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The dynamics of cereal cyst nematode infection differ between susceptible and resistant barley cultivars and lead to changes in (1,3;1,4)-β-glucan levels and HvCslF gene transcript abundance

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dc.contributor.authorAditya, J.
dc.contributor.authorLewis, J.
dc.contributor.authorShirley, N.
dc.contributor.authorTan, H.
dc.contributor.authorHenderson, M.
dc.contributor.authorFincher, G.
dc.contributor.authorBurton, R.
dc.contributor.authorMather, D.
dc.contributor.authorTucker, M.
dc.date.issued2015
dc.description.abstractHeterodera avenae (cereal cyst nematode, CCN) infects the roots of barley (Hordeum vulgare) forming syncytial feeding sites. In resistant host plants, relatively few females develop to maturity. Little is known about the physiological and biochemical changes induced during CCN infection. Responses to CCN infection were investigated in resistant (Rha2) and susceptible barley cultivars through histological, compositional and transcriptional analysis. Two phases were identified that influence CCN viability, including feeding site establishment and subsequent cyst maturation. Syncytial development progressed faster in the resistant cultivar Chebec than in the susceptible cultivar Skiff, and was accompanied by changes in cell wall polysaccharide abundance, particularly (1,3;1,4)-β-glucan. Transcriptional profiling identified several glycosyl transferase genes, including CELLULOSE SYNTHASE-LIKE F10 (HvCslF10), which may contribute to differences in polysaccharide abundance between resistant and susceptible cultivars. In barley, Rha2-mediated CCN resistance drives rapid deterioration of CCN feeding sites, specific changes in cell wall-related transcript abundance and changes in cell wall composition. During H. avenae infection, (1,3;1,4)-β-glucan may influence CCN feeding site development by limiting solute flow, similar to (1,3)-β-glucan during dicot cyst nematode infections. Dynamic transcriptional changes in uncharacterized HvCslF genes, possibly involved in (1,3;1,4)-β-glucan synthesis, suggest a role for these genes in the CCN infection process.
dc.description.statementofresponsibilityJessika Aditya, John Lewis, Neil J. Shirley, Hwei-Ting Tan, Marilyn Henderson, Geoffrey B. Fincher, Rachel A. Burton, Diane E. Mather and Matthew R. Tucker
dc.identifier.citationNew Phytologist, 2015; 207(1):135-147
dc.identifier.doi10.1111/nph.13349
dc.identifier.issn0028-646X
dc.identifier.issn1469-8137
dc.identifier.orcidShirley, N. [0000-0001-8114-9891]
dc.identifier.orcidBurton, R. [0000-0002-0638-4709]
dc.identifier.orcidMather, D. [0000-0001-7506-2589]
dc.identifier.orcidTucker, M. [0000-0003-4661-6700]
dc.identifier.urihttp://hdl.handle.net/2440/100637
dc.language.isoen
dc.publisherWiley-Blackwell
dc.relation.grantARC
dc.rights© 2015 The University of Adelaide. New Phytologist © 2015 New Phytologist Trust
dc.source.urihttps://doi.org/10.1111/nph.13349
dc.subjectBarley; cell wall; cellulose synthase-like; cereal cyst nematode (CCN); Heterodera avenae; Hordeum vulgare
dc.titleThe dynamics of cereal cyst nematode infection differ between susceptible and resistant barley cultivars and lead to changes in (1,3;1,4)-β-glucan levels and HvCslF gene transcript abundance
dc.title.alternativeThe dynamics of cereal cyst nematode infection differ between susceptible and resistant barley cultivars and lead to changes in (1,3;1,4)-beta-glucan levels and HvCslF gene transcript abundance
dc.typeJournal article
pubs.publication-statusPublished

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