Journal
PLANT AND CELL PHYSIOLOGY
Volume 51, Issue 9, Pages 1524-1536Publisher
OXFORD UNIV PRESS
DOI: 10.1093/pcp/pcq109
Keywords
Cyst nematode; Globodera rostochiensis; Plant pathogen; Resistance; Salicylic acid; Tomato
Categories
Funding
- Japan Society for Promotion of Science [21580058]
- Ministry of Economy, Trade Industry of Japan
- Northern Advancement Center for Science Technology
- Grants-in-Aid for Scientific Research [22405018, 21580058] Funding Source: KAKEN
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To understand the machinery underlying a tomato cultivar harboring the Hero A gene against cyst nematode using microarrays, we first analyzed tomato gene expression in response to potato cyst nematode (PCN; Globodera rostochiensis) during the early incompatible and compatible interactions at 3 and 7 days post-inoculation (dpi). Transcript levels of the phenylalanine ammonia lyase (PAL) and Myb-related genes were up-regulated at 3dpi in the incompatible interaction. Transcription of the genes encoding pyruvate decarboxylase (PDC) and alcohol dehydrogenase (ADH) was also up-regulated at 3dpi in the incompatible interaction. On the other hand, the four genes (PAL, Myb, PDC and ADH) were down-regulated in the compatible interaction at 3dpi. When the expression levels of several pathogenesis-related (PR) protein genes in tomato roots were compared between the incompatible and compatible interactions, the salicylic acid (SA)-dependent PR genes were found to be induced in the incompatible interaction at 3dpi. The PR-1(P4) transcript increased to an exceptionally high level at 3dpi in the cyst nematode-infected resistant plants compared with the uninoculated controls. The free SA levels were elevated to similar levels in both incompatible and compatible interactions. We then confirmed that PR-1(P4) was not significantly induced in the NahG tomato harboring the Hero A gene, compared with the resistant cultivar. We thus found that PR-1(P4) was a hallmark for the cultivar resistance conferred by Hero A against PCN and that nematode parasitism resulted in the inhibition of the SA signaling pathway in the susceptible cultivars.
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