Vallisneria americana declined in backwaters of the Upper Mississippi River, U.S.A., after a drought in 1988. To determine whether viable seeds of V. americana occurred in the seed bank of navigation pool 7, Lake Onalaska, the upper 5 cm of sediment was collected from 103 sites in May 1990. These sediment samples were kept in pots at a depth of 0.4, 0.8, and 1.2 m in an outdoor pond for 12 weeks. Vallisneria americana seeds germinated from sites throughout the lake, and some seedlings produced overwintering buds by the end of the study. Seeds, spores, or fragments of 12 other species of aquatic plants also germinated. Seed germination trials with fresh and stored seeds in both greenhouse and ponds in which light availability was reduced with shade cloths indicated that seed germination was insensitive to light level. To determine the light requirements for seedling survival and bud production, sediment from Lake Onalaska was incubated in ponds under neutral density shade screens reducing light to 2, 5, 9, and 25% of full sun. Seeds germinated under all shade treatments but survival was significantly higher in the 9 and 25% light treatments, and bud production was restricted to these light levels.
Large beds of Vallisneria americana declined in the backwaters of the Upper Mississippi River after a drought that occurred between 1987 and 1989. One hypothesis for this decline is that low light availability may have decreased net photosynthesis to the extent that overwintering tubers were not formed. Following the decline, light availability remained low. To determine what light levels would be necessary for the re-establishment of Vallisneria in the Upper Mississippi River, the long-term growth of plants in a backwater lake and in an experimental pond was measured while the surface and subsurface light were monitored continuously. Plants grown from tubers transplanted to 0.5, 1.0 and 1.5m depth in the lake grew and produced tubers only at 0.5m depth (9% of surface light). At I-Om, light availability was less than 1 % of the surface light. Plants grown from tubers in experimental ponds with four shade treatments (2,5,9 and 25% of surface light) for the same growing period produced replacement-weight tubers in 9% light. For a longer growing season, plants also produced replacement-weight tubers in treatments with at least 5% of surface light.An average light-extinction coefficient of 4.64 m-' was calculated for the backwater lake based on continuous data collected during 94 days during the growing season from eight widely separated sites. Using equations based on the average extinction coefficient for the lake and average leaf lengths of plants grown in experimental ponds, we predict that in years with comparable turbidity, plants grown from locally collected tubers will grow and produce replacement tubers only at depths of 0.8 m or less.
The effects of purified Helminthosporium maydis T (HmT) toxin on active Ca2" transport into isolated mitochondria and microsomal vesicles were compared for a susceptible (T) and a resistant (N) strain of corn (Zea mays). ATP, malate, NADH, or succinate could drive 4"Ca2" transport into mitochondria of corn roots. Ca2" uptake was dependent on the proton electrochemical gradient generated by the redox substrates or the reversible ATP synthetase, as oligomycin inhibited ATP-driven Ca2" uptake while KCN inhibited transport driven by the redox substrates.Purified native HmT toxin completely inhibited Ca" transport into T mitochondria at 5 to 10 nanograms per milliliter while transport into N mitochondria was decreased slightly by 100 nanograms per milliliter toxin. Malate-driven Ca2" transport in T mitochondria was frequently more inhibited by 5 nanograms per milliliter toxin than succinate or ATP-driven Ca2 uptake. However, ATP-dependent Ca2" uptake into microsomal vesicles from either N or T corn was not inhibited by 100 nanograms per milliliter toxin. Similarly, toxin had no effect on proton gradient formation (Q'4Cjmethylamine accumulation) in microsomal vesicles. These results show that mitochondrial and not microsomal membrane is a primary site of HmT toxin action. HmT toxin may inhibit formation of or dissipate the electrochemical proton gradient generated by substrate-driven electron transport or the mitochondrial ATPase, after interacting with a component(s) of the mitochondrial membrane in susceptible corn.The fungus HmT3 causes leaf blight in corn with Texas malesterile cytoplasm (T) while maize with nonsterile or normal (N) cytoplasm and the same nuclear background is resistant to the disease (4, 14, 15). H. maydis race T produces a toxin (HmT toxin) which causes multiple effects in susceptible (T) plants (1,4,5,8,9,20,23,24,27 (768 D). Availability of such a purified toxin preparation allows comparisons of data from several laboratories using standardized toxin concentrations. Furthermore, a purified toxin preparation is crucial for elucidating the toxin mode of action.To understand the toxin mode of action and determine its primary site of action, we have examined the effect of purified HmT toxin on energy-dependent ion transport in isolated mitochondria and microsomal vesicles. We wanted to determine whether the toxin affected various membrane systems capable of generating ion or proton gradients in susceptible corn as suggested by Daly and Barna (5). We also wanted to determine the site of toxin action in mitochondria. This paper illustrates that an in vitro approach and direct ion transport assays can provide some answers to these questions. HmT toxin at low concentrations decreased active Ca2+ transport into isolated mitochondria of T but not N corn. A primary site of toxin action appears to be the mitochondrial membrane as active ion transport across the microsomal vesicles from susceptible corn was not affected by the toxin. A preliminary report of these findings has been presented ( 12)....
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