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BBSRC announces its new ROPA awards
October 12, 1998The Biotechnology and Biological Sciences Research Council (BBSRC) has announced its 1998 round of Realising Our Potential Awards (ROPAs). BBSRC is making 40 awards under the updated scheme in which awards can be made across all areas of research in each Research Council.
The full list of BBSRC awards appears on pp10-11 of the current issue of bbsrc business. Projects of particular interest include:
1. Improving salt tolerance in plants
Usually plants will not grow very well in salty conditions. By understanding how plants cope with excess salt scientists may be able to modify them to grow better in adverse saline conditions. This could have significant implications for increased crop production on poor quality and irrigated land, for example rice production in developing countries.
Plant cells contain pumps that control the passage of chemicals (ions) in and out of the cell to maintain the conditions required for chemical reactions. The problems posed by saline conditions are mainly linked to an excess of sodium ions (Na+), and there is a specific Na+ transporter to pump sodium ions out of the cell in saline conditions.
Only some plant cells appear able to control salt tolerance. Plants that can prevent Na+ reaching their shoot cells do well in salty conditions; but this is only achieved by having efficient Na+ pumps in the root cells, which must pump the Na+ away from the plant transport system (xylem) that feeds the shoot.
This project will examine whether genes for Na+ transporters inserted into specific cells of the genetic model plant Arabidopsis thaliana can improve salt tolerance in the plant. Once this has been investigated, it may be possible to extend the work to plants of agricultural importance.
Contact: Dr Mark Tester, University of Cambridge Department of Plant Sciences
Tel 01223 333918
Fax 01223 333953
E-mail mat10@cam.ac.uk
2. How do cells cope with DNA mutations?
Much of our understanding of how genes work comes from observing what happens when a normal or wild-type gene goes wrong. The subsequent change in function can indicate how the gene and the protein it normally produces would be used.
Change or mutation in DNA may occur naturally or be induced by chemicals or radiation. Previous work has suggested that changes of single DNA bases accumulate at least 10 times faster in the sections of "packaging" DNA (introns) than in the DNA that actually codes for proteins (exons). This project aims to check this observation by measuring the rate and timing of new mutations in a broader sample of DNA.
The research will help us understand how the cell identifies mutations and the extent to which it can repair them. It will have important implications for work in plant and animal breeding, much of which relies on examining the effect of particular mutations. It may also have implications for evolutionary theory.
Contact: Professor James Parry, University of Wales Swansea Dept. Biol. Sci.
Tel 01792 295385
Fax 01792 295447
E-mail jmp@swansea.ac.uk
3. Potential improvements for cancer drug design
Cells have an in-built quality control mechanism to detect proteins that are incorrectly assembled and target them for destruction in the cell liquid or cytosol. Control is exerted within a network of membranes called endoplasmic reticulum (ER), which transports proteins throughout the cell. Certain toxic proteins can take advantage of the ER export machinery to reach the cytosol where they avoid destruction, and exert their toxicity, often by modifying other proteins and preventing them from functioning.
How do toxic proteins escape destruction in the cell? If we can identify the strategies that allow this to happen, it could be especially useful for improving the specificity of drugs whose toxicity is harnessed to destroy particular cells such as tumour cells. For example, ricin has shown particular promise as a cancer drug, but it currently causes unacceptable side effects in non-tumour cells. Improved understanding of how the drug gets through the ER means it might be possible to administer a form that is only activated in the ER of tumour cells, thus avoiding side effects in other cells.
Contact: Professor Mike Lord, University of Warwick Dept. Biol. Sci.
Tel 01203 523598
Fax 01203 523701
E-mail ml@dna.bio.warwick.ac.uk
Biotechnology and Biological Sciences Research Council (BBSRC)
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