Submitted to: Photosynthesis International Congress Symposium Proceedings and Abstracts
Publication Type: Proceedings
Publication Acceptance Date: 6/24/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: The low temperature sensitivity of photosynthesis is an important contributing element in limiting the growth and productivity of numerous economically significant crops of temperate North America (e.g. corn, soybean, tomato). These crops have in common a tropical or subtropical evolutionary origin and lack the genetic information necessary to cope with low temperature. Because of its significant impact on agriculture, the biochemical and molecular basis for chilling sensitivity of photosynthesis has been very active area of research for nearly two decades. One of the major challenges in this research arena is to trace the cause and effect relationship back to the primary events that actually distinguish chilling-sensitive from chilling-tolerant plant species. We have taken advantage of recent discovery in our lab that chilling causes the endogenous rhythm controlling many important functions in plants to lose its time keeping ability. Here we show that the timing of the activation of an important enzyme in sucrose metabolism is interrupted by chilling. This result, as well as the experimental approaches employed, should be of interest to wide range of plant biologist and agricultural scientists involved with environmental stress research.
Technical Abstract: Sucrose phosphate synthase (SPS), a key enzyme in sucrose biosynthesis, is regulated by protein phosphorylation and shows a circadian pattern of activity in tomato. SPS is most active in its dephosphorylated state which normally coincides with daytime. Applying okadaic acid, a potent phosphatase inhibitor, prevents SPS activation. More interesting is that a brief treatment with cycloheximide, a cytoplasmic translation inhibitor, also prevents the light activation of SPS, without any effect on the amount of SPS protein. Cordycepin, a transcription inhibitor, has the same effect. Both of these inhibitors also inhibit the activation phase of the cricadian rhythm in SPS activity. Conversely, cycloheximide and cordycepin do not prevent the decline in circadian SPS activity. These observations indicate that SPS-phosphatase activity, but not SPS-kinase activity, is controlled at the level of gene expression. Taken together, it seems clear that there is a circadian rhythm controlling the transcription of SPS-phosphatase which subsequently dictates the circadian rhythm in SPS activity via effects on its phosphorylation state.