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Abstract
Plants use diverse strategies to defend themselves from biotic stresses in nature, which include the activation of defense gene expression and a variety of signal transduction pathways. Previous studies have shown that protein ubiquitination plays a critical role in plant defense responses, however the details of its function remain unclear. Our previous work has shown that increasing expression levels of ATL9, an E3 ubiquitin ligase in Arabidopsis thaliana, increased resistance to infection by the fungal pathogen, Golovinomyces cichoracearum. In this study, we demonstrate that the defense-related proteins PDF1.2, PCC1 and FBS1 directly interact with ATL9 and are targeted for degradation to the proteasome by ATL9. The expression levels of PDF1.2, PCC1 and FBS1 are decreased in T-DNA insertional mutants of atl9 and T-DNA insertional mutants of pdf1.2, pcc1 and fbs1 are more susceptible to fungal infection. In addition, callose is more heavily deposited at infection sites in the mutants of atl9, fbs1, pcc1 and pdf1.2. Overexpression of ATL9 and of mutants in fbs1, pcc1 and pdf1.2 showed increased levels of cell death during infection. Together these results indicate that ubiquitination, cell death and callose deposition may work together to enhance defense responses to fungal pathogens.
Highlights
Plants face a variety of fungal pathogens in nature, which pose significant threats to successful growth and reproduction [1]
To confirm if PDF1.2, Pathogen and circadian controlled 1 (PCC1) and F-Box stress-induced 1 (FBS1) are involved in defense against fungal infection, T-DNA insertional mutants of pdf1.2, pcc1 and fbs1 were infected with powdery mildew and Pathogens 2022, 11, 68 their phenotype was evaluated
Six days post inoculation, leaves of atl9 (At2g35000), pdf1.2 (AT5G44420), pcc1 (AT3G22231), and fbs1 (AT1G61340) all had more extensive fungal growth and the fungi had generated more spores when compared to Columbia wild type (Col-0), demonstrating that these mutants are more susceptible to powdery mildew infection (Figure 1)
Summary
Plants face a variety of fungal pathogens in nature, which pose significant threats to successful growth and reproduction [1]. Pathogens that successfully colonize host plants can deliver virulence factors (effectors) into plant cells to counteract the effects of plant PTI, referred to as effectortriggered susceptibility (ETS) [2]. In this case, the second layer of the plant immune system comes into play which involves the recognition of effectors by plant nucleotide-binding leucine-rich repeat (NB-LRR) proteins, resulting in effector-triggered immunity (ETI) [4]. Both PTI and ETI activate complex immune responses, including the generation of reactive oxygen species, induction of phosphorylation cascades, the hypersensitive response (HR), the deposition of callose, and the production of antimicrobial compounds and defense hormones [5,6]
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