EXPRESSION OF THE GENE FOR A SMALL GTP-BINDING PROTEIN IN TRANSGENIC TOBACCO ELEVATES ENDOGENOUS CYTOKININ LEVELS, ABNORMALLY INDUCES SALICYLIC-ACID IN RESPONSE TO WOUNDING, AND INCREASES RESISTANCE TO TOBACCOMOSAIC-VIRUS INFECTION
H. Sano et al., EXPRESSION OF THE GENE FOR A SMALL GTP-BINDING PROTEIN IN TRANSGENIC TOBACCO ELEVATES ENDOGENOUS CYTOKININ LEVELS, ABNORMALLY INDUCES SALICYLIC-ACID IN RESPONSE TO WOUNDING, AND INCREASES RESISTANCE TO TOBACCOMOSAIC-VIRUS INFECTION, Proceedings of the National Academy of Sciences of the United Statesof America, 91(22), 1994, pp. 10556-10560
Tobacco plants transformed with rgp1, a gene encoding a Ras-related sm
all GTP binding protein, were previously shown to exhibit a distinct r
eduction in apical dominance with increased tillering. These abnormal
phenotypes were later found to be associated with elevated levels of e
ndogenous cytokinins (zeatin and zeatin riboside). Analysis of the exp
ression of several genes known to be affected by cytokinins identified
a clear increase in the mRNA levels of genes encoding acidic pathogen
esis-related proteins in both transgenic plants and their progenies. T
his increase was directly attributable to elevated levels of the acidi
c pathogenesis-related protein inducers, salicylic acid (SA) and salic
ylic acid P-glucoside, due to an abnormal and sensitive response of th
e transgenic plants to wounding. In contrast, mRNA levels of the gene
for proteinase inhibitor II, which is normally induced by wounding, we
re generally suppressed in the same wounded plants, probably due to SA
overproduction. The changes in SA and pathogenesis-related protein le
vels in the transgenic plants resulted in a distinct increase in their
resistance to tobacco mosaic virus infection. In normal plants, the w
ound and pathogen-induced signal transduction pathways are considered
to function independently. However, the wound induction of SA in the t
ransgenic plants suggests that overexpression of this small GTP bindin
g protein somehow interferes with the normal signal pathways, possibly
by affecting cytokinin biosynthesis, and results in cross-signaling b
etween these two transduction systems.