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.