Abstract
Pathogens overcome plant immunity by means of secreted effectors. Host effector targets often act in pathogen defense, but might also support fungal accommodation or nutrition. The barley ROP GTPase HvRACB is involved in accommodation of fungal haustoria of the powdery mildew fungus Blumeria graminis f.sp. hordei (Bgh) in barley epidermal cells. We found that HvRACB interacts with the ROP-interactive peptide 1 (ROPIP1) that is encoded on the active non-long terminal repeat retroelement Eg-R1 of Bgh. Overexpression of ROPIP1 in barley epidermal cells and host-induced post-transcriptional gene silencing (HIGS) of ROPIP1 suggested that ROPIP1 is involved in virulence of Bgh. Bimolecular fluorescence complementation and co-localization supported that ROPIP1 can interact with activated HvRACB in planta. We show that ROPIP1 is expressed by Bgh on barley and translocated into the cytoplasm of infected barley cells. ROPIP1 is recruited to microtubules upon co-expression of MICROTUBULE ASSOCIATED ROP GTPase ACTIVATING PROTEIN (HvMAGAP1) and can destabilize cortical microtubules. The data suggest that Bgh ROPIP targets HvRACB and manipulates host cell microtubule organization for facilitated host cell entry. This points to a possible neo-functionalization of retroelement-derived transcripts for the evolution of a pathogen virulence effector.
Highlights
Considerable effort is invested in the understanding of plant immunity against infection by pathogens (Spoel and Dong, 2012) and the underlying genes such as resistance genes (R-genes) or quantitative trait loci (QTLs) that might be used in breeding for crops with improved resistance
We found that HvRACB interacts with the Rho of plants (ROP)-interactive peptide 1 (ROPIP1) that is encoded on the active non-long terminal repeat retroelement Eg-R1 of Blumeria graminis f.sp. hordei (Bgh)
We identified the retroelement-encoded peptide ROPIP1 of Bgh that shows the potential to interact with the barley S-factor HvRACB and to promote fungal penetration success on barley
Summary
Considerable effort is invested in the understanding of plant immunity against infection by pathogens (Spoel and Dong, 2012) and the underlying genes such as resistance genes (R-genes) or quantitative trait loci (QTLs) that might be used in breeding for crops with improved resistance. Plant immunity towards invading pathogens is made up of two main layers,namely pattern-triggered immunity (Macho and Zipfel, 2014) and effector-triggered immunity (Spoel and Dong, 2012). Adapted pathogens evolved means to overcome host immunity, which is mainly attributed to secreted effector proteins that manipulate host cellular processes for the benefit of the pathogen. Plant hosts on the other hand evolved resistance proteins that directly or indirectly recognize the presence of a corresponding effector, or the action of effector proteins. The exerted mutual selection pressure drives co-evolution of host R-genes and pathogen effectors (Jones and Dangl, 2006)
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