Agrobacterium tumefaciens causes crown gall disease by transferring and 
integrating bacterial DNA (T-DNA) into the plant genome. To examine the 
physiological changes and adaptations during Agrobacterium-induced tumor 
development, we compared the profiles of salicylic acid (SA), ethylene (ET), 
jasmonic acid (JA), and auxin (indole-3-acetic acid [IAA]) with changes in the 
Arabidopsis thaliana transcriptome. Our data indicate that host responses were 
much stronger toward the oncogenic strain C58 than to the disarmed strain GV3101 
and that auxin acts as a key modulator of the Arabidopsis-Agrobacterium 
interaction. At initiation of infection, elevated levels of IAA and ET were 
associated with the induction of host genes involved in IAA, but not ET 
signaling. After T-DNA integration, SA as well as IAA and ET accumulated, but JA 
did not. This did not correlate with SA-controlled pathogenesis-related gene 
expression in the host, although high SA levels in mutant plants prevented tumor 
development, while low levels promoted it. Our data are consistent with a 
scenario in which ET and later on SA control virulence of agrobacteria, whereas 
ET and auxin stimulate neovascularization during tumor formation. We suggest 
that crosstalk among IAA, ET, and SA balances pathogen defense launched by the 
host and tumor growth initiated by agrobacteria.