Functionality of resistance gene Hero which controls plant root-infecting potato cyst nematodes, in leaves of tomato

A - Papers appearing in refereed journals

Caberera Poch, H. L., Manzanilla-Lopez, R. H. and Kanyuka, K. 2006. Functionality of resistance gene Hero which controls plant root-infecting potato cyst nematodes, in leaves of tomato. Plant, Cell & Environment. 29 (7), pp. 1372-1378.

AuthorsCaberera Poch, H. L., Manzanilla-Lopez, R. H. and Kanyuka, K.
Abstract

The expression of host genomes is modified locally by root endoparasitic nematode secretions to induce the development of complex cellular structures referred as feeding sites. In compatible interactions, the feeding sites provide the environment and nutrients for the completion of the nematode's life cycle, whereas in an incompatible (resistant) interaction, the host immune system triggers a plant cell death programme, often in the form of a hypersensitive reaction, which restricts nematode reproduction. These processes have been studied in great detail in organ tissues normally infected by these nematodes: the roots. Here we show that host leaves can support a similar set of programmed developmental events in the potato cyst nematode Globodera rostochiensis life cycle that are typical of the root-invading nematodes. We also show that a gene-for-gene type specific disease resistance that is effective against potato cyst nematodes (PCN) in roots also operates in leaves: the expression of the resistance (R) gene Hero and members of its gene family in leaves correlates with the elicitation of a hypersensitive response only during the incompatible interaction. These findings, and the ability to isolate RNA from relevant parasitic stages of the nematode, may have significant implications for the identification of nematode factors involved in incompatible interactions.

KeywordsPlant Sciences
Year of Publication2006
JournalPlant, Cell & Environment
Journal citation29 (7), pp. 1372-1378
Digital Object Identifier (DOI)doi:10.1111/j.1365-3040.2006.01517.x
PubMed ID17080958
Open accessPublished as non-open access
Funder project or code506
505
ISSN01407791
PublisherWiley

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