Transcriptional profiling reveals no response of fungal pathogens to the durable, quantitative Lr34 disease resistance gene of wheat
Sucher J, Menardo F, Praz C, Boni R, Krattinger SG and Keller B (2018) Transcriptional profiling reveals no response of fungal pathogens to the durable, quantitative Lr34 disease resistance gene of wheat. Plant Pathology 67, 792-798.
Durable resistance against fungal pathogens is highly valuable for
disease management in agriculture. For its sustainable use, and to avoid
pathogen adaptation, it is important to understand the underlying
molecular mechanisms. Many studies on durable disease resistance in
plants have focused exclusively on the host plant, whereas possible
reactions and adaptations of pathogens exposed to this type of
resistance have not been well researched. The wheat Lr34 gene,
encoding a putative ABC‐transporter, provides broad‐spectrum and durable
resistance against multiple fungal pathogens in wheat and is functional
as a transgene in all major cereals. Lr34‐based resistance is partial, meaning pathogens can grow and reproduce to some degree on Lr34‐containing plants. Therefore, Lr34‐expressing
plants are ideal for studying the response of pathogens to partial
resistance. Here, transcriptomic responses of the two fungal pathogens Blumeria graminis f. sp. hordei (barley powdery mildew) and Puccinia triticina (wheat leaf rust) during growth on their respective host plants containing Lr34 were compared to their responses on control plants without Lr34.
Two different time points after inoculation were chosen for analysis of
powdery mildew on barley and one time point for wheat leaf rust.
Transcriptome analyses revealed that there were no differences in the
expression patterns of the two pathogens growing on susceptible versus
partially resistant plants, even though pathogen growth was reduced in
the presence of Lr34. This reflects the absence of observable reaction in the pathogen to the presence of the Lr34 resistance gene and, consequently, no major alteration of fungal pathogen metabolism.