Education
M.S.,
Punjab Agricultural University, India - Genetics
Ph.D., Simon Fraser University, B.C., Canada -
Biological Sciences with emphasis on plant pathology
Background
July
2004 – present
Associate Professor of Plant Pathology, Department of Botany and Plant Pathology,
Purdue University
June 2002 – June
2004
Assistant Professor of Plant Pathology, Department of Botany and Plant Pathology,
Purdue University
March 1998 – June 2001
Senior Research Scientist, Disease Resistance Group, Pioneer Hi-Bred
International Inc.
March 1993 – February 1999
Assistant Professor of Maize Genetics, Department of Agronomy, University
of Missouri
Research
Interests
How is
it that plants are constantly exposed to potential pathogens but
seldom succumb to disease? My group is addressing this question in
maize by determining the nature of resistance mechanisms that are
called into action when confronted with fungal pathogens and how
these mechanisms are breached or avoided during interactions that
result in disease. Using a combination of genetic, genomic, molecular
and cell biological approaches, we are presently focusing our efforts
on two contrasting maize diseases. One of these diseases, characterized
by severe leaf blight and ear rot symptoms, is caused by race 1 of
Cochliobolus carbonum. A key perpetrator of this disease
is HC-toxin, a cyclic tetrapeptide, which the fungus needs to cause
disease. Answering how HC-toxin coaxes maize to change from a resistant
to a susceptible form is the major thrust of our research.
The
second disease is Fusarium ear mold, infamous not only for
the damage it does to ears but also for Fumonisin, a mycotoxin responsible
for many maladies in humans and the live stock. Virtually nothing
is known about how this disease develops, what part of the host allows
fungal ingress in developing kernels, and how resistant maize cultivars
succeed in fending off the pathogen.
In addition
to bona fide diseases, we also utilize a collection of maize mutations
- called disease lesion mimics – to elucidate genes
and pathways that may be of relevance to maize’s interaction with
pathogens. Of more than 50 disease lesion mimics presently available
in maize, genes responsible for five independent mimics have been recently
cloned and characterized in our group. While proving invaluable in enhancing
our knowledge of how plants cope with stresses, lesion mimics are also
providing excellent tools for dissecting cell death mechanisms and pathways
in plants.
Assistantships
and Positions
Please
contact me directly for information on assistantships and openings
in my program. Follow these links for general information on graduate
programs or employment announcements.
Selected
Publications
Penning, B.W., G.S. Johal and M.M. McMullen. 2004.
A major suppressor of cell death, slm1, modifies the expression
of the maize (Zea mays L.) lesion mimic mutation les23.
Genome 47: 961-969.
Yang, M.Y., E. Wardzala, G.S. Johal,
and Gray J. 2004.
The wound-inducible Lls1 gene
from maize is an ortholog of the Arabidopsis Acd1 gene, and
the LLS1 protein is present in non-photosynthetic tissues. Plant Molecular
Biology 54: 175-191.
Multani, D.S., S.P. Briggs, M.A. Chamberlin, J.J. Blakeslee, A.S.
Murphy, and G.S. Johal. 2003. Loss of an MDR transporter
in compact stalks of maize br2 and sorghum dw3 mutants.
Science 302: 81-4.
Links to Abstract or Full Text
Gray,
J., D. Janick-Buckner, B. Buckner, P. Close, and G.S. Johal.
2002. Light-dependent death of maize lls1 cells is mediated by functional
chloroplasts. Plant Physiology. 130: 1894-907.
Nadimpalli R., N. Yalpani, G.S. Johal, and C.R. Simmons.
2000. Prohibitins, stomatins, and plant disease response genes compose
a protein superfamily that controls cell proliferation, ion channel
regulation and death. J. Biological Chemistry 275: 29579-29586.
Buckner, B., D. Janick-Buckner and G.S. Johal. 2000.
Cell death in maize. Physiologia Plantarum 108: 231-239.
Hu, G., N. Yalpani, S.P. Briggs and G.S. Johal. 1998.
A porphyrin pathway impairment is responsible for the phenotype of
a dominant disease lesion mimic mutant of maize. Plant Cell 10: 1095-1105.
Buckner, B., D. Janick-Buckner, J. Gray and G.S. Johal.
1998. Cell death mechanisms in maize. Trends in Plant Science 3:
218-223.
Multani, D.S., R.B. Meeley, A.H. Paterson, J. Gray, S.P. Briggs and G.S. Johal.
1998. Plant-pathogen micro evolution: Molecular basis for the origin
of a fungal disease in maize. Proceedings of the
National Academy of Sciences U.S.A. 95: 1686-1691.
Gray, J., P.S. Close, S.P. Briggs and G.S. Johal. 1997.
A novel suppressor of cell death in plants encoded by the Lls1 gene
of maize. Cell 89: 25-31.
Johal, G.S., S. Hulbert and S.P. Briggs. 1995. Disease
lesion mimic of maize: a model for cell death in plants. BioEssays
17: 685-692.
Johal, G.S., J. Gray, D. Gruis and S.P. Briggs. 1995.
Convergent insights into mechanisms determining disease and resistance
responses in plant-fungal interactions. Canadian J. of Botany 73S:
468-474.
Briggs, S.P. and Johal, G.S. 1994. Genetic patterns
of host-pathogen interactions. Trends in Genetics 10: 12-16.
Johal, G.S. and S.P. Briggs. 1992. Reductase activity
encoded by the HM1 disease resistance gene in maize. Science 258:
985-987.
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