Biology subjects

Xu, S. S.

Publications and source records attributed to Xu, S. S..

4 recordsLinked to original sources

bioRxiv2026

Chromosomal rearrangements 1 and sequence similarity drivepreferential allosyndetic introgression from a wild relative into wheat

Recombination in polyploid genomes is generally constrained to homologous or homoeologous chromosomes; however, how chromosomal rearrangements influence recombination between chromosomes remains unclear. Here, we demonstrate that large-scale chromosomal rearrangements in the wild relatives of wheat are associated with recombination involving non-homoeologous chromosomes or arms during alien gene introgression under conditions that permit homoeologous recombination mediated by ph1b. Using a wheat chromosome 6A monosomic-induced 6AS*6CL Robertsonian translocation combined with ph1b-mediated recombination, we generated 17 independent recombinants carrying a new stem rust resistance gene, Sr69, from Aegilops caudata chromosome arm 6CL. Unexpectedly, 94.1% (16 of 17) of recombinants resulted from exchanges with wheat group-7 chromosomes rather than with the homoeologous group-6 chromosome. Comparative sequence- and marker-based analyses identified a 67-Mb rearranged interval on Ae. caudata 6CL that corresponds to telomeric regions of the long arms of wheat group-7 chromosomes. Sequence similarity within this interval was quantitatively associated with recombination frequency, with higher similarity corresponding to more frequent translocations. Physical and optical mapping showed that recombination within the rearranged interval generated compensating 7A/6C, 7B/6C, and 7D/6C translocations, whereas recombination outside this region produced non-compensating 6A/6C exchanges. An independent case involving the powdery mildew resistance gene Pm7C showed a similar correspondence between a rearranged 7CL region and preferential introgression into wheat 7DS. Together, these results indicate that ph1b-mediated recombination involving structurally altered chromosomes is driven by local chromosomal structure and sequence similarity rather than strict homoeologous group identity. This provides a mechanistic basis for harnessing untapped beneficial genes from structurally rearranged alien genomes. Significance StatementAlien gene introgression is a powerful strategy for wheat improvement, typically relying on ph1b-mediated recombination between homoeologous chromosomes. The genomic basis and outcomes of introgression from structurally rearranged alien chromosomes remain unclear. Here, we show that ph1b-induced recombination can efficiently target wheat-allosyntenic blocks in rearranged alien genomes, preferentially transferring genes from structurally altered alien segments into their syntenic regions on wheat chromosomes of different homoeologous groups. Crossover formation is governed by extended sequence similarity within corresponding intervals rather than strict collinearity across entire homoeologous chromosomes. As many wild species exhibit extensive genome rearrangement, these findings and methodologies expand access to underexploited genetic diversity embedded within highly rearranged wild genomes for wheat improvement.

genetics↗

bioRxiv2021

The Parastagonospora nodorum necrotrophic effector SnTox5 targets the wheat gene Snn5 and facilitates entry into the leaf mesophyll

Parastagonospora nodorum, causal agent of septoria nodorum blotch, is a destructive necrotrophic fungal pathogen of wheat. P. nodorum is known to secrete several necrotrophic effectors that target wheat susceptibility genes that trigger classical biotrophic resistance responses but resulting in susceptibility rather than resistance. SnTox5 targets the wheat susceptibility gene Snn5 to induce necrosis. In this study, we used full genome sequences of 197 P. nodorum isolates collected from the US and their disease phenotyping on the Snn5 differential line LP29, to perform genome wide association study analysis to localize the SnTox5 gene to chromosome 8 of P. nodorum. SnTox5 was validated using gene transformation and CRISPR-Cas9 based gene disruption. SnTox5 encoded a small secreted protein with a 22 and 45 amino acid secretion signal and a pro sequence, respectively. The SnTox5 gene is under purifying selection in the Upper Midwest but under strong diversifying selection in the South/East regions of the US. Comparison of wild type and SnTox5-disrupted strains on wheat lines with and without the susceptibility target Snn5 showed that SnTox5 has two functions, 1) facilitating colonization of the mesophyll layer, and 2) targeting Snn5 to induce programmed cell death to provide cellular nutrient to complete its necrotrophic life cycle.

pathology↗

bioRxiv2021

A triple threat: the Parastagonospora nodorum SnTox267 effector exploits three distinct host genetic factors to cause disease in wheat

Parastagonospora nodorum is a fungal pathogen of wheat. As a necrotrophic specialist, it deploys a suite of effector proteins that target dominant host susceptibility genes to elicit programmed cell death (PCD). Nine effector - host susceptibility gene interactions have been reported in this pathosystem, presumed to be governed by unique pathogen effectors. This study presents the characterization of the SnTox267 necrotrophic effector that hijacks two separate host pathways to cause necrosis. An association mapping approach identified SnTox267 and the generation of gene-disrupted mutants and gain-of-function transformants confirmed its role in Snn2-, Snn6-, and Snn7-mediated necrosis. The Snn2 and Snn6 host susceptibility genes were complementary, and together they functioned cooperatively to elicit SnTox267-induced necrosis in the same light-dependent PCD pathway. Additionally, we showed that SnTox267 targeted Snn7, resulting in light-independent necrosis. Therefore, SnTox267 co-opts two distinct host pathways to elicit PCD. SnTox267 sequence comparison among a natural population of 197 North American P. nodorum isolates revealed 20 protein isoforms conferring variable levels of virulence, indicating continuing selection pressure on this gene. Protein isoform prevalence among discrete populations indicated that SnTox267 has likely evolved in response to local selection pressures and has diversified more rapidly in the Upper Midwest. Deletion of SnTox267 resulted in the upregulation of the unrelated effector genes SnToxA, SnTox1, and SnTox3, providing evidence for a complex genetic compensation mechanism. These results illustrate a novel evolutionary path by which a necrotrophic fungal pathogen uses a single proteinaceous effector to hijack two host pathways to induce cell death.

pathology↗

bioRxiv2018

Resistance gene discovery and cloning by sequence capture and association genetics

Genetic resistance is the most economic and environmentally sustainable approach for crop disease protection. Disease resistance (R) genes from wild relatives are a valuable resource for breeding resistant crops. However, introgression of R genes into crops is a lengthy process often associated with co-integration of deleterious linked genes1, 2 and pathogens can rapidly evolve to overcome R genes when deployed singly3. Introducing multiple cloned R genes into crops as a stack would avoid linkage drag and delay emergence of resistance-breaking pathogen races4. However, current R gene cloning methods require segregating or mutant progenies5-10, which are difficult to generate for many wild relatives due to poor agronomic traits. We exploited natural pan-genome variation in a wild diploid wheat by combining association genetics with R gene enrichment sequencing (AgRenSeq) to clone four stem rust resistance genes in <6 months. RenSeq combined with diversity panels is therefore a major advance in isolating R genes for engineering broad-spectrum resistance in crops.

genomics↗