The sudden oak death pathogen infects a bay leaf tree. Photo: Doug Schmidt, Garbelotto Lab, UC Berkeley. |
The
virulence of plant-borne diseases depends on not just the particular
strain of a pathogen, but on where the pathogen has been before landing
in its host, according to a new study from researchers at the University
of California and the United States Department of Agriculture’s
Agricultural Research Service (USDA ARS).
The
study demonstrates that the pattern of gene regulation—how a cell
determines which genes it will express and how it will express
them—rather than gene make-up alone affects how aggressively a microbe
will behave in a plant host. The pattern of gene regulation is formed by
past environments, or by an original host plant from which the pathogen
is transmitted.
“If
confirmed, this finding could add a key new dimension to how we look at
microbes because their history is going to matter and their history may
be hard to reconstruct,” said Matteo Garbelotto, an adjunct professor
of environmental science, policy and management at UC Berkeley and
corresponding author of the study.
Epigenetic
factors—for example, gene regulation mechanisms controlled by diet or
exposure to extreme environments—are well known to affect the
susceptibility of humans to some diseases. The new study, published in
the journal PLoS ONE on April 18, is the first to show a similar process
for plant pathogens. Garbelotto said other scientists have hypothesized
that gene regulation has an effect on plant pathogens, based on the
evolutionary rates of portions of the genome that are known to have an
effect on gene regulation.
“Our work provides the concrete evidence those hypotheses were correct,” he said.
Researchers
showed that genetically identical strains of the sudden oak death
pathogen isolated from different plant hosts were strikingly different
in their virulence and their ability to proliferate, and showed that
these traits were maintained long after they had been isolated from
their hosts.
“We
show that an identical strain placed in two different plant hosts will
undergo distinct changes that will persistently affect the strain’s
virulence and fitness,” said Takao Kasuga, a molecular geneticist with
the USDA ARS, and the lead author on the study.
The
implications for disease control are significant. Researchers say that
it may not be enough to know what strain of pathogens they are dealing
with in order to make treatment decisions; it also may be necessary to
know how the pathogen’s genes are being regulated. This study shows that
gene regulation may be the result of the environments the strain
inhabited before being identified.
Garbelotto
used a parallel example of a well-known human pathogen: particular
strains of the H1N1 flu virus have been identified as highly virulent,
so a diagnosis of one of these strains indicates to doctors that they
should treat that flu aggressively.
“But,
hypothetically, if you caught one of these aggressive strains of H1N1
from a guy that went to, for example, Paris, it could be 10 times more
dangerous, and you may never know from whom you got it, and it’s even
less likely that you’ll be able to learn where your infector visited
before passing the germ on to you,” Garbelotto said.
In
plants, Garbelotto said, tracking a pathogen’s history may prove even
more difficult, but correct information could give scientists a new
weapon to use against virulent strains of diseases like sudden oak
death, which can devastate forests and the ecosystems that depend on
them.
The
researchers also identified two groups of genes that are capable of
affecting virulence and whose expression patterns are indicative of the
previous host species they inhabited. Over-expression of
transposons—mobile genetic elements—combined with under-expression of
crinkler genes—genes involved in host-pathogen interactions—is
consistently associated with lowered fitness of the pathogen.
Understanding the regulation of these genes may provide scientists with
some future approaches to control the disease, such as manipulating the
gene expression to artificially reduce the aggressiveness of plant
pathogens.
While
Garbelotto stresses that more study is needed, he says if the paper’s
findings are confirmed, it could influence not just treatment but
policymaking as well.
“Most
countries impose regulations on microbes based on their genetic make
up—which ones can and can’t cross state and international lines and how
they must be transported,” he said. “Our findings suggest that when
making regulatory policy, we may also need to identify gene expression
levels and take into account the history of a microbe.”
Coauthors
on the study include Melina Kozanitas and Daniel Huberli also of UC
Berkeley, Mai Bui of the USDA ARS and David M. Rizzo, a professor of
Plant Pathology at UC Davis. The National Science Foundation’s Ecology
and Evolution of Infectious Diseases program funded the study. The US
Department of Agriculture-Forest Service’s Pacific Southwestern Research
Station Sudden Oak Death research program was also a funder.
Source: National Science Foundation