长链非编码RNA Cslnc256通过CsmiR395介导的硫酸盐代谢调控茶树炭疽病抗性

Abstract

SUMMARY Long non-coding RNAs (lncRNAs) are critical regulators of stress responses in plants. Fungal pathogens such as Colletotrichum camelliae severely impair the development of tea plants ( Camellia sinensis ); however, mechanisms involving long ncRNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) remain poorly understood in this pathosystem. Through transcriptome profiling of tea leaves 6 days post-pathogen inoculation, a ceRNA regulatory network was constructed based on expression correlation analysis. A lncRNA localized in both the nucleus and cytoplasm, Cslnc256 , was identified to function as a molecular decoy for CsmiR395 , thereby protecting the sulfate transporter gene CsSULTR2;1 from CsmiR395 -mediated degradation. Our findings revealed that CsmiR395 -directed cleavage of CsSULTR2;1 positively regulated sulfate metabolism and enhanced disease resistance. Silencing Cslnc256 enhanced pathogen resistance, whereas transient overexpression reduced the plant defense capacity. Single-base substitution mapping, coupled with Nicotiana benthamiana transient expression and β-glucuronidase reporter assays, confirmed that the 1345–1356 bp region of Cslnc256 constitutes the critical interaction domain for CsmiR395 . This study elucidated the molecular mechanism by which the Cslnc256–CsmiR395–CsSULTR2;1 module dynamically regulates sulfur metabolism to coordinate tea plant responses, providing novel insights into RNA-mediated regulatory networks that govern plant–pathogen interactions. These findings offer a new perspective for deciphering RNA-layered responses in crop protection strategies.