Contribution of proteomic studies towards understanding plant heavy metal stress response

Abstract

Modulation of plant proteome composition is an inevitable process to cope with the environmental challenges including heavy metal (HM) stress. Soil and water contaminated with hazardous metals not only cause permanent and irreversible health problems, but also result substantial reduction in crop yields. In course of time, plants have evolved complex mechanisms to regulate the uptake, mobilization, and intracellular concentration of metal ions to alleviate the stress damages. Since, the functional translated portion of the genome plays an essential role in plant stress response, proteomic studies provide us a finer picture of protein networks and metabolic pathways primarily involved in cellular detoxification and tolerance mechanism. In the present review, an attempt is made to present the state of the art of recent development in proteomic techniques and significant contributions made so far for better understanding the complex mechanism of plant metal stress acclimation. Role of metal stress-related proteins involved in antioxidant defense system and primary metabolism is critically reviewed to get a bird's-eye view on the different strategies of plants to detoxify HMs. In addition to the advantages and disadvantages of different proteomic methodologies, future applications of proteome study of subcellular organelles are also discussed to get the new insights into the plant cell response to HMs.

Keywords: HSPs; PR protein; antioxidant; heavy metal; phytochelatins; proteomics.

FIGURE 1

Schematic illustration of various cellular mechanisms for mitigating heavy metal (HM) stress. Information about highlighted proteins gathered from published proteomic articles related to plant HM-toxicity. Up and down arrows indicate HM-induced increase and decrease protein abundance respectively. ATPase β, ATP synthase subunit beta; AH, aconitate hydratase; AsA-Glu, ascorbate glutathione; APX, ascorbate peroxidase; ACC, 1-aminocyclopropane-1-carboxylic acid; ACO, aconitase; CAT, catalase; CAX, cation/proton exchanger; CS, cysteine synthase; CSy, citrate synthase; ENO, enolase; FDH, formate dehydrogenase; G3PDH, glyceraldehyde-3-phosphate dehydrogenase; GR, glutathione reductase; Gly-I, glyoxalase I; GS, glutamine synthetase; GSH, reduced glutathione; LHC, light harvesting complex; LhcII-4, light-harvesting chlorophyll-a/b binding protein; LSU, large subunit; MTs, metallothioneins; MG, methylglyoxal; MDAR, monodehydroascorbate reductase; MDH, malate dehydrogenase; OEE, oxygen-evolving enhancer protein; PC, Phytochelatin; Prx, peroxidoxin; PR, pathogenesis-related; PDH, pyruvate dehydrogenase; PSII-OEC 2, photosystem II oxygen-evolving complex protein 2; PS, photosystem; ROS, reactive oxygen species; RuBisCO, ribulose-1,5-bisphosphate carboxylase oxygenase; SD, succinate dehydrogenase; SAM, S-adenosylmethionine; SSU, small subunit; Trx, thioredoxin; TPI, triosephosphate isomerase; TCA, tricarboxylic acid.