Abstract
It has been several decades since Skoog and Miller described the contrasting behavior of auxin and cytokinin in promoting the growth of root and shoot, respectively [1]. In recent years, a lot of progress has been made in understanding the regulation of stem cell niche and cell fate in both shoot and root apical meristems. Developmental processes such as the maintenance of root meristems [2], lateral root formation [3], leaf position determination [4], and de novo auxin-induced organogenesis [5] are finetuned by the mutual interactions between auxin and cytokinin. Auxin exerts its inhibition on cytokinin on several levels; mechanisms range from its biosynthesis to the suppression of its signaling [6]. Reciprocally, cytokinin antagonistically impacts the flux, distribution, and signaling of auxin [7]. Antagonism between auxin and cytokinin is not the only type of interaction that governs developmental outputs in plants. Rather, synergistic interaction between auxin and cytokinins also exists in processes such as nodule organogenesis [8], light-mediated leaf initiation, and organ positioning [9]. With the majority of previous studies focusing on these hormones in development, auxin-cytokinin interplay has not been extensively analyzed in the context of plant immunity. Mutual interactions between stress-specific hormones such as salicylic acid and jasmonic acid/ethylene (SA-JA/ET) are regarded as the central backbone of the immunity [10]. However, growth-promoting hormones (auxin, cytokinins, gibberellic acid, and abscisic acid) either inhibit or potentiate this balance in mediating the protection or susceptibility of the plant against the invading pathogen [10,11]. For a comprehensive understanding of hormonal crosstalk in disease, a systems-biological perspective is critical, as plant hormones act in concert [11]. We focus on recent progress regarding the individual effects of auxin and cytokinins and their combined effect on immune dynamics in plant-pathogen systems.
Highlights
It has been several decades since Skoog and Miller described the contrasting behavior of auxin and cytokinin in promoting the growth of root and shoot, respectively [1]
To assess the impact of the auxin-cytokinin antagonism on plant immune defense, we have focused on a single model plant-pathogen system: Arabidopsis infected by pv. tomato DC3000 (Pto) (Figure 1)
We propose a working model for the auxin-cytokinin antagonism (Figure 1): To cause susceptibility, Pto enhances the in planta level of auxin, which attenuates the SA responses and decreases resistance against infection by a pathogen
Summary
It has been several decades since Skoog and Miller described the contrasting behavior of auxin and cytokinin in promoting the growth of root and shoot, respectively [1]. The impact of auxin has already been analyzed with respect to immune dynamics of plant-pathogen interactions [13]. The transgenic expression of the AvrRpt2 (bacterial effector protein) gene in Arabidopsis restores optimal growth of the Pto strain defective in TTSS, thereby linking the effector and auxin (Figure 1) in mediating susceptibility of the host [15].
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