Rhynchosporium commune


Rhynchosporium commune is a haploid ascomycete fungus causing rhynchosporium, scald or leaf blotch, one of the most destructive and economically important diseases of barley worldwide. R. commune is a hemibiotroph with a prolonged asymptomatic phase followed by increasing development of plant tissue damage. It causes lesions on leaves, leaf sheaths and ears, starting as pale grey and developing a dark brown margin over time. R. commune is a polycyclic pathogen with primary inoculum coming from crop debris or infected seeds, and secondary spread occurring through splash dispersal of conidia from infected leaves. It produces characteristic beak‐shaped one‐septate conidia both on leaves and in culture. R. commune is predominantly controlled by fungicides with different modes of action. However, cultivar resistance combining a broad range of ‘major’ and horizontal resistance genes represents the most sustainable and cost‐effective approach to protection against fungal pathogens, including R. commune. Sequencing of R. commune genomes led to the identification of many genes coding for novel candidate effectors, potentially crucial for host colonisation and pathogenicity.

Key Concepts

  • Rhynchosporium commune causes rhynchosporium, scald or leaf blotch, one of the most destructive and economically important diseases of barley.
  • R. commune is an apoplastic hemibiotrophic pathogen.
  • R. commune effectors are crucial for fungal communication with, and manipulation of the host.
  • Rhynchosporium is controlled predominantly by fungicides in combination with cultivar resistance.
  • Prolonged asymptomatic infection makes chemical treatment challenging.
  • Relatively high genetic diversity of R. commune leads to the development of insensitivity to fungicides and reduction in effectiveness of individual major resistance genes.
  • Barley cultivars with a broad range of resistances provide the most cost‐effective and sustainable protection against fungal pathogens, including R. commune.

Keywords: Rhynchosporium; scald; pathogen; barley; disease; asymptomatic infection; hemibiotroph; genome; effectors; resistance

Figure 1. (a) Symptoms on a highly susceptible spring barley cultivar Optic, (b) typical lesions with dark brown borders on susceptible barley leaves caused by Rhynchosporium commune, (c) typical R. commune conidia, (d) R. commune conidia germinated in water.
Figure 2. Representative confocal microscopy images of (a) susceptible barley cultivar Alexis and (b) barley line SBCC154 containing Rrs1 at 2 days post inoculation (dpi) of leaf fragments from 3 weeks old barley seedlings inoculated with a 2 × 104 spores per mL suspension of GFP expressing Rhynchosporium commune strain T‐R214‐GFP. Green colour represents GFP fluorescence and shows fungal spores and hyphae, with blue colour showing chlorophyll auto‐fluorescence. Resistant interactions typically show germinated spores, less extensive hyphal networks, with random growth directions, whilst susceptible lines show much more extensive growth following the anticlinal wall of the epidermal cells. Scale bars represent 50 μm.
Figure 3. Physical map positions of R. commune major resistance genes, including Rrs1–Rrs4 and Rrs18 from H. vulgare (in red), Rrs12Rrs15 from H. vulgare ssp. spontaneum (in blue) and Rrs16 from H. bulbosum (in green). Physical positions of R gene flanking markers are based on the 2017 Morex genome assembly (Mascher et al., ).


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Further Reading

Bjornstad A, Patil V, Tekauz A, et al. (2002) Resistance to scald (Rhynchosporium secalis) in barley (Hordeum vulgare) studied by near‐isogenic lines: I. Markers and differential isolates. Phytopathology 92: 710–720.

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Gierlich A, van 't Slot KAE, Li VM, et al. (1999) Heterologous expression of the avirulence gene product, NIP1, from the barley pathogen Rhynchosporium secalis. Protein Expression and Purification 17: 64–73.

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van't Slot KAE, van den Burg HA, Kloks CPAM, et al. (2003) Solution structure of the plant disease resistance‐triggering protein NIP1 from the fungus Rhynchosporium secalis shows a novel β‐sheet fold. Journal of Biological Chemistry 278: 45730–45736.

van't Slot KAE, Gierlich A and Knogge W (2007) A single binding site mediates resistance‐ and disease‐associated activities of the effector protein NIP1 from the barley pathogen Rhynchosporium secalis. Plant Physiology 144: 1654–1666.

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Avrova, Anna(Mar 2020) Rhynchosporium commune. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0028895]