Sanjib Kumar Panda

Chromium stress in plants

The article presents an overview of the mechanism of chromium stress in plants. Chromium is known to be a toxic metal that can cause severe damage to plants and animals. Chromium-induced oxidative stress involves induction of lipid peroxidation in plants that causes severe damage to cell membranes. Oxidative stress induced by chromium initiates the degradation of photosynthetic pigments causing decline in growth. High chromium concentration can disturb the chloroplast ultrastructure thereby disturbing the photosynthetic process. Like copper and iron, chromium is also a redox metal and its redox behaviour exceeds that of other metals like Co, Fe, Zn, Ni, etc. The redox behaviour can thus be attributed to the direct involvement of chromium in inducing oxidative stress in plants. Chromium can affect antioxidant metabolism in plants. Antioxidant enzymes like SOD, CAT, POX and GR are found to be susceptible to chromium resulting in a decline in their catalytic activities. This decline in antioxidant efficiency is an important factor in generating oxidative stress in plants under chromium stress. However, both metallothioneins and organic acids are important in plants as components of tolerance mechanisms and are also involved in detoxification of this toxic metal.

Reactive oxygen species signaling in plants under abiotic stress

Abiotic stresses like heavy metals, drought, salt, low temperature, etc. are the major factors that limit crop productivity and yield. These stresses are associated with production of certain deleterious chemical entities called reactive oxygen species (ROS), which include hydrogen peroxide (H2O2), superoxide radical (O2−), hydroxyl radical (OH−), etc. ROS are capable of inducing cellular damage by degradation of proteins, inactivation of enzymes, alterations in the gene and interfere in various pathways of metabolic importance. Our understanding on ROS in response to abiotic stress is revolutionized with the advancements in plant molecular biology, where the basic understanding on chemical behavior of ROS is better understood. Understanding the molecular mechanisms involved in ROS generation and its potential role during abiotic stress is important to identify means by which plant growth and metabolism can be regulated under acute stress conditions. ROS mediated oxidative stress, which is the key to understand stress related toxicity have been widely studied in many plants and the results in those studies clearly revealed that oxidative stress is the main symptom of toxicity. Plants have their own antioxidant defense mechanisms to encounter ROS that is of enzymic and non-enzymic nature . Coordinated activities of these antioxidants regulate ROS detoxification and reduces oxidative load in plants. Though ROS are always regarded to impart negative impact on plants, some reports consider them to be important in regulating key cellular functions; however, such reports in plant are limited. Molecular approaches to understand ROS metabolism and signaling have opened new avenues to comprehend its critical role in abiotic stress. ROS also acts as secondary messenger that signals key cellular functions like cell proliferation, apoptosis and necrosis. In higher eukaryotes, ROS signaling is not fully understood. In this review we summarize our understanding on ROS and its signaling behavior in plants under abiotic stress.

Aluminum stress signaling in plants

Aluminum (Al) toxicity is a major constraint for crop production in acidic soil worldwide. When the soil pH is lower than 5, Al3+ is released to the soil and enters into root tip cell ceases root development of plant. In acid soil with high mineral content, Al is the major cause of phytotoxicity. The target of Al toxicity is the root tip, in which Al exposure causes inhibition of cell elongation and cell division, leading to root stunting accompanied by reduced water and nutrient uptake. A variety of genes have been identified that are induced or repressed upon Al exposure. At tissue level, the distal part of the transition zone is the most sensitive to Al. At cellular and molecular level, many cell components are implicated in the Al toxicity including DNA in nucleus, numerous cytoplastic compounds, mitochondria, the plasma membrane, and the cell wall. Although it is difficult to distinguish the primary targets from the secondary effects so far, understanding of the target sites of the Al toxicity is helpful for elucidating the mechanisms by which Al exerts its deleterious effects on root growth. To develop high tolerance against Al stress is the major goal of plant sciences. This review examines our current understanding of the Al signalling with the physiological, genetic, and molecular approaches to improve the crop performance under the Al toxicity. New discoveries will open up new avenues of molecular/physiological inquiry that should greatly advance our understanding of Al tolerance mechanisms. Additionally, these breakthroughs will provide new molecular resources for improving the crop Al tolerance via molecular-assisted breeding and biotechnology.

