Beneficial use of lignosulfonates in in vitro plant cultures: stimulation of growth, of multiplication and of rooting

peer reviewedLignosulfonates (LIGNs), low-cost by-products from the paper industry, are already commercialized as fertilizers; they stimulate both vegetative and reproductive growths and fructification. LIGNs have been tested in in vitro cultures and here too, they improve shoot growth and vigor, and rooting of various plant materials. This study aimed at to extend the in vitro application of LIGNs at different developmental stages in order to increase the productivity of systems generating vitroplants. The present results showed the beneficial effects of various LIGN applications on growth of a tropical orchid, Phalaenopsis, multiplication of Saint-paulia ionantha and rooting of poplar and Sequoiadendron sempervirens shoot cuttings. One of the most interesting observations was the stimulating effect of Ca-chelated LIGN on growth of Phalaenopsis and on rooting of Sequoiadendron. The significant and reproducible effects of LIGNs at several steps of micropropagation of different plant materials represent a potential tool improve quality without embarrassing side-effects

Loss of plant organogenic totipotency in the course of in vitro neoplastic progression

The aptitude for organogenesis from normal hormone-dependent cultures very commonly decreases as the tissues are serially subcultured. The reasons for the loss of regenerative ability may vary under different circumstances: genetic variation in the cell population, epigenetic changes, disappearance of an organogenesis-promoting substance, etc. The same reasons may be evoked for the progressive and eventually irreversible loss of organogenic totipotency in the course of neoplastic progressions from hormone-independent tumors and hyperhydric teratomas to cancers. As in animal cells, plant cells at the end of a neoplastic progression have probably undergone several independent genetic accidents with cumulative effects. They indeed are characterized by atypical biochemical cycles from which they are apparently unable to escape. The metabolic changes are probably not the primary defects that cause cancer, rather they may allow the cells to survive. How these changes, namely an oxidative stress, affect organogenesis is not known. The literature focuses on somatic mutations and epigenetic changes that cause aberrant regulation of cell cycle genes and their machinery