Soil salinity, a prevalent abiotic stress, causes enormous losses in global crop yields annually. Previous studies have shown that salt stress-induced reprogramming of gene expression contributes to the survival of plants under this stress. However, mechanisms regulating gene expression in response to salt stress at the posttranscriptional level are not well understood. Here, we show that salt stress increases the level of Signal Responsive 1 (SR1) mRNA, a member of signal-responsive Ca2+/calmodulin-regulated transcription factors, by enhancing its stability. We present multiple lines of evidence indicating that reactive oxygen species generated by NADPH oxidase activity mediate salt-induced SR1 transcript stability. Using mutants impaired in either nonsense-mediated decay, XRN4 or mRNA decapping pathways, we show that neither the NMD pathway, XRN4 nor the decapping of SR1 mRNA is required for its decay. We analyzed the salt-induced accumulation of eight truncated versions of the SR1 coding region (∼3 kb) in the sr1 mutant background. This analysis identified a 500 nts region at the 3' end of the SR1 coding region to be required for the salt-induced stability of SR1 mRNA. Potential mechanisms by which this region confers SR1 transcript stability in response to salt are discussed.

中文翻译：

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盐诱导的 SR1/CAMTA3 mRNA 稳定性由活性氧介导，需要其开放阅读框的 3' 端。

土壤盐分是一种普遍存在的非生物胁迫，每年都会造成全球作物产量的巨大损失。先前的研究表明，盐胁迫诱导的基因表达重编程有助于植物在这种胁迫下的生存。然而，在转录后水平上调节基因表达以应对盐胁迫的机制尚不清楚。在这里，我们显示盐胁迫通过增强其稳定性来增加信号响应 1 (SR1) mRNA 的水平，该 mRNA 是信号响应 Ca2+/钙调蛋白调节的转录因子的成员。我们提出了多条证据表明由 NADPH 氧化酶活性产生的活性氧物质介导盐诱导的 SR1 转录物稳定性。使用在无意义介导的衰变、XRN4 或 mRNA 脱帽途径中受损的突变体，我们表明，无论是 NMD 途径，XRN4 也不需要 SR1 mRNA 的去盖，因为它的衰变是必需的。我们分析了 sr1 突变体背景中八个截短版本的 SR1 编码区（~3 kb）的盐诱导积累。该分析确定了 SR1 编码区 3' 端的 500 nts 区域是盐诱导的 SR1 mRNA 稳定性所必需的。讨论了该区域响应盐分赋予 SR1 转录物稳定性的潜在机制。