A plethora of abiotic and biotic environmental stresses exert their in
fluence on plants via the gaseous hormone ethylene. In addition, aspec
ts of plant development and climacteric fruit ripening are regulated b
y ethylene. Sensitivity to ethylene is presumably mediated by a specif
ic ethylene receptor whose activation signal is then transduced via an
unknown cascade pathway. We have used the plant pathogenesis response
, exemplified by the induction of pathogenesis-related (PR) genes, as
a paradigm to investigate ethylene-dependent signal transduction in th
e plant cell. Ethylene application induced very rapid and transient pr
otein phosphorylation in tobacco leaves. In the presence of the kinase
inhibitors H-7 and K-252a, the transient rise in phosphorylation and
the induced expression of PR genes were abolished. Similarly, these in
hibitors blocked the response induced by an ethylene-dependent elicito
r, alpha-AB. Reciprocally, application of okadaic acid, a specific inh
ibitor of phosphatases type 1 and type 2A, enhanced total protein phos
phorylation and by itself elicited the accumulation of PR proteins. In
the presence of H-7 and K-252a, PR protein accumulation induced by ok
adaic acid was blocked. In contrast to the action of ethylene and alph
a-AB, xylanase elicits the accumulation of PR protein by an ethylene-i
ndependent pathway. Xylanase-induced PR protein accumulation was not a
ffected by H-7 and K-252a. The results indicate that responsiveness to
ethylene in leaves is transduced via putative phosphorylated intermed
iates that are regulated by specific kinases and phosphatases.