Genetic and biochemical studies on the suppression of and a recovery from the tumorous state in higher plants.
Four neoplastic diseases of plants: crown gall, which is caused by Ti plasmid DNA; Black's wound tumor disease by an RNA virus; the Kostoff genetic tumors by chromosomal imbalance; and habituation, which results from a spontaneous activation of select biosynthetic systems, have been analyzed and compared. It has been found that both the development of a capacity for autonomous growth and the nature of the heritable cellular change that underlies tumorigenesis are similar in the four instances. All develop a capacity for autonomous growth as a result of the persistent activation of select biosynthetic systems, the products of which are concerned with cell growth and division. That the persistent activation of these biosynthetic systems does not involve heritable changes of an irreversible type is indicated by the finding that a reversal of the neoplastic state occurred in three of the test systems. Since the tumor cells in these instances were found to remain totipotent the results suggest that whether the normal or tumor phenotype is expressed is determined by how the genetic information is regulated in a cell. Regulation appears to be accomplished in part through positive feedback control mechanisms. Foreign genetic information could act either in a regulatory manner to persistently activate normal biosynthetic systems or it could code for one or more essential but normally limiting substance(s) and thus replace a substance(s) that in the case of the Kostoff tumors or habituation is specified by host cell genes, or it could do both. In either case, the foreign genetic information can be regulated in much the same manner as are the host cell genes to give rise to either the normal or tumor phenotype.
D002453:Cell Cycle; D002875:Chromosomes / Q000378:metabolism; D000242:Cyclic AMP / Q000032:analysis; D004273:DNA, Neoplasm / Q000096:biosynthesis; D007399:Interphase; D010941:Plant Tumors / Q000032:analysis / Q000209:etiology / Q000382:microbiology; D010942:Plant Viruses / Q000472:pathogenicity; D010957:Plasmids
D004273:DNA, Neoplasm; D000242:Cyclic AMP