Loss of Plant Organogenic Totipotency in the Course of in vitro Neoplastic Progression

• Published in: In vitro cellular & developmental biology. Plant Vol. 36; no. 3; pp. 171 - 181
• Main Authors: Gaspar, Thomas, Claire Kevers, Badia Bisbis, Thierry Franck, Crevecoeur, Michèle, Greppin, Hubert, Jacques Dommes
• Format: Journal Article Web Resource
• Language: English
• Published: CABI Publishing 01.05.2000; Springer Science & Business Media B.V
• Subjects: Aneuploidy; Animal cells; Biologie végétale (sciences végétales, sylviculture, mycologie...); Callus; Cell cycle; Habituation; hyperhydricity; Life sciences; neoplastic progression; organogenic totipotency; oxidative stress; Phytobiology (plant sciences, forestry, mycology...); plant cancer; Plant cells; Plants; Sciences du vivant; Special Symposium: In vitro Plant Recalcitrance; Stem cells; Totipotent stem cells; Tumors
• ISSN: 1054-5476; 1475-2689; 1475-2689
• DOI: 10.1007/s11627-000-0033-3

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.