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Researchers at Yale have identified a gene that regulates the major immune
response in plants, programmed cell death (PCD), according to a recent
report in the journal Cell, June 2005.

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
(NIGMS). "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 (NIGMS / NIAID) and a NSF
Plant Genome grant.

[www.yale.edu]

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