Membrane degradation, accumulation of Phosphatidic acid, stimulation of catalase activity and nuclear DNA fragmentation during 2,4-d-induced leaf senescence in mustard

Abstract

We investigated 2,4-D-induced leaf senescence in young mustard seedlings. A set of morphometric, biochemical and molecular parameters were analyzed to characterize senescence markers. In accordance with earlier reports, chloroplast-membrane degradation marked the early phase of leaf senescence based on the analysis of the galactolipid fraction. Degradation of grana occurred earlier to that of the envelope, as revealed by the relative level of their specific galactolipids, namely, monogalactosyl diglyceride and digalactosyl diglyceride. Phospholipids showed extensive degradation resulting in the accumulation of lyso-derivatives of major phospholipids and phosphatidic acid (PA) in senescing leaves. Catalase activity was stimulated by 2,4-D and reflected scavenging of reactive oxygen species. Nuclear DNA degradation, a previously known death signal that represented a point of no return from progression of senescence, occurred late on the 4th day subsequent to 2,4-D supplementation. AgNO3, an inhibitor of ethylene biosynthesis, inhibited leaf senescence by ca. 54% based on PA content. Involvement of 2,4-D, ethylene and abscisic acid in leaf senescence is discussed in relation to hormonal interplay.

2,4-dichlorophenoxyacetic acid-induced leaf senescence in mung bean (Vigna radiata L. Wilczek) and senescence inhibition by co-treatment with silver nanoparticles

“…Effect of 2,4-D on activities of antioxidative enzymes and AA-GSH cycle-related intermediates 2,4-D-treatment has previously been shown to regulate the activities of several antioxidative enzymes, including CAT, POX, and SOD, and also affects enzymes of the AA-GSH cycle, such as MDHAR, DHAR, and GR [4,9]. Supplementation with 2,4-D caused an increase in the activities of POX, SOD, MDHAR, DHAR, and GR by 2-to 3-fold compared to controls ( Table 2).…”

“…The optimum concentration of auxin needed to induce senescence varies, even in the same plant system, depending on the type of auxin used, e.g., a natural auxin or synthetic analog (NAA, picloram, dicamba, quinclorac, etc) [4,7,9].…”

“…nDNA degradation has been reported in a variety of plant tissues that are undergoing senescence, and the degradation of nDNA is detected in most cases by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay [3]. While most studies on leaf senescence focus on nDNA degradation, very little information is available on the labeling of degraded nDNA in situ [1,4,11].…”

“…Cell membrane damage is a marked symptom of leaf senescence that is attributed to lipid peroxidation, stimulation of antioxidative enzyme activity [4e6], and overproduction of cytotoxic reactive oxygen species (ROS), including hydrogen peroxide (H 2 O 2 ), superoxide radical (O $À 2 ), and hydroxyl radical (OH ) [7e9]. Plant cells are protected from ROS by complex enzymatic antioxidative systems, such as catalase (CAT), peroxidase (POX), and superoxide dismutase (SOD), as well as ascorbate-glutathione cycle (AA-GSH cycle)-related enzymes, including monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), and glutathione reductase (GR) [4,9]. The main non-enzymatic antioxidants in plant cells are ascorbate and glutathione, which are also components of the AA-GSH cycle [6,10].…”

Effects of sucrose, inoculum density, auxins, and aeration volume on ceil growth ofGymnema sylvestre

“…Although the synthetic auxin 2,4-D has been extensively used in plant cell cultures, this member of the chlorophenoxy acid group can have deleterious consequences to human health (Manoharan et al, 2005). Therefore, tests are needed that determine the efficacy of other synthetic auxins, e.g., NAA and IBA, in culturing systems.…”