| 1997
McCoy Award Recipient
Gregory B. Martin
Professor Agronomy
Pathogen Recognition
and Signal Transduction
in Plant Disease Resistance
The recipient
of the Herbert Newby McCoy
Award for 1997 is Gregory
B. Martin, Associate
Professor of Agronomy.
Professor Martin was born
in East Lansing, Michigan,
where he later attended
Michigan State University,
obtaining a B.S. in crop
science and a Ph.D. in
genetics at the MSU/DOE
" Plant Research Laboratory.
Martin held an NSF plant
biology fellowship to conduct
postdoctoral research at
Cornell University. He
joined the Purdue agronomy
department in 1992, where
he teaches Introduction
to Genetics, AGRY 320.
Martin was awarded a David
and Lucile Packard fellowship
in 1995. In addition to
the Packard fellowship,
Professor Martin's research
is supported by the NSF,
USDA, USDA-BARD, and Monsanto.
His research on plant disease
resistance is described
in over 25 publications
and he has presented more
than 50 lectures at universities
and various national and
international meetings
over the past five years.
Abstract of talk
Diseases caused by bacteria, fungi, viruses, and nematodes cause major economic losses to crops throughout the world.
Research in Professor Martin's laboratory focuses on understanding the molecular basis of pathogen recognition and
subsequent signal transduction events that are involved in plant disease resistance. The work focuses on resistance to
bacterial speck disease in tomato that is governed by a "gene-for-gene" interaction in which the Pto resistance gene in
the plant recognizes the expression of the avrPto avirulence gene in the pathogen. Pto encodes a protein kinase and avrPto
encodes a small hydrophilic protein. Martin's research team investigated the role of Pto and AvrPto in plant-pathogen
recognition and found that the two proteins physically interact in the plant cell. The team currently is determining the
recognition specificity domains of both AvrPto and Pto and is testing specific models to understand how the physical
interaction of these two proteins initiates disease resistance. To understand the role of the Pto kinase in signal
transduction, researchers in Professor Martin's laboratory isolated genes from tomato that encode Pto-interacting (Pti)
proteins. Pti proteins include a protein kinase (Pti1) and a class of DNA-binding proteins (Pti4/5/6). Martin will discuss
these data and present a model for the molecular basis of Pto- mediated disease resistance.
Research
Professor Martin's work focuses on understanding the molecular basis of disease resistance in plants, Most of his work has
been with tomato bacterial speck disease, which is caused by the organism Pseudomoeas syringae pv. tomato. Resistance to
bacterial speck is typical of many "gene-for-gene" interactions, in which a single resistance (R) gene in the plant
responds to the expression of a single "avirulence" (avr) gene in the pathogen. In the case of bacterial speck disease, the
Pto resistance gene in tomato responds to the expression of the avrPto gene in the bacterium. Disease susceptibility results
if either Pto or avrPto is absent in the corresponding organisms. Martin applied a new gene isolation strategy termed
"map-based" cloning to isolate the Pto resistance gene. Pto was the first gene to be isolated from a crop plant species
using map-based cloning and was the first plant disease resistance gene that participates in a gene-for-gene interaction to
be molecularly characterized. Pto proved to encode a serine-threonine protein kinase that has roles in both recognition of
the pathogen and in signal transduction leading to the activation of plant defense responses. Since the early 1980s, it had
been proposed that the molecular basis of gene-for-gene interactions might be the physical interaction of a signal molecule
produced by the pathogen and a receptor produced by the plant R gene. However, it had been unclear how such an interaction
could occur in bacterial speck resistance since Pto is probably a cytoplasmic protein and there was no evidence that the
AvrPto protein is secreted from the bacterial cell. Martin's team recently showed that the bacterial AvrPto protein
functions directly in plant cells and physically interacts with the Pto kinase. These observations provided the first
explanation of the molecular basis of a recognition process that occurs between plants and their bacterial pathogens. To
understand the steps in the Pto signaling pathway, Martin's laboratory used the yeast two-hybrid system to identify
several Pto-interacting (Pti) proteins. One of these, Ptil, encodes a protein kinase that appears to lie downstream of
Pto in a pathway leading to the localized cell death termed the "hypersensitive response." Another series of proteins,
Pti4, Pti5, and Pti6, encode putative transcription factors that are implicated in the activation of a large family of
"pathogenesis-related" (PR) genes. Professor Martin's research over the past five years at Purdue permitted the development
of a comprehensive model to explain the molecular basis of bacterial speck disease resistance. In this model, it is
proposed that the AvrPto protein is secreted by Pseudomonas directly into plant cells where it physically interacts with
the cytoplasmic kinase Pto. The physical interaction of Pto and AvrPto determines the specific recognition between plants
with the Pto gene and Pseudomonas bacteria carrying avrPto. This recognition event, which also may involve the Prf protein
(known to be required for Pto-mediated resistance), activates the Pto kinase. In response, the Pto kinase phosphorylates
and activates diverse downstream target proteins, each of which plays a unique role in signaling the resistance response.
Ultimately, disease resistance is determined by the activation of a variety of defense responses including the oxidative
burst, defense gene expression, and the hypersensitive response. In the course of his research at Purdue, Gregory Martin
has worked with Professors Ray Bressan, Alan Friedman, Phil Low, Sally MacKenzie, Randy Woodson, and many outstanding
graduate students and postdoctoral scientists.
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