Mechanisms of Water Transport Mediated by PIP Aquaporins and Their Regulation Via Phosphorylation Events Under Salinity Stress in Barley Roots

Water homeostasis is crucial to the growth and survival of plants under water-related stress. Plasma membrane intrinsic proteins (PIPs) have been shown to be primary channels mediating water uptake in plant cells. Here we report the water transport activity and mechanisms for the regulation of barley (Hordeum vulgare) PIP aquaporins. HvPIP2 but not HvPIP1 channels were found to show robust water transport activity when expressed alone in Xenopus laevis oocytes. However, the co-expression of HvPIP1 with HvPIP2 in oocytes resulted in significant increases in activity compared with the expression of HvPIP2 alone, suggesting the participation of HvPIP1 in water transport together with HvPIP2 presumably through heteromerization. Severe salinity stress (200 mM NaCl) significantly reduced root hydraulic conductivity (Lp(r)) and the accumulation of six of 10 HvPIP mRNAs. However, under relatively mild stress (100 mM NaCl), only a moderate reduction in Lp(r) with no significant difference in HvPIP mRNA levels was observed. Sorbitol-mediated osmotic stress equivalent to 100 and 200 mM NaCl induced nearly identical Lp(r) reductions in barley roots. Furthermore, the water transport activity in intact barley roots was suggested to require phosphorylation that is sensitive to a kinase inhibitor, staurosporine. HvPIP2s also showed water efflux activity in Xenopus oocytes, suggesting a potential ability to mediate water loss from cells under hypertonic conditions. Water transport via HvPIP aquaporins and the significance of reductions of Lp(r) in barley plants during salinity stress are discussed.

Changes in antioxidant levels in Oryza sativa L. roots subjected to NaCl-salinity stress

Imposition of NaCl-salinity stress induced oxidative reactions in root tissue of rice seedlings. A uniform accumulation of proline was marked with the increasing NaCl concentrations. Both peroxide content and lipid peroxidation level (MDA) increased with the salt treatment from the control. CAT, GPx and SOD activities decreased with the increasing NaCl concentrations suggesting a possible oxidative damage to root tissue.

Molecular Physiology of Aluminum Toxicity and Tolerance in Plants

Aluminum being the third most abundant metal in the earth’s crust poses a serious threat to crop productivity in acid soils, which comprise almost half of the arable land. This review travels across time and updates research done on aluminum stress in plants. In its phytotoxic forms, aluminum affects root growth by acting in the root apical zone, resulting in growth inhibition in a very short time at micromolar concentrations. The mechanisms of aluminum toxicity in plants may proceed by growth inhibition, callose accumulation, cytoskeletal distortion, disturbance of plasma membrane surface charge, and H+-ATPase activity, lipid peroxidation of membranes, production of reactive oxygen species in cytosol and mitochondria, respiratory dysfunction, opening of mitochondrial permeability transition pores, collapsing of inner mitochondrial membrane potential, activation of mitochondrial protease, and induction of nuclear apoptosis, resulting ultimately in programmed cell death. In contrast, the mechanism of tolerance involves the exudation of organic acid anions, complexation of aluminum with organic acids, and subsequent detoxification. Many oxidative stress genes and other metabolically important genes have also been found to be induced under aluminum stress and overexpression analyses have also shown some plants to develop some degree of tolerance. In the future, researchers in the area of aluminum research should investigate more basic mechanisms of aluminum toxicity and discover and study more aluminum-responsive genes that confer resistance against this toxic metal, to ensure food security for ever-increasing human populations in the future.

An insight into the drought stress induced alterations in plants

Plants are subjected to several abiotic stresses that adversely affect growth, metabolism and yield. The dynamic research in plant genetics complemented by genome sequencing has opened up avenues to address multiple problems caused by abiotic stresses. Though many drought-induced genes have been phytoengineered in a wide range of plants, the drought signal transduction pathways, and the alteration of plant sensing and signaling systems to adverse environments still remain an intriguing subject for comprehensive investigation. To impart enhanced drought tolerance in plants, a thorough perception of physiological, biochemical and gene regulatory networks is essential. Recent functional genomics tools have facilitated the progress in our understanding of stress signaling and of the linked molecular regulatory networks. This has revealed several stress-inducible genes and various transcription and signaling factors that regulate the drought stress-inducible systems. Translational genomics of these drought specific genes using model plants have provided encouraging outcomes, but the in-depth knowledge of the specific roles of various metabolites in plant stress tolerance will lead to evolvement of strategies for the phytoengineering of drought tolerance in plants in future.

