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Baig, D. I.

Publications and source records attributed to Baig, D. I..

2 recordsLinked to original sources

The variable wheat stripe rust effector AvrYr7 evades Yr7 recognition through sequence and expression polymorphisms

Introductory paragraphWheat provides about 20% of total dietary calories worldside1. Wheat diseases, including wheat stripe (yellow) rust, cause billions of dollars in losses each year2. Wheat stripe (yellow) rust is caused by the fungal pathogen Puccinia striiformis f. sp. tritici (Pst) which is best controlled by fungicide application and disease resistant wheat cultivars3. To-date, there are over 80 catalogued and >10 cloned yellow rust resistance genes (Yr genes)4. Yet our knowledge of corresponding avirulence (Avr) genes lags far behind5-8. The absence of cloned Avrs reflects Psts complex genome and the lack of robust transformation and genetic systems3. Recent advances in generating high-quality genome assemblies and the development of wheat defense assays have addressed these challenges9-11. Here we clone AvrYr7 which is recognized by Yr712. We further identify six additional alleles of AvrYr7 that escape recognition due to non-synonymous genetic variations, transposable element activity, missense mutation, and expression polymorphism. These findings provide critical insights into virulence evolution in one of the worlds most important wheat pathogens.

plant biology↗

A conserved stripe rust effector elicits variable resistance responses in wheat

Plant resistance (R) and pathogen avirulence (Avr) gene interactions are central to pathogen recognition and disease resistance in crops. Functional characterisation of recognised Avr effectors of Puccinia striiformis f. sp. tritici (Pst) lags other key fungal pathogens of wheat. Here, we used a wheat protoplast-based screen to identify Avr/R interactions via the proxy of effector-induced defence responses in a set of diverse wheat cultivars. We identified an Avr candidate, termed AvrPstB48, that triggers defence responses in 16 out of 24 cultivars tested. AvrPstB48 is hemizygous, and the Pst genome carries four divergent paralogs within a gene cluster. Analysis of these paralogs revealed partial redundancy in their ability to activate wheat defences and enabled us to identify a single amino acid in AvrPstB48 that is necessary but not sufficient for defence activation. Notably, the activation of defence signalling by AvrPstB48 in protoplasts did not directly correlate with disease outcomes. Whole-plant infection assays revealed that some cultivars which exhibited strong defence activation in the protoplast assay are susceptible to the Pst isolate Pst104E137A- from which AvrPstB48 is derived. Comparison of infection dynamics of two wheat cultivars that differ in their AvrPstB48 recognition capacity revealed a delay in disease progression in the recognising cultivar Avocet S compared to the non-recognising cultivar Morocco. While correlative only, our observations, combined with other recent reports, support a recognize-then-suppress model of plant-pathogen interaction where disease outcomes are driven not only by simple Avr/R interactions but also by pathogen effectors that suppress defence signalling downstream of effector recognition.

plant biology↗