Calcium disrupts CML38/WRKY46-NAC187-CCR cascade to inhibit the formation of lignin-related physiological disorders in pear fruit.

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 Ca 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 Ca levels. This module plays a dual role in both lignin accumulation and Ca level reduction, shedding new light on the role of calcium in modulating fruit quality.