Changes in tissue deformability accompanying actinomycin D inhibition of plant growth and ribonucleic acid synthesis.

Demonstrationi of a necessary role for RNA and protein synthesis in maintenance of rapid rates of cell expansion in planit tissues has been greatly facilitated through use of actinomycin D, puromycin., 8azaguanine and other specific inhibitors (5, 6, 7, 11). For example, a low concentration of the antibiotic actinomycin D will partially inhibit protein synthesis (5, 7, 11), and at the same time greatly inihibit growth (5, 6, 7, 11) and RNA synthesis (5, 7) in the elongating zone of plant stems. Actinomycin D is considered to be inhibitory through a specific blocking of DNA-dependent RNA synthesis (3, 7). Implicit in the interpretation of the above observations is the assumiption that some pre-existing RNA must also be rendered nonifunctional by the system before actiniomiiyciii D can be effective in the inhibition of proteiin synthesis and of growth (7). Furthermore, the necessity for RNA synithesis in mainteniance of growtth rate may not be directly attributed to RNA sniithesis per se but rather to RNA-directed protein synlthesis (7, 11). If this possibility is also considered, then the protein fractions limiting cell expansion in soybean hypocotyl tissue must also be characterized by rapid turnover, i.e., with a mean life of a few hours (7). Thus, regardless of the constituent directlv involved, the effective cellular concentration of the rate limiting fraction must be reduced below some threshold level no longer capable of supporting rapid growth, if growth is to be inhibited by an effect of actinomycin D on RNA synthesis. As a new approach toward understanding of the partial processes of expansion growth, the effect of actinomvcin D on tissue deformability was assessed. The relative ease by which cells may be deformed has long been associated with relative rates of cell expansion (4). Growth rate is considered to be proportional to the rate of yielding of the cell wall with the driving force being turgor pressure (1). The property ascribed to auxin of increasing rate of expansion by enhancing cell wall softening (1) was