Conifer stem pest resistance includes constitutive defenses that discourage invasion and inducible defenses, including phenolic and
terpenoid resin synthesis. Recently,
methyl jasmonate (MJ) was shown to induce conifer resin and phenolic defenses; however, it is not known if MJ is the direct effector or if there is a downstream signal. Exogenous applications of MJ,
methyl salicylate, and
ethylene were used to assess inducible defense signaling mechanisms in conifer stems. MJ and
ethylene but not
methyl salicylate caused enhanced phenolic synthesis in polyphenolic parenchyma cells, early sclereid lignification, and reprogramming of the cambial zone to form traumatic resin ducts in Pseudotsuga menziesii and Sequoiadendron giganteum. Similar responses in internodes above and below treated internodes indicate transport of a signal giving a systemic response. Studies focusing on P. menziesii showed MJ induced
ethylene production earlier and 77-fold higher than wounding.
Ethylene production was also induced in internodes above the MJ-treated internode. Pretreatment of P. menziesii stems with the
ethylene response inhibitor
1-methylcyclopropene inhibited MJ and
wound responses. Wounding increased
1-aminocyclopropane-1-carboxylic acid (
ACC) oxidase protein, but MJ treatment produced a higher and more rapid
ACC oxidase increase.
ACC oxidase was most abundant in ray parenchyma cells, followed by cambial zone cells and resin duct epithelia. The data show these MJ-induced defense responses are mediated by
ethylene. The cambial zone xylem mother cells are reprogrammed to differentiate into resin-secreting epithelial cells by an MJ-induced
ethylene burst, whereas polyphenolic parenchyma cells are activated to increase
polyphenol production. The results also indicate a central role of ray parenchyma in
ethylene-induced defense.