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Shee, R.

Publications and source records attributed to Shee, R..

3 recordsLinked to original sources

Designer grass pea for transgene-free minimal neurotoxin-containing seeds with CRISPR-Cas9

Grass pea seeds are consumed as food in several South Asian and Sub-Saharan African nations. However, the presence of the neurotoxic compound N-oxalyl-L-diamino propionic acid ({beta}-ODAP) has restricted its cultivation. Although various cultivars with low {beta}-ODAP levels have been developed, their cultivation is still limited due to the risk of neurolathyrism from long-term grass pea seed ingestion. In this study, we employed the CRISPR-Cas9-mediated gene editing technique to generate grass pea seeds with zero or minimal {beta}-ODAP levels. We targeted the BAHD-AT3 gene that encodes a key enzyme in the {beta}-ODAP biosynthesis pathway. We developed bahd-at3 knock-out lines using three gRNAs targeting different regions of this gene and characterized them. Cas9-free independent lines from each event carrying the desired on-target mutation were selected and backcrossed twice with the wild-type to eliminate any off-target mutation present therein. Various agronomical parameters were analyzed from the backcrossed mutant lines and they displayed no phenotypic abnormalities. Interestingly, the seed {beta}-ODAP content ranged between 0.001 % - 0.002 % of dry weight which is 99 % lower than the wild-type. Together, our study reports the development of transgene-free, genome-edited grass peas with insignificant levels of {beta}-ODAP in seeds for safer food in the future.

plant biology↗

Glutathione activates PHT1;5 gene via WRKY75 transcription factor to regulate phosphate homeostasis in Arabidopsis

Phosphorus (P) is essential for plant growth, yet inorganic phosphate (Pi) is often limiting in soil. Plants respond to Pi limitation by activating P transporters and starvation genes, which boost Pi uptake or redistribute P. While glutathione (GSH) regulates iron and zinc homeostasis in Arabidopsis, its role in P homeostasis under Pi limitation remains elusive. Here, we show that GSH-S-nitrosoglutathione (GSNO) module regulates source-to-sink P allocation in Arabidopsis by transcriptionally activating the phloem-localised transporter AtPHT1;5 via the transcription factor AtWRKY75. GSH-deficient mutants, cad2-1 and pad2-1, exhibited sensitivity to Pi-starvation with altered root system architecture, reduced anthocyanin accumulation, and disrupted root-to-shoot P transport. AtPHT1;5 transcript levels were markedly reduced in these mutants but were positively responsive to exogenous GSH or GSNO. The pht1;5 mutant failed to respond to GSH treatments, demonstrating that AtPHT1;5 is essential for GSH-mediated P mobilisation. Pharmacological and genetic manipulation of nitric oxide (NO)/GSNO levels implicated GSNO as an essential intermediary. In depth molecular analyses identified AtWRKY75 as a Pi- and GSH/GSNO-responsive activator that binds w-box motifs in the AtPHT1;5 promoter. This was further supported by the lack of AtPHT1;5 induction in the wrky75 mutants. Finally, AtWRKY75 is S-nitrosylated and stabilised by GSH/GSNO, providing a mechanistic link between redox/NO signalling and transcriptional control of P transport. We propose that elevated GSH under Pi limitation is converted to GSNO, which S-nitrosylates AtWRKY75 and promotes AtPHT1;5 expression, thus driving source-to-sink P reallocation. This pathway integrates redox and NO signalling with transcriptional regulation to maintain P homeostasis under Pi starvation. Summary statementGlutathione-S-nitrosoglutathione module regulates phosphate translocation in Arabidopsis under phosphate starvation via transcriptional activation of AtPHT1;5 gene by AtWRKY75 transcription factor.

plant biology↗

Glutathione regulates subcellular iron homeostasis via transcriptional activation of iron responsive genes in Arabidopsis

While glutathione (GSH) is known to regulate iron (Fe) deficiency response in plants, its involvement in modulating subcellular Fe homeostasis remained elusive. In this study, we report that the GSH depleted mutants, cad2-1 and pad2-1 displayed increased sensitivity to Fe deficiency with significant down-regulation of the vacuolar Fe exporters, AtNRAMP3 and AtNRAMP4 and the chloroplast Fe importer, AtPIC1. Moreover, the pad2-1 mutant accumulated higher Fe content in vacuoles and lower in chloroplasts compared with Col-0 under Fe limited condition. Exogenous GSH treatment could enhance the chloroplast Fe content in Col-0 plants but failed to do so in the nramp3nramp4 double mutant demonstrating the role of GSH in modulating subcellular Fe homeostasis. Pharmacological experiments, mutant analysis and promoter assay revealed that this regulation involved transcriptional activation of the transporter genes by a GSH-GSNO module. The Fe responsive bHLH transcription factors (TFs), AtbHLH29, AtbHLH38 and AtbHLH101 were identified to interact with the promoters of these genes which were in turn activated via S-nitrosylation. Together, the present study delineates the role of GSH-GSNO module in regulating subcellular Fe homeostasis by transcriptional activation of the Fe transporters AtNRAMP3, AtNRAMP4 and AtPIC1 via S-nitrosylation of the bHLH TFs during Fe deficiency. Summary statementGlutathione regulates subcellular iron homeostasis under iron deficiency via GSNO dependent transcriptional activation of AtNRAMP3, AtNRAMP4 and AtPIC1 genes by S-nitrosylation of the iron responsive bHLH transcription factors, AtbHLH29, AtbHLH38 and AtbHLH101.

plant biology↗