Accumulation of small heat shock proteins, including mitochondrial HSP22, induced by oxidative stress and adaptive response in tomato cells

Abstract

SummaryChanges in gene expression, by application of H 2 O 2 , O 2°-generating agents (methyl viologen, digitonin) and gamma irradiation to tomato suspension cultures, were investigated and compared to the well-described heat shock response. Two-dimensional gel protein mapping analyses gave the first indication that at least small heat shock proteins (smHSP) accumulated in response to application of H 2 O 2 and gamma irradiation, but not to O 2°-generating agents. While some proteins seemed to be induced specifically by each treatment, only part of the heat shock response was observed. On the basis of Northern hybridization experiments performed with four heterologous cDNA, corresponding to classes I-IV of pea smHSP, it could be concluded that significant amounts of class I and II smHSP mRNA are induced by H 2 O 2 and by irradiation. Taken together, these results demonstrate that in plants some HSP genes are inducible by oxidative stresses, as in micro-organisms and other eukaryotic cells. HSP22, the main stress protein that accumulates following H 2 O 2 action or gamma irradiation, was also purified. Sequence homology of amino terminal and internal sequences, and immunoreactivity with Chenopodium rubrum mitochondrial smHSP antibody, indicated that the protein belongs to the recently discovered class of plant mitochondrial smHSP. Heat shock or a mild H 2 O 2 pretreatment was also shown to lead to plant cell protection against oxidative injury. Therefore, the synthesis of these stress proteins can be considered as an adaptive mechanism in which mitochondrial protection could be essential.

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

“…An RNA blot was prepared with 32 Arabidopsis, in CaM-mediated cell death. We demonstrate that (i) oxidative stress, involved in plant PCD processes, [40][41][42][43] induces the transient expression of AtBAG6, (ii) AtBAG6 physically interacts with AtCaMs, (iii) the IQ motif in the AtBAG6 is required for Ca 2 þ -independent CaM complex formation, and (iv) the CaM-binding IQ motif and BAG domain are required for AtBAG6-mediated cell death in both yeast and plant. In animals, Ca 2 þ released into the cytoplasm can induce mitochondrial permeability transition (PT) pore opening, which induces release of apoptotic activators to the cytoplasm and consequently activates caspase-mediated PCD.…”

“…52 Abiotic stresses, including temperature, salinity, drought, light, ROS, and ozone, are now often regarded not as toxins, but rather as elicitors of PCD, when plant cells are chronically exposed to physiological levels of these stresses. 41,[73][74][75][76][77] However, necrosis, which represents an uncontrolled form of cell death, does occur in plant cells when they are exposed to high levels of abiotic stress that the plant cannot override with their tolerance mechanisms. ROS are pivotal mediators of PCD in plants.…”

“…Transcription of AtBAG6 was specifically induced by SA, H 2 O 2 , and high temperature, all of which are known to be involved in plant PCD processes. [40][41][42][43] To further determine the biological roles of AtBAG6 in plants, we constructed each plasmid containing CDD or CDD I575S under the control of the constitutive cauliflower mosaic virus 35S promoter using the pCAMBIA1302 binary vector and used these plasmids to transform Arabidopsis. Transgenic CDD plants showed midget (dwarfism) phenotypes and formed disease-like necrotic lesions on their leaves (Figure 9b and c).…”

In Vivo Modifications of the Maize Mitochondrial Small Heat Stress Protein, HSP22

“…Presumably, the HSPs function as chaperones that stabilize denatured proteins. These stresses include oxidative (20,21), ␥ irradiation (20), cold stress (22,23), and drought (24). Exposure to heat stress increases subsequent resistance of plants to other stresses (25)(26)(27)(28), which supports a general protective function for HSPs.…”

Effect of extreme temperatures on powdery mildew development and Hsp70 induction in tomato and wild Solanum spp.

“…Plant Hsp70s, together with their cochaperones DnaJ/Hsp40 and GrpE, are localised in the cytosol, endoplasmic reticulum, mitochondria, chloroplasts, and peroxisomes (Vierling 1991;Boston et al 1996;Bukau & Horwich 1998). The members of the 70-kDa Hsp family are most commonly associated with the cellular defence against high temperatures and their accumulation thus confers thermotolerance (Vierling 1991), protection against oxidative stress (Banzet et al 1998), and inhibition of apoptosis through the prevention of DNA fragmentation (Cho & Choi 2009). A general protective role of Hsp70 was demonstrated in Arabidopsis thaliana mutants deficient in Hsp70 synthesis which exhibited higher sensitivity to the heat injury (Burke 2001).…”