Wound-induced expression of a tobacco peroxidase is not enhanced by ethephon and suppressed by methyl jasmonate and coronatine

Citation
S. Hiraga et al., Wound-induced expression of a tobacco peroxidase is not enhanced by ethephon and suppressed by methyl jasmonate and coronatine, PLANT CEL P, 41(2), 2000, pp. 165-170
Citations number
40
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT AND CELL PHYSIOLOGY
ISSN journal
00320781 → ACNP
Volume
41
Issue
2
Year of publication
2000
Pages
165 - 170
Database
ISI
SICI code
0032-0781(200002)41:2<165:WEOATP>2.0.ZU;2-4
Abstract
In tobacco plants, wounding induces production of a set of defense-related proteins such as basic pathogenesis-related (PR) proteins and proteinase in hibitors (PIs) via the jasmonate/ethylene pathway. Although class III plant peroxidase (POX) is also wound-inducible, the regulatory mechanism for its wound-induced expression is not fully understood. Here, we describe that a tobacco POX gene (tpoxN1), which is constitutively expressed in roots, is induced locally 30 min after wounding and then systemically in tobacco plan ts. Infection of necrotizing virus also induced tpoxN1 gene. The wound-indu ced expression was not enhanced by known wound-signal compounds such as met hyl jasmonate (MeJA) and ethephon in contrast to other wound-inducible gene s such as basic PR-1 and PI-II genes. And treatment with MeJA and coronatin e, biological analogs of jasmonate, rather suppressed the tpoxN1 expression . Salicylic acid, an antagonist of jasmonate-based wound signaling, did not suppress the wound-induced expression of tpoxN1, Only spermine, which is r eported as an endogenous inducer for acidic PR genes in tobacco mosaic viru s-infected tobacco leaves, could induce tpoxN1 gene expression, These resul ts suggest that,wound-induced expression of the tpoxN1 gene is regulated di fferently from that of the basic PR and PI-II genes.