Reference : Loss of plant organogenic totipotency in the course of in vitro neoplastic progression
Scientific journals : Article
Life sciences : Phytobiology (plant sciences, forestry, mycology...)
http://hdl.handle.net/2268/3295
Loss of plant organogenic totipotency in the course of in vitro neoplastic progression
English
Gaspar, Thomas mailto [> > Botanique, radiobotanique & serres expér. >]
Kevers, Claire mailto [Université de Liège - ULg > Département des sciences de la vie > Biologie moléculaire et biotechnologie végétales >]
Bisbis, Badia [Université de Liège - ULg > > Hormonologie végétale > >]
Franck, Thierry mailto [Université de Liège - ULg > Département clinique des animaux de compagnie et des équidés > Anesthésiologie gén. et pathologie chirurg. des grds animaux >]
Crèvecoeur, Michèle [Université de Genève - UNIGE > > > > Physiologie et Biochimie Végétales > >]
Greppin, Hubert [Université de Genève - UNIGE > > Physiologie et Biochimie Végétales > >]
Dommes, Jacques mailto [Université de Liège - ULg > Département des sciences de la vie > Biologie moléculaire et biotechnologie végétales >]
2000
In Vitro Cellular & Developmental Biology-Plant
Springer Science & Business Media B.V.
36
3
171-181
Yes (verified by ORBi)
International
1054-5476
Wallingford
United Kingdom
[en] organogenic totipotency ; neoplastic progression ; habituation ; hyperhydricity ; oxidative stress ; plant cancer
[en] 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.
Researchers
http://hdl.handle.net/2268/3295

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