Kinetin's role is connected with the growth and development of plants. It stimulates seed germination, regulates cell division and reaction to stress, and determines apical dominance, formation, and activity of shoot meristems. Kinetin and 6-BAP counteract the inhibitory effect of darkness on epicotyl shoot formation and sprouting and raise it to the same level as in tissue incubated in light . It is also implicated in the vascular development and synthesis of secondary metabolites like indol alkaloids and anthocyanins. Kinetin influences chloroplast differentiation and chlorophyll biosynthesis by stimulation of 5-aminolevulinc acid synthesis , [14-16]. Cytokinin inhibits lateral root initiation by blocking the peri-cycle founder cells' cell division cycle at the G2 to M transition phase. It stimulates lateral root elongation by stimulating the G1 to S phase transition [17-19] and strongly inhibits of RNase from the Pisum sativum isolated leaf, inhibits proteolysis, and maintains the integrity of cell membranes . Since the majority of plant hormones bear a charge, cytokinin can be absorbed into specific membrane lipid domains . It induces a rapid response at the outer face of membrane modulating ion transport . The hormones affect the surface pressure decrease observed in the phospholipid monolayer relaxation. The greatest decay of surface pressure has been recorded in the presence of auxins in all systems, the lowest in the presence of cytokinins. Negatively charged hormones like IAA and 2,4-D affect monolayer disorganization to the highest degree, while the effect of positively charged compounds (kinetin, zeatin) is less pronounced. Both the cytokinins, zeatin and kinetin, display very similar effects, which suggests that the purine ring is the main steric parameter that determinines interaction with the lipid monolayer built from phospho-lipids as phosphatidylcholine and phosphatidic acid, having the same hydrophobic parts .
Exogenously applied kinetin stimulates promoter-dependent rRNA transcription of the repeated genes that encode the precursor of 17-18, 5.8, and 25-28 S riboso-mal RNA in Arabidopsis thaliana. RNA polymerase I enhanced activity in growing cells and decreased it in quiescent cells. On average it accounts for approx. 34% of total nuclear transcription, but in cytokinin-treated cells this figure is approx. 60%. Kinetin was suggested to operate at the level of transcription initiation rather than rRNA stabilization and acts as a general regulator of protein synthesis activity and growth modulator in plant cells .
Kinetin influences the cell cycle. In N. plumbaginifolia it was shown to be indispensable in cell transition to the G2 phase and to histone kinase H1 p34cdc2 normal functioning . Kinetin and 1-naphthylacetic acid (auxin) increases phosphorylation of the S6 ribosomal protein and activation of its cognate kinase, AtS6K, as well as translationaly up-regulating S6 and S18A mRNAs in Arabidopsis suspension cell culture .
Kinetin delays aging and leaf senescence and causes nutrient mobilization. It influences the activity of extracellular invertase, an enzyme responsible for nutrition remobilization from senescing leaves to other parts of the plant. The expression is inhibited by the invertase inhibitors expressed under the control of the cytokinin-inducible promoter. As a result, kinetin contributes to nutrition retention and thus inhibits senescence .
Kinetin interacts with the pathogenesis-related protein c (PR-10c) of the PR-10 protein family from a birch tree. PR-10c shows a low ribonuclease activity and is known to take part in response to stress. Kinetin interacts with the glycine-rich loop through its adenine moiety .
Kinetin serves as a chitinase inhibitor and could be an effective antifungal compound. It is considered to be the most potent of 880 druglike molecules tested. It acts as a competitive inhibitor, with its furfuran group occupying a deep pocket of the enzyme. In the pocket, oxygen atoms could interact with Tyr32, which probably determines unusually strong molecule binding .
It can also play a protective role. The cytokinin reduces membrane damage caused by fungal toxin fusaric acid and necrosis brought about by mercuric chloride .
It also combats viral infections. Kinetin treatment of Xanthic-nc tobacco reduces the number of lesions induced by tobacco mosaic viral infection but only slightly affects virus multiplication .
BT37 is a crown gall teratoma induced on tobacco by Agrobacterium tumefa-ciens containing pTi-T37, a nopaline-type Ti plasmid. The BT37 tissue treated with kinetin at 1 mg/L results in the development of relatively normal-appearing shoots. The shoots can produce viable seeds and are susceptible to A. tumefaciens infection. The cells lose most of the Ti plasmid sequences (T-DNA) found in BT37 DNA containing a highly conserved region of the Ti plasmid that has been found to be incorporated into all tumors. However, the cells retain sequences homologous to the ends of the T-DNA present in the teratoma tissue .
Kinetin brings about an increase in cytoplasmic calcium, an early event in vegetative bud formation in the moss Physcomitrella patens through stimulation of azidopine binding to 1,4-dihydropyridine-sensitive calcium channels . The cy-tokinin has also been suggested to enhance phosphoinositide catabolism in soybean suspension cultures . Kinetin as well as the cyclic guanosine-3',5'-mono- phosphate (cGMP) analog 8-Br-cGMP induces a stomatal opening in Tradescantia albi-flora. Its effect is reversibly inhibited by guanylate cyclase inhibitors .
It has been shown that kinetin is present in a root nodule of Casuarina equiseti-folia modulated by Frankia . Probably it is produced as a result of oxidative stress during infection. In that process reactive oxygen species (ROSs) are generated in high amounts in the root cells , which could provoke DNA damage and result in kinetin formation. In the same process the cytokinin could serve as a factor that regulates ROS amounts as its balance is necessary for infection thread progression.
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