Fine Mapping of Two Wheat Powdery Mildew Resistance Genes Located at the Pm1 Cluster

Abstract

Powdery mildew caused by Blumeria graminis (DC.) f. sp. tritici (Bgt) is a globally devastating foliar disease of wheat (Triticum aestivum L.). More than a dozen genes against this disease, identified from wheat germplasms of different ploidy levels, have been mapped to the region surrounding the Pm1 locus on the long arm of chromosome 7A, which forms a resistance (R)-gene cluster. Mlm2033 and Mlm80 from einkorn wheat (T. monococcum L.) were two of the R genes belonging to this cluster. This study was initiated to fine map these two genes toward map-based cloning. Comparative genomics study showed that macrocolinearity exists between Brachypodium distachyon L. chromosome 1 (Bd1) and the Mlm2033-Mlm80-Pm1a region, which allowed us to develop markers based on the wheat sequences orthologous to genes contained in the Bd1 region. With these and other newly developed and published markers, high-resolution maps were constructed for both Mlm2033 and Mlm80 using large F 2 populations. Moreover, a physical map of Mlm2033 was constructed through chromosome walking with bacterial artificial chromosome (BAC) clones and comparative mapping. Eventually, Mlm2033 and Mlm80 were restricted to a 0.12-and 0.86-cM interval, respectively. Based on the closely linked common markers, Mlm2033, Mlm80, and MlIW172 (another powdery mildew resistance gene in the Pm1 cluster) were not allelic to one another. Severe recombination suppression and disruption of synteny were noted in the region encompassing Mlm2033. These results provided useful information for mapbased cloning of the R genes in the Pm1 cluster and interpretation of their evolution.

A highly differentiated region of wheat chromosome 7AL encodes a Pm1a immune receptor that recognizes its corresponding AvrPm1a effector from Blumeria graminis

“…dicoccoides (tetraploid). Intriguingly, Liang et al (2016) did observe strong recombination suppression in this region of two T. monococcum accessions (diploid). It could be possible that an ancient introgression(s) predisposed this region to its present structure, which in turn promoted a diversification of NLRs that culminated in the linked resistance cluster carrying Pm1a and Sr15-Lr20.…”

“…It was suggested that all the genes sharing the marker interval with Pm1 were allelic to Pm1. However, Liang et al (2016) showed that et al, 2018) was concluded to occupy the same locus as PmU (Zhang et al, 2018), within the same interval as Pm1. However, sequence comparison of Pm1a with Pm60 showed they were quite dissimilar (Fig.…”

The Wild Emmer Wheat Gene PmG16, Conferring Resistance to Powdery Mildew, is an Orthologue of Pm60 from Triticum Urartu

“…Axminster is quite dissimilar to Pm60, therefore, it is unlikely that they represent orthologous genes (Hewitt et al 2020). These ndings suggest that an R-gene cluster is present within this genomic region of cultivated and wild wheat species of different ploidy levels, conferring powdery mildew resistance (Liang et al 2016;Zhang et al 2018). Recently, a multi-genome comparisons showed huge differences in NLR content between wheat genotypes; Among ~ 2,500 loci with NLR signatures identi ed in the 16 wheat cultivars, 31-34% of them are shared across all genomes, while the number of unique signatures ranged from 22 to 192 per cultivar (Walkowiak et al 2020).…”

Identification, High-Density Mapping, and Characterization of New Major Powdery Mildew Resistance Loci From the Emmer Wheat Landrace GZ1

“…The QPm.GZ1-7A was mapped to a large region of chromosome 7AL (144 Mb). So far, about 20 Pm genes have been localized on chromosome 7AL: Pm1 consisting of five different alleles: Pm1a, Pm1b, Pm1c (Pm18), Pm1d (Hsam et al, 1998), and Pm1e (Pm22; Singrün et al, 2003), Pm9 (Schneider et al, 1991), mlRd30 (Singrün et al, 2004), Pm37 (Srnić et al, 2005;Perugini et al, 2007), NC96BGTA4 (Srnić et al, 2005), MlIW172 (Ouyang et al, 2014), PmU (Qiu et al, 2005), NCA6 (Miranda et al, 2007), Mlm2033 and Mlm80 (Yao et al, 2006;Liang et al, 2016), MlIw72 (Ji et al, 2007), MlAG12 (Maxwell et al, 2009), MlWE18 (Han et al, 2009), PmG16 (Ben-David et al, 2010, PmTb7A.1 and PmTb7A.2 (Chhuneja et al, 2011), HSM1 (Li et al, 2013), MlUM15 (Worthington et al, 2014, Pm59 (Tan et al, 2018), and QPm.gb-7A (Desiderio et al, 2021). According to Desiderio et al (2021), most of these genes are likely to be closely linked and create clusters.…”