Methylgyoxal signalling in Phaseolus vulgaris under phosphate deficiency

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Date

2020

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Publisher

UWC

Abstract

In this study, we observed that phosphate (P) deficiency stunted plant growth and produced plants with poor morphological characteristics (yellow and small leaves). Furthermore, we treated plants with 0.8 mM (control) and 0.02 mM P (deficient) in addition to 6 μM methylglyoxal (MG) and we observed that the plants treated with MG had a higher germination, and better morphological characteristics (the leaves were more dark green and bigger in size) compared to the P deficient plants. However, we also observed that the P deficient plants treated with MG had low levels of both O2- and H2O2 and this could be a possible reason for the improved growth and morphological characteristics. In contrast, the P deficient plants not treated with MG had high levels of O2- and H2O2 which could be the possible reason for the observed cell death. We also performed biochemical assays including superoxide dismutase, ascorbate peroxidase, malondialdehyde content, ascorbic acid content, catalase, and most of the assays showed high levels of reactive oxygen species (ROS) and low levels of antioxidant activities in plants not treated with MG while high levels of antioxidant activities and low levels of ROS were observed in plants treated with exogenous MG. Since nitric oxide (NO) is also known to be a signalling molecule, we did a NO assay and observed that NO content increased under low exogenous doses of MG. From our findings we came to a hypothesis that MG modulates P deficiency stress in P. vulgaris through NO signalling or it might be that NO and MG work in tandem to modulate signalling pathways under P deficiency. Finally, we looked at the nutrient profile and the results showed that while there was a poor nutrient profile generally under P deficiency, there was an improvement in nutrient profile when MG was administered at low doses.

Description

Masters of Science

Keywords

Antioxidant enzymes, Ascorbate peroxidase, Biomass, Cell death, Heavy metal, Hydrogen peroxide, Lipid peroxidation, Methylglyoxal, Nitric oxide, P. vulgaris, Phosphate deficiency, Reactive oxygen species, Superoxide dismutase, Superoxide

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