New papers from Hückelhoven/Stam lab.
Good Riddance? Breaking Disease Susceptibility in the Era of New Breeding Technologies.
Stefan Engelhardt, Remco Stam, Ralph Hückelhoven
Despite a high abundance and diversity of natural plant pathogens, plant disease susceptibility is rare. In agriculture however, disease epidemics often occur when virulent pathogens successfully overcome immunity of a single genotype grown in monoculture. Disease epidemics are partially controlled by chemical and genetic plant protection, but pathogen populations show a high potential to adapt to new cultivars or chemical control agents. Therefore, new strategies in breeding and biotechnology are required to obtain durable disease resistance. Generating and exploiting a genetic loss of susceptibility is one of the recent strategies. Better understanding of host susceptibility genes (S) and new breeding technologies now enable the targeted mutation of S genes for genetic plant protection. Here we summarize biological functions of susceptibility factors and both conventional and DNA nuclease-based technologies for the exploitation of S genes. We further discuss the potential trade-offs and whether the genetic loss of susceptibility can provide durable disease resistance.
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A Barley powdery mildew fungus non-autonomous retrotransposon encodes a peptide that supports penetration success on barley.
Mathias Nottensteiner, Bernd Zechmann, Christopher McCollum, Ralph Hückelhoven
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 uorescence complementation and co-localization supported that ROPIP1 can interact with acti- vated 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 viru- lence effector.
