Samir Sharma

Effect of Fe Deficiency on the Photosynthetic System of Maize

Summary We investigated the effect of Fe deficiency on the photosynthetic system of maize ( Zea mays var. Ganga 5). Chlorophyll content, PSI and PSII electron transport rates, P700, Q, cytochrome f, cytochrome b559 HP and CO 2 fixation by intact leaves show a decrease in Fe deficient plants. Maximum reduction is observed in the amount of cyt f, which may be the component that limits overall photosynthetic rates, instead of PSI, which has been described as the component most severely effected by Fe deficiency in other plants. Loss in carbon fixing ability is much greater than the loss of chlorophyll, but corresponds closely to the reduction in cytochrome content, further implicating cyt f as the limiting factor. Reaction centers of the photosystems were not reduced as much as other components, suggesting that in the case of Fe deficiency the plant shows selectivity when loss of electron transport components is imminent.

Reactive oxygen species mediate axis-cotyledon signaling to induce reserve mobilization during germination and seedling establishment in Vigna radiata.

Seeds represent an excellent opportunity to investigate the role of reactive oxygen species (ROS) in control of metabolism during germination and seedling establishment. Cotyledons, the storage organs in Vigna, do not display growth/cell division while the embryonic axis shows rapid growth and intense metabolic activity. The present study investigates the possibility of ROS generated during respiration in the axis serving as messengers guiding storage reserve mobilization from cotyledons at the pre-greening stage. Seeds were germinated in the presence of hydroxyurea to halt cell division in the S-phase and separately in Edaravone, a potent free radical scavenger. Both treatments caused a decrease in germination percentage, seedling growth and protein mobilization. In the growing axis, both treatments resulted in a decrease in hydrogen peroxide (H2O2), total ROS, MDA and protein carbonyls. The picture in cotyledons was quite different, owing to the physiological dissimilarities between the tissues. The status of redox as evident by GSH/GSSG ratios tended toward oxidizing in axis in comparison to the highly reducing environment found in cotyledons. This is construed as a tendency to maintain redox buffering on the oxidizing side in the axis, to facilitate the passage of ROS message. These results strongly indicate that suppression of cell division or scavenging of ROS adversely affects protein reserve mobilization. It is proposed that apart from H2O2 being a transportable signal, the final message perceived in cotyledons also comprises lipid peroxidation, protein carbonylation and alteration of redox status of the glutathione pool.

Nickel Toxicity, Altering ROS Scavenging Mechanism and Impairing Sugar Based Signaling in Vigna radiata (L.) Wilczek during Germination and Seedling Establishment

Nickel is a heavy metal that has a minor requirement in plants and exerts strong toxic effects at low concentrations. Seed germination and pre-greening stages of seedling establishment represent a brief heterotrophic phase in the life of an otherwise autotrophic organism. Germination is also a stage when the seed relies on stored reserves, including minerals rather than carrying out their uptake and has not been studied. The present work is a study of alteration of germination-related biochemical parameters in the presence of Nickel. Manifestations of Nickel induced oxidative stress as well as antioxidant defenses together with sugar sensing and respiratory enzymatic factors were investigated in seeds of Vigna radiata. Ni treatment increased electron flow through complex IV in cotyledons. It is proposed that inactivation of α-amylase adversely affects sugar movement to the growing seedling, leading to poor sugar sensing by hexokinase. These factors, including possible mis-metallation of electron transport complexes, combine to produce the observed symptoms of Nickel toxicity. The altered antioxidants activity can be correlated with Reactive Oxygen Species production and subsequent changes in seed metabolism.

Interaction of Calcium Signalling with Reactive Oxygen and Reactive Nitrogen Species

Reactive oxygen species (ROS) are inevitable by-products of cellular redox reactions and are considered an index of redox status in the cell. The origin of the main reactive nitrogen species (RNS), nitric oxide (NO), has been elusive so far, occurring either via reductive production from nitrate/nitrite or via oxidative synthesis from arginine. NO interacts with superoxide to yield more species of RNS. Both RNS and ROS are known to covalently modify proteins. At least some of these oxidative or nitrosative modifications alter the structure and/or function of the target protein and convey a signal to alter the metabolic state of the cell. Ca2+, the simplest messenger, is supported in its signalling actions by a very large set of proteins referred to as the ‘Ca2+ toolkit’ comprising ion channels, ion pumps, Ca2+ binding and sensing proteins, etc. The three signalling entities mentioned, employ extensive interactions and cross-talk to arrive at a particular state of metabolism. Cellular metabolic status is strongly influenced by the dynamic concentration range of ROS and RNS and arrived at by the interaction of these species with the Ca2+ toolkit proteins altering the Ca2+ signature at any given point of time. Similar to Ca2+ signature, ROS signature has also been proposed, but has remained difficult to delineate due to the interactions and highly transitory status of these species. In the final analysis, it is suggested that the relative status of ROS, RNS, and cytosolic Ca2+ is highly dynamic due to the modifications these entities make in each other’s level and interpretation.