Bacterial leaf streak caused by Xanthomonas translucens threatens cereal production, however, the temporal coordination of host transcriptional responses during resistant and susceptible interactions in polyploid crops remains partially understood. Here, we used time-resolved transcriptomics to characterize responses of synthetic hexaploid triticale to two X. translucens pv. undulosa strains that produce contrasting disease outcomes. The resistant interaction with non-virulent LB10 showed a strong early transcriptional response that subsequently declined, whereas responses to the virulent strain P3 progressively intensified as water-soaking symptoms developed. Analysis of syntenic A-, B-, and R-subgenome homoeologs revealed extensive regulatory asymmetry, with R-subgenome homoeologs disproportionately represented among transcriptionally suppressed genes. Despite their conserved coding sequences, homoeologs often showed divergent transcriptional responses during infection, whereas greater similarity in upstream regulatory regions was associated with more coordinated responsive trajectories. We next examined pathogen-mediated transcriptional regulation through transcription activator-like (TAL) effectors. Among eight TAL effector templates identified in LB10 and P3, TAL5-associated predicted targets showed the strongest preferential induction during P3 infection. Disruption of TAL5 in P3 predominantly reduced host gene expression, including genes involved in immune signaling, cell wall-associated defense and photosynthetic function, accompanied by reduced maximum photosystem II quantum efficiency at 72 h post-inoculation. Together, our results show that bacterial leaf streak outcomes are shaped by temporally distinct host responses and pathogen effector-associated transcriptional reprogramming, providing insight into the dynamic regulation underlying cereal-Xanthomonas interactions.
Fahad Hasan, Fazal Manan, Edward Cedrick J. Fernandez et al.· bioRxiv· 0 citations
Tan spot is an economically important fungal disease of wheat that occurs globally. In this necrotrophic pathosystem, pathogen effectors are recognized by wheat genes in an inverse gene-for-gene manner, leading to the hijacking of host defense mechanisms and ultimately disease susceptibility. Here, we identified the tan spot susceptibility gene
Tsc2
through positional cloning, mutagenesis, and transgenic complementation.
Tsc2
encodes a diverged form of the exocyst subunit Exo70FX15 that localizes to the nucleus and cytoplasm and does not interact directly with the fungal effector. A 21‑nucleotide deletion in
Tsc2
occurred in durum wheat more than a century ago and subsequently spread to common wheat through breeding practices, which allowed recognition of the pathogen effector and subsequent hijacking of the host immune system. We demonstrate that elimination of
Tsc2
through conventional breeding using a diagnostic marker or disruption of
Tsc2
by gene editing can be used to improve tan spot resistance in wheat.
Gurminder Singh, Katherine L. D. Running, Zeng-Cui Zhang et al.· Nature Communications· 0 citations
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