Effect of morphactine on differentiation and development of Cymbidium Sw. protocorms cultured in vitro

The morphogenetic effect of morphactine IT 3456 on meristematic tissue of <i>Cymbidium </i>Sw. was investigated within the dose range 0.01 to 10 ppm in <i>in vitro</i> culture on liquid and agar-solidified medium. In the doses applied, morphactine increased the number of protocorms differentiating from isolated meristematic tissues, and, in dependence on the dose, affected their shape and proliferation. Morphactine retards, and in large doses completely inhibits, the development of rhizoids, shoots and roots. Various developmental anomalies were observed under the influence of morphactine: leaf syncotylia, and their deformation, thickening, shortening, flattening and branching of shoots as well as formation of 2-3 shoots by one protocorm and development of secondary protocorms on the leaves.

Cytokinin-induced decrease in ribonuclease activity and initiation of gametophore buds in the protonema of mosses

As early as after 4 hours of kinetin treatment a decrease in RNase activity was found in the moss protonema and it was maintained to at least 10 hours. It was shown that this decrease was correlated with the morphogenetic effect of kinetin (bud induction). No allosteric inhibition of RNase toy kinetin could be found. The decrease in enzyme activity was more pronounced When additionally inhibitors of protein and RNA synthesis were used. It is concluded that kinetin affects the RNase rather by an inhibition of de novo synthesis of the enzyme than by an increase of its decomposition by proteases.

Role of TGF-β1 and JNK signaling in capillary tube patterning

The transforming growth factor (TGF) family of secretory polypeptides comprises signaling proteins involved in numerous physiological processes, including vascular development and vessel wall integrity. Both pro- and anti-angiogenic effects of TGF-β1 have also been documented. To study the intracellular mechanisms involved in capillary tube morphogenesis, endothelial cell aggregates were cultured in a fibrin matrix. It was found that the pattern of capillary tubes formed in a fibrin matrix was altered in response to TGF-β1 treatment such that the capillary-like structures displayed a bipolarized pattern. In contrast, in untreated control and fibroblast growth factor-2-treated cells, the pattern of capillary tubes formed was random. TGF-β1 also downregulated urokinase-type plasminogen activator (uPA) activity while upregulating PA inhibitor (PAI)-1 and thrombospondin (TSP)1 gene expression. To investigate the signaling cascade mediating the phenotypic changes observed, pharmacological inhibitors of p38 MAPK, Sp1 transcription factor, c-Jun NH2-terminal kinase (JNK), and the cytokine TNF-α were used. The p38 MAPK inhibitor SB203580 reversed the TGF-β1-dependent inhibition of uPA activity but not its morphogenetic effect. In contrast, the DNA intercalator WP631 and TNF-α counteracted the TGF-β1-induced morphogenetic effect while the JNK inhibitor SP600125 effectively inhibited capillary tube formation. These results indicate that the TGF-β1-induced capillary tube pattern is independent of the p38 MAPK-activated PAI-1 and TSP1 expression, but the mechanism involves Sp1-dependent transcriptional regulation. The results also raise the possibility that the JNK pathway, which controls convergent extension in Xenopus, may be involved in vessel wall patterning in mammalian systems.