In tobacco plants, wounding induces production of a set of defense-related
proteins such as basic pathogenesis-related (PR)
proteins and
proteinase inhibitors (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 plants.
Infection of necrotizing virus also induced tpoxN1 gene. The
wound-induced expression was not enhanced by known
wound-signal compounds such as
methyl jasmonate (MeJA) and
ethephon in contrast to other
wound-inducible genes such as basic PR-1 and PI-II genes. And treatment with MeJA and
coronatine,
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 reported as an endogenous inducer for acidic PR genes in tobacco mosaic virus-infected tobacco leaves, could induce tpoxN1 gene expression. These results suggest that
wound-induced expression of the tpoxN1 gene is regulated differently from that of the basic PR and PI-II genes.