ArticleCommunications biology2022
Temporally coordinated expression of nuclear genes encoding chloroplast proteins in wheat promotes Puccinia striiformis f. sp. tritici infection.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Homoeolog expression in polyploid wheat mutants shows limited transcriptional compensation.The New phytologist · 2026Article
- Durum wheat mutants with enhanced disease resistance to stripe rust show differential responses to other fungal diseases.Molecular breeding : new strategies in plant improvement · 2025Article
- Phytophthora infestans RXLR effector Pi23014 targets host RNA-binding protein NbRBP3a to suppress plant immunity.Molecular plant pathology · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Targeting host processes that allow pathogens to thrive can be invaluable in resistance breeding. Here, we generated a deep-sequencing transcriptome time course for Puccinia striiformis f. sp. tritici (Pst) infection on wheat and compared datasets from three wheat varieties with different levels of susceptibility to two tested pathogen isolates. We sought genes specifically altered in a susceptible host as candidates that might support colonisation. Host responses differed between Pst-varietal pairs most prominently early during infection. Notably, however, nuclear genes encoding chloroplast-localised proteins (NGCPs) exhibited temporal coordination of expression profiles that differed at later time points in relation to Pst susceptibility. Disrupting one such NGCP, encoding the chloroplast-localised RNA binding protein TaCSP41a, led to lower Pst susceptibility. These analyses thus highlight NGCPs as prime targets for Pst manipulation during infection and point to TaCSP41a disruption as a potential source of Pst resistance for breeding programmes.
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