Combinations of ethylene and methyl jasmonate (E/MeJA) synergistically
induced members of both groups 1 and 5 of the pathogenesis-related (P
R) superfamily of defense genes. E/MeJA caused a synergistic induction
of PR-1b and osmotin (PR-5) mRNA accumulation in tobacco seedlings. E
/MeJA also synergistically activated the osmotin promoter fused to a b
eta-glucuronidase marker gene in a tissue specific manner. The E/MeJA
responsiveness of the osmotin promoter was localized on a -248 to +45
fragment that exhibited responsiveness to several other inducers. E/Me
JA induction also resulted in osmotin protein accumulation to levels s
imilar to those induced by osmotic stress. Of the several known induce
rs of the osmotin gene, including salicylic acid (SA), fungal infectio
n is the only other condition known to cause substantial osmotin prote
in accumulation in Wisconsin 38, a tobacco cultivar that does not resp
ond hypersensitively to tobacco mosaic virus. Based on the ability of
the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpip
e to block ethylene induction of PR-1b mRNA accumulation and its inabi
lity to block osmotin mRNA induction by ethylene, these two PR gene gr
oups appeared to have at least partially separate signal transduction
pathways. Stimulation of osmotin mRNA accumulation by okadaic acid ind
icated that another protein kinase system is involved in regulation of
the osmotin gene. SA, which is known to induce pathogen resistance in
tobacco, could not induce the osmotin gene as much as E/MeJA and neit
her could it induce PR-1b as much as SA and MeJA combined.