Hard-end, superficial scald and cork spot are prevalent physiological disorders in pear fruit, characterized by an increase in lignin deposition, which impairs the fruit quality and reduces farmer income. Although calcium deficiency is known to exacerbate symptoms of these lignin-related disorders, the underlying mechanisms remain poorly understood. In this study, we aimed to elucidate the regulatory network through which calcium modulates lignin deposition-induced physiological disorders, using hard-end disorder as a model. Our results showed that WRKY46, a transcription factor, is upregulated in hard-end fruit but downregulated by calcium treatment. WRKY46 directly activates the transcription of NAC187, which in turn activates the expression of CCR, promoting lignin accumulation. Furthermore, CML38, a calcium sensor protein, enhances the transactivation capacity of WRKY46 via physical interaction. Calcium disrupts the CML38/WRKY46-NAC187-CCR cascade, ultimately suppressing lignin biosynthesis. Additionally, the upregulation of WRKY46, CML38 and NAC187 correlates with reduced Ca²⁺ levels in the fruit. Collectively, these data suggest that the development of lignin-related physiological disorders in pear fruit is mediated by the CML38/WRKY46-NAC187-CCR regulatory module, which is enhanced by reduced Ca²⁺ levels. This module plays a dual role in both lignin accumulation and Ca²⁺ level reduction, shedding new light on the role of calcium in modulating fruit quality.

中文翻译：

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钙破坏 CML38/WRKY46-NAC187-CCR 级联反应，抑制梨果实中木质素相关生理紊乱的形成

硬端、浅表烫伤和软木斑是梨果实中普遍存在的生理疾病，其特征是木质素沉积增加，从而损害果实质量并降低农民收入。尽管已知钙缺乏会加剧这些木质素相关疾病的症状，但其潜在机制仍然知之甚少。在这项研究中，我们旨在以硬端疾病为模型，阐明钙调节木质素沉积诱导的生理疾病的调节网络。我们的结果表明，转录因子 WRKY46 在硬端水果中上调，但在钙处理下调。WRKY46 直接激活 NAC187 的转录，进而激活 CCR 的表达，促进木质素积累。此外，钙传感器蛋白 CML38 通过物理相互作用增强 WRKY46 的反式激活能力。钙会破坏 CML38/WRKY46-NAC187-CCR 级联反应，最终抑制木质素的生物合成。此外，WRKY46、CML38 和 NAC187 的上调与果实中 Ca²⁺ 水平降低相关。总的来说，这些数据表明，梨果实中木质素相关生理障碍的发展是由 CML38/WRKY46-NAC187-CCR 调节模块介导的，该模块通过降低 Ca²⁺ 水平而增强。该模块在木质素积累和 Ca²⁺ 水平降低中起双重作用，为钙在调节水果品质中的作用提供了新的思路。