Transgenic cowpea (Vigna unguiculata) seeds expressing a bean α-amylase inhibitor 1 confer resistance to storage pests, bruchid beetles

Cowpea is one of the important grain legumes. Storage pests, Callosobruchus maculatus and C. chinensis cause severe damage to the cowpea seeds during storage. We employ a highly efficient Agrobacterium-mediated cowpea transformation method for introduction of the bean (Phaseolus vulgaris) α-amylase inhibitor-1 (αAI-1) gene into a commercially important Indian cowpea cultivar, Pusa Komal and generated fertile transgenic plants. The use of constitutive expression of additional vir genes in resident pSB1 vector in Agrobacterium strain LBA4404, thiol compounds during cocultivation and a geneticin based selection system resulted in twofold increase in stable transformation frequency. Expression of αAI-1 gene under bean phytohemagglutinin promoter results in accumulation of αAI-1 in transgenic seeds. The transgenic protein was active as an inhibitor of porcine α-amylase in vitro. Transgenic cowpeas expressing αAI-1 strongly inhibited the development of C. maculatus and C. chinensis in insect bioassays.

Copper-induced growth inhibition, oxidative stress and ultrastructural alterations in freshly grown water lettuce (Pistia stratiotes L.)

The effects of increasing concentrations of copper on the growth, ultra-structure and on certain biochemical parameters of water lettuce (Pistia stratiotes L.) were investigated under controlled conditions in the nutrient solutions containing increased copper sulfate concentrations ranging from 0 to 100 microM. Copper treatment for 12, 18 or 24 h resulted in inhibition of roots and leaves dry biomass. Atomic absorption spectrometry analysis of roots and leaves showed that copper accumulation increased with increase in concentration and duration of metal treatment. It is seen that copper resulted in increased production of hydrogen peroxide and superoxide radical in both roots and leave cells, showed a significant change after 24 h of treatment. Also, the significant decrease in the contents of total protein and photosynthetic pigments was observed. The antioxidant enzymes, viz., peroxidase (POX, E.C.1.11.1.7), catalase (CAT, E.C.1.11.1.6) and superoxide dismutase (SOD, E.C.1.15.1.1) showed significant variation with the increase in lipid peroxidation. Increasing trends was observed in levels of ascorbate and glutathione. The rapid inducibility of some of these enzymes are useful early and sensitive indicators of heavy metal toxicity. The results demonstrated that exposure to elevated concentration of Cu had a remarkable effect on the biochemistry and physiology, induced oxidative stress in water lettuce characterized by the initiation of lipid peroxidation that inhibited growth and disintegration of major antioxidant systems.

Mitochondrial alterations related to programmed cell death in tobacco cells under aluminium stress.

The present investigation was undertaken to verify whether mitochondria play a significant role in aluminium (Al) toxicity, using the mitochondria isolated from tobacco cells (Nicotiana tabacum, non-chlorophyllic cell line SL) under Al stress. An inhibition of respiration was observed in terms of state-III, state-IV, succinate-dependent, alternative oxidase (AOX)-pathway capacity and cytochrome (CYT)-pathway capacity, respectively, in the mitochondria isolated from tobacco cells subjected to Al stress for 18 h. In accordance with the respiratory inhibition, the mitochondrial ATP content showed a significant decrease under Al treatment. An enhancement of reactive oxygen species (ROS) production under state-III respiration was observed in the mitochondria isolated from Al-treated cells, which would create an oxidative stress situation. The opening of mitochondrial permeability transition pore (MPTP) was seen more extensively in mitochondria isolated from Al-treated cells than in those isolated from control cells. This was Ca(2+) dependent and well modulated by dithioerythritol (DTE) and Pi, but insensitive to cyclosporine A (CsA). The collapse of inner mitochondrial membrane potential (DeltaPsi(m)) was also observed with a release of cytochrome c from mitochondria. A great decrease in the ATP content was also seen under Al stress. Transmission electron microscopy analysis of Al-treated cells also corroborated our biochemical data with distortion in membrane architecture in mitochondria. TUNEL-positive nuclei in Al-treated cells strongly indicated the occurrence of nuclear fragmentation. From the above study, it was concluded that Al toxicity affects severely the mitochondrial respiratory functions and alters the redox status studied in vitro and also the internal structure, which seems to cause finally cell death in tobacco cells.