|Sauter, J - CHRISTIAN ALBRECHT UNIV|
|Fuchigami, L - CHRISTIAN ALBRECHT UNIV|
|Stepien, V - CHRISTIAN ALBRECHT UNIV|
Submitted to: Physiologia Plantarum
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 15, 1996
Publication Date: N/A
Interpretive Summary: Deciduous trees (including fruit trees) undergo a period of rest (dormancy) during the winter months in response to environmental conditions that are not conducive to growth. This is a protective adaptation. To prevent buds of trees from growing during short, unseasonable warm periods during the winter, a defined period of exposure to chilling temperatures is required in order for normal budbreak to occur in the spring. Understanding how dormancy is regulated is important in order to develop technologies to extend dormancy and/or delay budbreak during cold spring weather. The ability to delay and manipulate dormancy could provide a method of protecting flower buds of fruit trees from spring frosts. In the present study, we examined the ability of mild heat stresses to release buds of poplar trees from dormancy and induce the production of a family of protective proteins (heat shock proteins). It was determined that dormancy ycould be broken at any time by the exposure of buds to mild heat stress an was accompanied by a loss in the membrane permeability of bud tissue, as well as the production of specific heat shock proteins. Based on this data, we suggest that the accumulation of mild stresses may play a universal role in releasing buds from dormancy in nature. This data has been extended to fruit trees, and will serve as the foundation for studying the underlying biochemical and genetic regulation of dormancy.
Technical Abstract: The present investigation was conducted to determine the effects of near-lethal heat stress on budbreak, heat-shock proteins (HSP(s)), and ubiquitin in hybrid poplar (populus nigra Charkowiensis x P. nigra incrassata). Shoots were collected monthly for 1.5 years exposed to 20-60 degrees C and then placed in a greenhouse at 18-22 degrees C and supplemental light. Cumulative budbreak was recorded over a four-week period. Samples of bud tissues were collected during and up to 96h after a heat treatment for electrophoretic analysis. De novo synthesis of proteins was monitored by exposing excised buds to (35S)methionine for 3h. Results indicated that heat treatments of 40-45 degrees C resulted in both a release from endodormancy and a decrease in thermal units needed for budbreak during ecodormancy. The response to near-lethal heat stress was complex and affected by intrinsic levels of thermal sensitivity. The treatments were least effective during August and became more effective as endodormancy progressed. In late ecodormancy, buds were inhibited or killed by 45 degrees C. Labeling experiments indicated the synthesis of several HSPs in response to temperatures of 40-45 degrees C. Temperatures of 42.5-45 degrees C caused a shut down of protein synthesis for at least 48h. Immunoblots indicated one of the proteins was related to HSP70. Increases in free and conjugated forms of ubiquitin were also observed. The role of heat-induced protein degradation, HSPs, and ubiquitin in overcoming dormancy by near-lethal heat stress is discussed.