Dissecting the Roles of the Cytokinin Signaling Network: The Case of De Novo Shoot Apical Meristem Formation.

Numerous biotechnological applications require a fast and efficient clonal propagation of whole plants under controlled laboratory conditions. For most plant species, the de novo regeneration of shoots from the cuttings of various plant organs can be obtained on nutrient media supplemented with plant hormones, auxin and cytokinin. While auxin is needed during the early stages of the process that include the establishment of pluripotent primordia and the subsequent acquisition of organogenic competence, cytokinin-supplemented media are required to induce these primordia to differentiate into developing shoots. The perception of cytokinin through the receptor ARABIDOPSIS HISTIDINE KINASE4 (AHK4) is crucial for the activation of the two main regulators of the establishment and maintenance of shoot apical meristems (SAMs): SHOOTMERISTEMLESS (STM) and the WUSCHEL-CLAVATA3 (WUS-CLV3) regulatory circuit. In this review, we summarize the current knowledge of the roles of the cytokinin signaling cascade in the perception and transduction of signals that are crucial for the de novo establishment of SAMs and lead to the desired biotechnological output-adventitious shoot multiplication. We highlight the functional differences between individual members of the multigene families involved in cytokinin signal transduction, and demonstrate how complex genetic regulation can be achieved through functional specialization of individual gene family members.

Cytokinin deficiency confers enhanced tolerance to mild, but decreased tolerance to severe salinity stress in in vitro grown potato.

Cytokinin (CK) is a plant hormone that plays crucial roles in regulating plant growth and development. CK-deficient plants are widely used as model systems for investigating the numerous physiological roles of CK. Since it was previously shown that transgenic or mutant CK-deficient Arabidopsis and Centaurium plants show superior tolerance to salinity, we examined the tolerance of three CK-deficient potato lines overexpressing the Arabidopsis thaliana CYTOKININ OXIDASE/DEHYDROGENASE2 (AtCKX2) gene to 50 mM, 100 mM, 150 mM, and 200 mM NaCl applied in vitro. Quantification of visible salinity injury, rooting and acclimatization efficiency, shoot growth, water saturation deficit, and chlorophyll content confirmed that the CK-deficient potato plants were more tolerant to low (50 mM) and moderate (100 mM) NaCl concentrations, but exhibited increased sensitivity to severe salinity stress (150 and 200 mM NaCl) compared to non-transformed control plants. These findings were corroborated by the data distribution patterns according to principal component analysis. Quantification of the activity of superoxide dismutases, peroxidases, and catalases revealed an impaired ability of AtCKX2-transgenic lines to upregulate the activity of antioxidant enzymes in response to salinity, which might contribute to the enhanced sensitivity of these potato lines to severe salt stress. Our results add complexity to the existing knowledge on the regulation of salinity tolerance by CK, as we show for the first time that CK-deficient plants can exhibit reduced rather than increased tolerance to severe salt stress.