Salicylic acid and the plant pathogen Erwinia carotovora induce defense genes via antagonistic pathways

被引:115
作者
Vidal, S
deLeon, IP
Denecke, J
Palva, ET
机构
[1] SWEDISH UNIV AGR SCI, UPPSALA GENET CTR, DEPT MOL GENET, S-75007 UPPSALA, SWEDEN
[2] INST INVEST BIOL CLEMENTE ESTABLE, DIV BIOL MOL, MONTEVIDEO 11600, URUGUAY
关键词
D O I
10.1046/j.1365-313X.1997.11010115.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Infection of tobacco plants with the plant pathogenic bacterium Erwinia carotovora subsp. carotovora or treatment of plants with Erwinia-derived elicitor preparations reads to the induction of a number of genes thought to play a role in plant defense response to pathogens. In order to determine the role of salicylic acid (SA) in the induction of the Erwinia responsive genes, the accumulation of mRNAs for these and other genes encoding pathogenesis-related proteins (PR genes) in response to both Erwinia elicitors and SA was determined. PR genes were identified which were preferentially induced by Erwinia elicitor preparations, one gene was induced by SA but not by Erwinia, and another gene was induced by both type of treatments. The differential expression of these genes and the timing of induction suggest that SA is not the signal molecule leading to the early response of plants to Erwinia. This was demonstrated by experiments using transgenic NahG plants that overproduce a salicylate hydroxylase inactivating SA. The elicitation of PR genes by Erwinia was similar in NahG and wild-type plants. Therefore, induction of plant defense genes by Erwinia and SA seems to be by two distinct pathways leading to expression of separate sets of genes. Furthermore, we could demonstrate that Erwinia elicitors antagonize the SA-mediated induction of PR genes. Similarly, SA appeared to inhibit the induction of PR genes elicited by Erwinia. The observed antagonism between the two signal transduction pathways indicates the presence of a common regulatory element in both pathways that acts downstream of SA in the SA-mediated response.
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页码:115 / 123
页数:9
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