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How cell suicide protects plants from infection

Yale University : 09 June, 2005  (New Product)
To protect themselves from viruses, plants create a zone of dead cells around an infection site that prevents the infection from spreading. Savithramma Dinesh
Researchers at Yale have identified a gene that regulates the major immune response in plants, programmed cell death, according to a recent report in the journal Cell.

To protect themselves from viruses, plants create a zone of dead cells around an infection site that prevents the infection from spreading. Savithramma Dinesh–Kumar, associate professor of Molecular, Cellular and Developmental Biology at Yale and his colleagues discovered how the plants keep from killing themselves after they turn on the cell–suicide PCD process.

Dinesh–Kumar first developed a technique for silencing or inactivating plant genes, a technique that is now used by several research groups. His group studies the interaction between plants and viruses using tobacco as a model system.

They identified and silenced a 'pro–survival' gene, BECLIN–1, that is important in the PCD response. When BECLIN–1 is active, infection is localized to a small number of cells that later die and form discrete brown lesions on the leaves. When the gene is inactivated, the plant can no longer regulate PCD, leading to cell death throughout the leaf and plant.

PCD has been described in virtually all cell types, both plant and animal. It is an important aspect of many biological processes including immune system function, embryonic development and elimination of defective cells. Failure of PCD can result in devastating diseases such as cancer, Alzheimer's and AIDS.

'This work gives us a better understanding of how plants fend off microbial attacks through carefully controlled destruction of infected cells,' said James Anderson, of the Division of Genetics and Developmental Biology at the National Institute of General Medical Sciences. 'Like other studies carried out in model organisms, these findings shed light on similar processes that occur in mammals, and may eventually be used to better human health.'

Collaborators in the research include Yule Liu and Michael Schiff at Yale, Kirk Czymmek at Delaware Biotechnology Institute, Zsolt Tallóczy at Columbia University and Beth Levine at Texas Southwestern.The work was supported by grants from the National Institutes of Health and a NSF Plant Genome grant.
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