More than a quarter of the world's irrigated acreage is so salty that it limits agricultural productivity. This has galvanized efforts to develop crops more tolerant of high-sodium conditions. But as a high sodium environment is likely to affect many processes within plant cells, it had been thought that engineering salt-tolerant plants would require the manipulation of many genes. However, a US—Canadian team of researchers has now provided a much simpler solution: By introducing into tomatoes a single gene that encodes a protein that pumps out excess salt before it does its damage, they have engineered plants able to not only flourish in salty water, but also produce edible fruit.
Plants mediate the inflow of sodium ions (Na+) and outflow of hydrogen ions (H+) from membrane-bound cellular compartments called vacuoles by special membrane channels known as Na+/H+ antiports. This led researchers Hong-Xia Zhang and Eduardo Blumwald to hypothesize that plants may be able to avoid damage from excessive salt if they were to segregate Na+ from intracellular water for storage in vacuoles. To find out whether this could work for tomato plants, they introduced a DNA sequence that contained a gene, AtNHX1, from thale cress (Arabidopsis thaliana), resulting in the overexpression of the Na+/H+ antiport. The transgenic plants were then grown in water containing 200 mM sodium chloride-a concentration known to inhibit growth of nearly all crop plants. Nontransgenic tomato plants grown in the same salty conditions either died or were severely stunted. In contrast, the transgenic tomatoes grew, flowered, and produced fruit. What's more, although the leaves of the transgenic plants contained very high concentrations of sodium, the fruits were not tainted by salt.
Transgenic salt-tolerant tomato plants accumulate salt in foliage but not in fruitpp 765 - 768 Hong-Xia Zhang & Eduardo Blumwald doi:10.1038/90824 Abstract|Full
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Diphtheria toxin is so poisonous to humans that a single molecule may be enough to kill a cell. However, biotechnology researchers have harnessed that toxicity to develop a model of hepatitis, a fatal disease of the liver that affects millions of people worldwide: They have shown that a transgenic mouse containing the human receptor for diphtheria in its liver can easily be induced by the toxin to replicate the symptoms of hepatitis—an approach that will aid efforts to understand and treat liver disease.
Scientists often try to selectively kill specific types of cells in mice in order to see whether the resulting effects mimic certain diseases, but current methods for doing this have serious limitations: Removing cells using surgery or lasers, for instance, cannot target cells at the molecular level, and chemicals that home to specific cell types are rare. And while some researchers have attempted to use genetic engineering to induce specific tissues to express protein toxins, cell death occurs early in the life of the animal and cannot be controlled experimentally, with these methods. The new strategy, however, developed by Kenji Kohno and colleagues in Japan, allows researchers to destroy mouse liver cells at will by injecting the mice with diphtheria toxin.
Diphtheria toxin can enter a cell only by fitting into a specific receptor molecule on the cell's surface, like a key into a lock. Mice are naturally resistant to diphtheria toxin because their receptor is a slightly different shape than that in humans. So the researchers genetically modified mice to produce the human diphtheria toxin receptor in their livers, making their liver cells susceptible to diphtheria toxin: When these transgenic mice were injected with toxin, their liver cells were selectively killed and the mice developed liver disease, while unmodified mice were unaffected.
By redirecting expression of the diphtheria toxin receptor to different tissues, it is likely that this strategy could be used to model diseases in other organs.
One of the leading sources of pollution is the phosphate in animal manure that is spread on fields as fertilizer, which leaks into rivers and streams wrecking havoc on aquatic life. Animals such as pigs and chickens are major culprits because they lack the enzyme phytase, which is needed to digest phytates, the main source of phosphorus in plant feed. Now Cecil Forsberg and colleagues at the University of Guelph (Ontario, Canada) explain how genetic modification could help pigs clean up their act.
The team genetically engineered pigs to produce the missing phytase in their saliva, creating animals that can now digest the phytates. The genetically modified pigs excrete 75% less phosphorus in their manurean improvement on the 56% reduction that can be achieved by supplementing animal feed with phytase enzyme. Moreover, because the transgenic swine can now digest plant phosphorus, which is essential for their health, no dietary supplement of this mineral is needed, further reducing pollution.
Transgenic herds of swine could be a unique biological strategy for cleaning up the environment.
Pigs expressing salivary phytase produce low-phosphorus manurepp 741 - 745 Serguei P. Golovan, Roy G. Meidinger, Ayodele Ajakaiye, Michael Cottrill, Miles Z. Wiederkehr, David J. Barney, Claire Plante, John W. Pollard, Ming Z. Fan, M. Anthony Hayes, Jesper Laursen, J. Peter Hjorth, Roger R. Hacker, John P. Phillips & Cecil W. Forsberg doi:10.1038/90788 Abstract|Full
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