Submitted to: American Society of Cell Biology Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: April 10, 1999
Publication Date: N/A
Technical Abstract: At harvest and for a finite period thereafter, potato tubers will not sprout and are in a state of endodormancy. The length of this endodormant period is dependent on both the cultivar (genotype) and on environmental conditions during tuber formation and typically lasts up to 4-6 months. At the cellular level, tuber meristem dormancy is a result of an inhibition of cell division. Meristematic cells in the tuber buds (eyes) are arrested in the G1-phase of the cell cycle prior to the onset of DNA replication. The resumption of bud growth following the termination of dormancy is accompanied by a large increase in DNA synthesis and in the number of cells traversing the cell cycle. At the molecular level, the events regulating entry into and exit from bud endodormancy are unknown. However at the physiological level, it is becoming increasingly clear that endogenous tuber hormones play a critical role in the regulation of bud dormancy. The hypothesis that hormones are involved in tuber dormancy is not new. In 1947, Hemberg suggested that dormancy is the result of a temporal excess of growth inhibitors. Later a role for growth promoters was envisaged. In total, four classes of endogenous hormones (abscisic acid, ethylene, cytokinins, and gibberellins) were implicated in tuber dormancy control. In spite of its attractiveness, experimental support for this hypothesis was based exclusively on the effects of exogenous hormones and on correlative studies examining changes in hormone content (as determined by bioassay) and dormancy status. As a result, this paradigm was subject to much justifiable criticism.