Cytokinin cross-talking during biotic and abiotic stress responses

Abstract

As sessile organisms, plants have to be able to adapt to a continuously changing environment. Plants that perceive some of these changes as stress signals activate signaling pathways to modulate their development and to enable them to survive. The complex responses to environmental cues are to a large extent mediated by plant hormones that together orchestrate the final plant response. The phytohormone cytokinin is involved in many plant developmental processes. Recently, it has been established that cytokinin plays an important role in stress responses, but does not act alone. Indeed, the hormonal control of plant development and stress adaptation is the outcome of a complex network of multiple synergistic and antagonistic interactions between various hormones. Here, we review the recent findings on the cytokinin function as part of this hormonal network. We focus on the importance of the crosstalk between cytokinin and other hormones, such as abscisic acid, jasmonate, salicylic acid, ethylene, and auxin in the modulation of plant development and stress adaptation. Finally, the impact of the current research in the biotechnological industry will be discussed.

Keywords: abscisic acid; cytokinin; hormonal crosstalk; salicylic acid; stress.

FIGURE 1

CK and crosstalks during abiotic stress responses. Under non-stress conditions, CK activates signaling mediated through AHK receptors, AHPs, and type-B response regulators ARRs. Type-B ARRs stimulate the expression of the early CK response genes, including type-A ARR genes that provide a negative feedback loop of the CK signaling. Besides this negative feedback loop, type-A ARRs also repress the expression of ABI5 and interfere with the ABA signaling, through the physical interaction with ABI5. In response to stress, ABA levels increase and, simultaneously, CK levels decrease. The recognition of ABA by the receptors PYR/PYL/RCAR promotes the interaction with PP2C proteins that will activate downstream responses through signaling components including ABI5 and ABI4. At the same time, ABA interferes with the activity of CK and auxin and via ABI4 attenuates the expression of the PIN1 auxin efflux carrier and enhances the transcription of the CK signaling repressor ARR5. Interestingly, type-A ARRs, such as ARR5, are upregulated, despite the low CK levels, probably because of the indirect activation of the CK signaling pathway by alternative receptors of the histidine kinase family, such as AHK1.

FIGURE 2

CK and hormonal crosstalks during biotic stress responses. Pathogen attacks stimulated by PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI) correlate with a dramatic production of SA and CK. The accumulation of CK will induce the production and accumulation of phytoalexins in a SA-independent manner and also enhance the SA-dependent immunity. In response to pathogens, NPR1 monomerizes and translocates to the nucleus where it interacts with TGA3. The NPR1-TGA3 activity is further regulated through interaction with the type-B ARR2 response regulator, a component of the CK signaling pathway. The TGA3-NPR1-ARR2 complex is required to induce the SA-mediated resistance and to trigger the expression of PR1 and PR2. High CK levels, induced after pathogen attacks, can activate the CRF5-mediated branch of the CK signaling pathway and contribute to the regulation of the PR1, PR3, PR4, and PR5 expression.