Simple Summary Potato early blight caused by Alternaria solani poses a serious threat to potato yield and quality. Catalase regulates plant immunity against necrotrophic pathogens, yet its function in early blight remains unclear. In this study, A. solani infection induces hydrogen peroxide accumulation in plants, and exogenous H2O2 application markedly accelerates early blight infection. Furthermore, we identified StCAT1 as a positive regulator of resistance to early blight in potato, with its expression significantly upregulated following A. solani induction. Silencing StCAT1 impaired antioxidant capacity and disease resistance, while overexpression exerted the opposite effect. Additionally, StABI5 was identified as an upstream transcription factor that activates StCAT1 expression, and silencing StABI5 compromised potato resistance to early blight. These results indicate that StABI5 can activate the expression of StCAT1 and by mediating the reactive oxygen species (ROS) signaling pathway regulates potato resistance to early blight, which provides a theoretical basis and genetic resources for the molecular breeding of potato resistance to early blight.
This study investigated the morphoanatomical and molecular mechanisms underlying grafting-mediated reproductive compatibility using a potato (
Solanum tuberosum
L.) and wolfberry (
Lycium barbarum
L.) grafting system. Phenotypic analysis demonstrated that heterologous pollination on grafted plants significantly enhanced early reproductive success, achieving an ovary enlargement rate of 35.2% and a cross fruit setting rate of 15.5%. However, anatomical tracking revealed that hybrid embryos underwent progressive abortion starting 12 days postpollination (DPP) and completely aborted by 20 DPP, thereby preventing the formation of viable seeds. To elucidate the underlying molecular triggers, transcriptomic profiling of 4 DPP ovary tissues was conducted. A total 2542 differentially expressed genes (DEGs) were identified and enriched in plant hormone signal transduction and phenylpropanoid biosynthesis pathways. Further pathway dissection revealed a complex hormonal trade-off: while grafting facilitated early ovary expansion via the localized compensatory activation of auxin (IAA), cytokinin (CTK), and abscisic acid (ABA), it subsequently induced profound systemic hormonal imbalances. Specifically, the downregulation of progrowth hormone [IAA, CTK, and gibberellin (GA)] biosynthesis, coupled with the overactivation of ABA-induced precocious senescence and salicylic acid (SA)-mediated defense stress, collectively disrupted the late embryogenic program. Collectively, this study provides an integrated dataset for understanding how grafting may affect early ovary enlargement and subsequent embryo abortion. The results provide a valuable basis for further exploration of grafting-mediated reproductive compatibility.
Yue Li, Kuan Wang, Ya-Ting Luo et al.· J. Amer. Soc. Hort. Sci.· 0 citations
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