<p>Soil salinization is one of the important abiotic stresses that limit rice yield, and salt tolerance in rice is often attributed to the magnitude of transcriptional responses. Here, we demonstrate that the tolerant landrace rice Pokkali (ssp.: indica) and the sensitive cultivar 9311 (ssp.: indica) deploy fundamentally different molecular strategies under salinity stress at the seedling stage via comparative transcriptomics. Compared to the 9311 seedling under stress, the Pokkali maintained higher survival, sustained growth, with minimal oxidative damage, indicating markedly superior physiological resilience. RNA-seq analysis showed that there was widespread genotype-dependent transcriptional reprogramming i<i>n</i> these two genotypes, with 18,329 and 18,761 DEGs, respectively. The 9311 genotype retained a small conserved core of 1,227 genes, whereas the tolerant Pokkali did 10,599 genes, indicating greater regulatory stability. Only 134 DEG genes were shared by these two genotypes, suggesting a limited but robust universal stress-responsive core, indicating extensive transcriptional specialization. Pokkali preferentially activated a chloroplast-centered protective network involving LOC_Os02g01340 (<i>petH</i>) and LOC_Os01g22010 (<i>metK</i>), accompanied by coordinated enrichment of phenylpropanoid, glutathione, flavonoid, lipid, and photosynthesis-related pathways that collectively reinforce redox buffering, membrane stabilization, and metabolic homeostasis. In contrast, 9311 had a translation-centered stress program that activated LOC_Os03g04590 (<i>RPL23e</i>) and stopped chloroplast biogenesis through LOC_Os03g20700 (<i>chlH</i>). The results showed salt-sensitive rice verities under stress can trigger a response that prioritizes making more proteins (via enhanced translation machinery, highlighted by RPL23e), but at the cost of halting the production and development of chloroplasts (via suppression involving chlH). qRT-PCR and haplotype analysis across the 3&#xa0;K Rice Genome panel showed that these different regulatory adaptive mechanisms are genetically controlled and not just temporary transcriptional plasticity. Our work maps out how rice copes with salt at the molecular level and points to practical ways breeders and genetic engineers can create more salt-resilient rice varieties to improve food security in saline areas.</p>

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Comparative transcriptomic analysis reveals chloroplast- and translation-centered salt-adaptation difference between two rice genotypes

  • Sirinthorn Kongpraphrut,
  • Zhangqiang Wang,
  • Marsuton Sanyapeung,
  • Mohamed Hazman,
  • Galal Anis,
  • Samer Fawzy,
  • Ahmed Elshiref,
  • Longbiao Guo,
  • Lianguang Shang

摘要

Soil salinization is one of the important abiotic stresses that limit rice yield, and salt tolerance in rice is often attributed to the magnitude of transcriptional responses. Here, we demonstrate that the tolerant landrace rice Pokkali (ssp.: indica) and the sensitive cultivar 9311 (ssp.: indica) deploy fundamentally different molecular strategies under salinity stress at the seedling stage via comparative transcriptomics. Compared to the 9311 seedling under stress, the Pokkali maintained higher survival, sustained growth, with minimal oxidative damage, indicating markedly superior physiological resilience. RNA-seq analysis showed that there was widespread genotype-dependent transcriptional reprogramming in these two genotypes, with 18,329 and 18,761 DEGs, respectively. The 9311 genotype retained a small conserved core of 1,227 genes, whereas the tolerant Pokkali did 10,599 genes, indicating greater regulatory stability. Only 134 DEG genes were shared by these two genotypes, suggesting a limited but robust universal stress-responsive core, indicating extensive transcriptional specialization. Pokkali preferentially activated a chloroplast-centered protective network involving LOC_Os02g01340 (petH) and LOC_Os01g22010 (metK), accompanied by coordinated enrichment of phenylpropanoid, glutathione, flavonoid, lipid, and photosynthesis-related pathways that collectively reinforce redox buffering, membrane stabilization, and metabolic homeostasis. In contrast, 9311 had a translation-centered stress program that activated LOC_Os03g04590 (RPL23e) and stopped chloroplast biogenesis through LOC_Os03g20700 (chlH). The results showed salt-sensitive rice verities under stress can trigger a response that prioritizes making more proteins (via enhanced translation machinery, highlighted by RPL23e), but at the cost of halting the production and development of chloroplasts (via suppression involving chlH). qRT-PCR and haplotype analysis across the 3 K Rice Genome panel showed that these different regulatory adaptive mechanisms are genetically controlled and not just temporary transcriptional plasticity. Our work maps out how rice copes with salt at the molecular level and points to practical ways breeders and genetic engineers can create more salt-resilient rice varieties to improve food security in saline areas.