Unraveling NbCML30-mediated defense against Sclerotinia sclerotiorum and Phytophthora capsici in Nicotiana benthamiana: A transcriptomic perspective.

Calcium signaling plays a crucial role as a second messenger in plant immune responses. However, the regulatory mechanisms that govern host responses to infections caused by Sclerotinia sclerotiorum and Phytophthora capsici remain unclear. This study investigated the expression pattern of Nicotiana benthamiana calmodulin-like protein 30 (NbCML30) following infections. Our results reveal a significant downregulation of NbCML30 expression after S. sclerotiorum infection, with no changes observed in NbCML30 expression following P. capsici infection. Importantly, transient silencing of NbCML30 using tobacco rattle virus-mediated methods promoted infections caused by both S. sclerotiorum and P. capsici. In contrast, transgenic plants overexpressing NbCML30 exhibited a suppressive effect on the infections caused by S. sclerotiorum and P. capsici. Subsequent transcriptome sequencing uncovered that NbCML30 silencing markedly upregulated the expression of host endogenous genes, particularly activating pathways associated with protein processing in endoplasmic reticulum (ER) associated degradation (ERAD) pathway. These findings highlight the affirmative regulatory role of NbCML30 in conferring resistance against necrotrophic and hemibiotrophic pathogens, shedding light on its potential inhibitory mechanism. In conclusion, our study provides a theoretical basis for crop resistance genetic breeding strategies by elucidating the regulatory function of NbCML30 in plant defense against these pathogens. • Silencing NbCML30 enhances susceptibility to S. sclerotiorum and P. capsici infections. • Silencing NbCML30 activates pathways associated with endoplasmic reticulum-associated degradation (ERAD). • NbCML30 overexpression inhibits S. sclerotiorum and P. capsici infection. [ABSTRACT FROM AUTHOR]