Abstract
Effects of cytokinins on trigonelline's promotion of cell arrest in G2 were determined. Previous results demonstrate that trigonelline, (N-methyl nicotinic acid), a hormone present in cotyledons of young seedlings of Pisum sativum L. and Glycine max Merrill, is transported to roots and shoots where it stops cell progression in the G2 stage of the cell cycle during normal cell maturation. In P. sativum, two natural cytokinins, isopentenyl adenine and zeatin, and both their ribosides (all at 10 −7 M) were antagonistic to trigonelline's function when placed individually in aseptic culture with trigonelline at 10 −6 M. Elevated trigonelline concentrations (10 −4 M) negated the antagonistic effect on these cytokinins. Kinetin and benzyl adenine (synthetic cytokinins) were not antagonistic to trigonelline at any concentration. In G. max, two natural cytokinins, isopentenyl adenine and zeatin, at 10 −7 and 10 −8 M, promoted cell arrest in G2 in the absence of trigonelline. Moreover, the proportion of cells arrested in G2 was higher in roots cultured with isopentenyl adenine in combination with trigonelline, than with either hormone alone. In both legumes, these natural cytokinins did not influence trigonelline concentrations in roots. These results demonstrate an interaction between natural cytokinins and trigonelline in control of the cell cycle in peas and soybeans. This is the first report of an interaction of two naturally occurring hormones that affect cell arrest in either G1 or G2 in tissues of either plants or animals.
Published Version
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