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How does a wound in certain plants like roses and grapevines develop into a
tumor? The answer appears to lie in a common soil bacterium that is able to
"smell" the wound and speed up the infection process, October 2005 by
Cornell University microbiologist Steve Winans says that the pathogen
Agrobacterium tumefaciens enters the wound where it copies the genes
required for infection, which can slip into the plant's cells and their
nuclear DNA, causing a cancer-like disease called crown gall. The cells of
the crown gall tumor synthesize compounds called opines, which serve as food
for the bacterial invaders.
The discovery may lead to a cure for crown gall disease, which takes a large
economic toll on fruit and wine-grape crops each year.
"Mutant forms of Agrobacterium are also widely used in agricultural
biotechnology for their ability to create transgenic plants containing new
genes of scientific or economic interest," said Winans, a professor in
Cornell's Department of Microbiology. "Perhaps these findings could be
exploited to get more effective delivery of DNA for biotechnology uses."
He is the senior author of a paper published in a recent issue of the
Proceedings of the National Academies of Science (PNAS, Vol. 102, No. 41).
"Many other disease-causing bacteria are like Agrobacterium, in that they
can detect specific chemical signal molecules that are released from plants
or animals, and respond by initiating an attack on these host organisms,"
Winans said. "For example, others have shown that the bacteria that cause
cholera express protein toxins only when they detect bile salts in the
host's intestine. It will be interesting to see whether those bacteria also
increase the replication of the genes necessary for disease."
The bacterium A. tumefaciens employs a large tumor-inducing plasmid to do
its dirty deed. The plasmid is a ring of DNA that is separate from the
chromosome and is not essential for the bacterium's survival but is required
for tumor growth. The plasmid can also transmit itself from one bacterial
cell to another when the two cells touch one another, in bacterial congress.
The plasmid recognizes organic compounds called phenols that leak out of
damaged cells when a plant is wounded. A bacterial protein called VirA acts
like an antenna, detecting phenols in a plant wound; the phenols, in turn,
signal VirA to add a phosphate (PO4) group to a related protein, VirG,
converting it into an active form.
The new study shows that the activated form of VirG causes the
tumor-inducing plasmid to replicate up to five times faster than normal by
increasing the expression of a protein called RepC, which is required for
replication of the plasmid. The extra copies of this DNA enhance the ability
of the bacterium to cause tumors, which grow when a fragment of the plasmid
DNA invades the plant's own DNA.
Crown gall tumors mostly strike the trunks or stems of dicot plants, tree or
vines near the ground where freezing occurs during winter and a wound forms
in spring. Such fruit trees as cherries and peaches, raspberries and
high-quality vine grapes like chardonnay and cabernet sauvignon tend to be
susceptible to the disease, which can stunt or kill a plant. Grafting can
also lead to infections.
"There are really no chemicals, no sprays that can control this disease,"
said Tom Burr, a plant pathology professor at Cornell and an expert on crown
gall disease. "This is really the cutting-edge research on the biology of
the pathogen, so now we can think about how to develop novel controls for
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