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Background: Phosphorus (P), being one of the essential components of nucleic acids, cell membranes and enzymes, indispensable for diverse cellular processes like photosynthesis/carbohydrate metabolism, energy production, redox homeostasis and signaling. Crop yield is severely affected due to Phosphate (Pi) deficiency; and to cope with Pi-deficiency, plants have evolved several strategies. Some rice genotypes are compatible with low Pi availability, whereas others are sensitive to Pi deficiency. However, the underlying molecular mechanism for low Pi tolerance remains largely unexplored., Result: Several studies were carried out to understand Pi-deficiency responses in rice at seedling stage, but few of them targeted molecular aspects/responses of Pi-starvation at the advanced stage of growth. To delineate the molecular mechanisms for low Pi tolerance, a pair of contrasting rice (Oryza sativa L.) genotypes [viz. Pusa-44 (Pi-deficiency sensitive) and its near isogenic line (NIL-23, Pi-deficiency tolerant) harboring Phosphorus uptake 1 (Pup1) QTL from an aus landrace Kasalath] were used. Comparative morphological, physiological, and biochemical analyses confirmed some of the well-known findings. Transcriptome analysis of shoot and root tissues from 45-day-old rice plants grown hydroponically under P-sufficient (16 ppm Pi) or P-starved (0 ppm Pi) medium revealed that Pi-starvation stress causes global transcriptional reprogramming affecting several transcription factors, signaling pathways and other regulatory genes. We could identify several significantly up-regulated genes in roots of NIL-23 under Pi-starvation which might be responsible for the Pi starvation tolerance. Pathway enrichment analysis indicated significant role of certain phosphatases, transporters, transcription factors, carbohydrate metabolism, hormone-signaling, and epigenetic processes in improving P-starvation stress tolerance in NIL-23., Conclusion: We report the important candidate mechanisms for Pi acquisition/solubilization, recycling, remobilization/transport, sensing/signalling, genetic/epigenetic regulation, and cell wall structural changes to be responsible for P-starvation tolerance in NIL-23. The study provides some of the novel information useful for improving phosphorus-use efficiency in rice cultivars.

A germplasm assembly of 128 finger millet genotypes from 18 countries was evaluated for seedling-stage phosphorus (P) responses by growing them in P sufficient (Psuf) and P deficient (Pdef) treatments. Majority of the genotypes showed adaptive responses to low P condition. Based on phenotype behaviour using the best linear unbiased predictors for each trait, genotypes were classified into, P responsive, low P tolerant and P non-responsive types. Based on the overall phenotype performance under Pdef, 10 genotypes were identified as low P tolerants. The low P tolerant genotypes were characterised by increased shoot and root length and increased root hair induction with longer root hairs under Pdef, than under Psuf. Association mapping of P response traits using mixed linear models revealed four quantitative trait loci (QTLs). Two QTLs (qLRDW.1 and qLRDW.2) for low P response affecting root dry weight explained over 10% phenotypic variation. In silico synteny analysis across grass genomes for these QTLs identified putative candidate genes such as Ser-Thr kinase and transcription factors such as WRKY and basic helix-loop-helix (bHLH). The QTLs for response under Psuf were mapped for traits such as shoot dry weight (qHSDW.1) and root length (qHRL.1). Putative associations of these QTLs over the syntenous regions on the grass genomes revealed proximity to cytochrome P450, phosphate transporter and pectin methylesterase inhibitor (PMEI) genes. This is the first report of the extent of phenotypic variability for P response in finger millet genotypes during seedling-stage, along with the QTLs and putative candidate genes associated with P starvation tolerance.

Phosphorus (P) is an essential macronutrient required for respiration, photosynthesis/carbohydrate metabolism, redox homeostasis, signaling, and synthesis/function of nucleic acids, cellular membranes, enzymes, etc. To cope with P-deficiency, plants reprogram gene expression for necessary alterations in metabolic/signaling pathways. To attain P homeostasis, plants readjust metabolism through transcriptional, post-transcriptional, and/or post-translational machinery involving biochemical, physiological, genomic, epigenomic, proteomic, and metabolomic functions. However, the underlying molecular mechanisms/pathways/genes for P-deficiency tolerance in crop plants remain elusive. To decipher the mechanisms/pathways adopted by rice under P-starvation/deficiency stress, a pair of contrasting rice [Pusa-44 (high-yielding, P-deficiency sensitive) and its near-isogenic line (NIL)-23, P-deficiency tolerant) for Pup1 QTL] genotype was used for comparative analyses. Omics analyses of shoot and root tissues from 45-day-old plants grown hydroponically in P-sufficient (16 ppm Pi), P-deficient (4 ppm Pi) or P-starved (0 ppm Pi) medium revealed important roles of P transporters, transcription factors (TFs), Transposable elements (TEs), auxin-responsive proteins, cell wall modulation, fatty acid metabolism, and chromatin architecture/epigenetic modifications in making NIL-23 tolerant to stress. The proteins involved in photosynthesis, sucrose-/starch-/energy-metabolism, transcription factors, and phytohormone signaling were observed to be differentially expressed in NIL-23. Since only a few coding genes are located on the QTL, modulations in morpho-physio-biochemical and molecular parameters under P-starvation/deficiency stress were attributed to the regulatory functions of Pup1 through TFs, TEs, epigenetic/chromatin architectural changes, etc. introgressed in Pusa-44 genetic background. Thus, the study provides new insights into molecular/regulatory functions of Pup1 under P-starvation/deficiency stress in rice, which might be useful to improve P-use efficiency in rice for better productivity in P-deficient soils. [ABSTRACT FROM AUTHOR]