Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine-insensitive (coi1) mutation occurs through two distinct mechanisms

Citation
Ap. Kloek et al., Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine-insensitive (coi1) mutation occurs through two distinct mechanisms, PLANT J, 26(5), 2001, pp. 509-522
Citations number
68
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT JOURNAL
ISSN journal
0960-7412 → ACNP
Volume
26
Issue
5
Year of publication
2001
Pages
509 - 522
Database
ISI
SICI code
0960-7412(200106)26:5<509:RTPSCB>2.0.ZU;2-D
Abstract
A new allele of the coronatine-insensitive locus (COI1) was isolated in a s creen for Arabidopsis thaliana mutants with enhanced resistance to the bact erial pathogen Pseudomonas syringae. This mutant, designated coi1-20, exhib its robust resistance to several P. syringae isolates but remains susceptib le to the virulent pathogens Erisyphe and cauliflower mosaic virus. Resista nce to P. syringae strain PstDC3000 in coi1-20 plants is correlated with hy peractivation of PR-1 expression and accumulation of elevated levels of sal icylic acid (SA) following infection, suggesting that the SA-mediated defen se response pathway is sensitized in this mutant. Restriction of growth of PstDC3000 in coi1-20 leaves is partially dependent on NPR1 and fully depend ent on SA, indicating that SA-mediated defenses are required for restrictio n of PstDC3000 growth in coi1-20 plants. Surprisingly, despite high levels of PsdDC3000 growth in coi1-20 plants carrying the salicylate hydroxylase ( nahG) transgene, these plants do not exhibit disease symptoms. Thus resista nce to P. syringae in coi1-20 plants is conferred by two different mechanis ms: (i) restriction of pathogen growth via activation of the SA-dependent d efense pathway; and (ii) an SA-independent inability to develop disease sym ptoms. These findings are consistent with the hypotheses that the P. syring ae phytotoxin coronatine acts to promote virulence by inhibiting host defen se responses and by promoting lesion formation.