However, Rottner et al.[ 6] suggested that Rac and Rho influence the development of focal contacts and focal complexes, respectively, through mutually antagonistic pathways.
WRKY70 protein activates SA-induced genes but represses JA-responsive genes, i.e. controls how the signals converge from these mutually antagonistic pathways [ 49], and WRKY50 proteins mediate SA-mediated repression of JA signalling [ 50].
It has been reported that two mutually antagonistic signalling pathways, the ROP2-actin and ROP6-MT pathways, regulate the development of leaf pavement cells and that defects in the two pathways lead to deficient polarity during leaf pavement cell growth [ 20, 31, 32, 40], similar to the phenotype of OE plants.
Given that Th1 and Th2 responses are mutually antagonistic, CCR4 antagonists may act as adjuvants that direct the immune response towards a Th1-type response.
SA and ET/JA signaling pathways are mutually antagonistic [ 36].
It is also known that these (SA and JA/ET) signaling pathways are mutually antagonistic [ 54].
Moreno and Kintner showed that the FGF and RA pathways were mutually antagonistic, so that FGF repression was associated with enhanced RA signalling (Moreno and Kintner, 2004).
Canonical and non-canonical pathways are thought to be mutually antagonistic (Grumolato et al., 2010; Weidinger and Moon, 2003).
Furthermore, the link between adipose cell inflammation and WNT/LRP5 signaling is likely to have its basis in the mutually antagonistic actions of the β-catenin and PCP pathways (Grumolato et al., 2010).
Based on studies using Arabidopsis mutants impaired in hormone biosynthesis and perception, as well as pharmacological treatments, it is well established that SA, ET and JA are vital components of plant defense responses, SA and JA/ET regulated defense pathways are believed to be mutually antagonistic, but examples of synergistic interactions have also been reported.
Taken together with previous findings, the present results indicate that TGF-ß and PPAR-γ are engaged in a mutually antagonistic reciprocal cross-talk, whereby the PPAR-γ pathway abrogates cellular responses induced by TGF-ß, while TGF-ß-Smad inhibits the expression of PPAR-γ and its target genes.
