Shade avoidance response (SAR) is an important adaptive mechanism that enables plants to optimize light capture in dense canopies, but excessive shade-induced hypocotyl elongation can negatively affect plant architecture, yield, and quality in Chinese cabbage. In this study, we investigated the genetic basis of SAR using an advanced intercross recombinant inbred line (AI RIL) population derived from a cross between the oil type Chinese cabbage ‘R500’ with significantly longer hypocotyls and the vegetable type Chinese cabbage ‘L58’ with shorter hypocotyls. Quantitative trait locus (QTL) mapping under simulated shade, represented by a low red/far-red light ratio of 0.5, and non-shade conditions, represented by a high red/far-red light ratio of 2.0, identified several candidate genes associated with hypocotyl elongation, including COP1, XTH17, HYH and SRR1. Among these genes, BrSRR1 was selected for functional validation by introducing two alleles of BrSRR1 coding sequences into the Arabidopsis srr1 mutant. Under simulated shade, the srr1 mutant exhibited significantly longer hypocotyl than wild-type Col-0, whereas the BrSRR1-L58 restored hypocotyl length to a level statistically indistinguishable from that of wild-type Col-0. In contrast, the BrSRR1-R500 failed to complement the mutant phenotype, indicating ecotype-specific and allele-dependent functional divergence. Collectively, these findings indicate that BrSRR1 is implicated as a candidate gene involved in negative regulation of shade-induced hypocotyl elongation, though pending validation in the native species, providing insights into the genetic regulation of SAR in Chinese cabbage and a potential target for breeding varieties with reduced shade-induced hypocotyl elongation suited to high-density planting.
Ya-Kun Zheng, Daling Feng, Shu-Xin Xuan et al.· Horticulturae· 0 citations
ABSTRACT Plant fungal pathogens secrete a plethora of effectors into host cells to facilitate their infection by interfering with the normal physiological processes of the host plant. However, the role of guanyl‐specific ribonuclease T1 effector protein in the virulence of fungal pathogens remains largely unexplored. Here, we show that an effector protein EC19, secreted by the soil‐borne fungus Fusarium oxysporum f. sp. lycopersici (Fol) that causes tomato wilt disease, contributes to the full virulence of Fol. In‐locus knockout of EC19 significantly reduced the virulence of Fol, while complementing EC19 in the knockout mutant restored the pathogenicity of Fol on tomato. EC19, which contains the ribonuclease T1‐like domain, is highly conserved across fungal species and exhibited the ability to cleave single‐stranded RNA isolated from tomato. EC19 was specifically induced during Fol infection. The AlphaFold3‐predicted structure of EC19 shows a high degree of structural similarity with ribonuclease T1 from Aspergillus oryzae, with limited similarity to RNase T2. Using Agrobacterium‐mediated transient assay in the leaves of Nicotiana benthamiana, we found that EC19 predominantly localised to the nucleus of plant cells. Stable transgenic susceptible tomato plants overexpressing EC19 exhibited increased susceptibility to Fol infection compared to wild‐type plants. RNA‐seq analysis of EC19‐overexpressing tomato lines revealed that downregulated differentially expressed genes were predominantly enriched in plant hormone signal transduction, phenylpropanoid biosynthesis, and plant–pathogen interaction pathways. Taken together, these findings indicate that EC19 with ribonuclease activity promotes Fol infection, expanding our understanding of the molecular mechanisms underlying Fol virulence.
Min Li, Yi-Fei Wang, Haoqian Li et al.· Molecular plant pathology· 0 citations
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