hsp70/Hsc70 accumulation, but were found to induce apoptosis. In contrast, SA in combination with HS potentiated heat‐induced Hsp70/Hsc70 accumulation in tobacco protoplasts that correlated negatively with apoptosis, illustrated by decreased PS exposure and DNA fragmentation and enhanced mitochondrial membrane potential. We propose that this correlation supports a possible role for apoptosis suppression by Hsp70 under elevated temperatures during pathogen infection. © 2004 Wiley‐Liss, Inc.