Associate Professor of Plant Pathology

Purdue University
Botany and Plant Pathology, Lilly Hall
915 West State Street
West Lafayette, IN 47907-2054

Office:  Lilly G-317
Phone:  (765) 494-4448
FAX:      (765) 494-0363
E-mail:   

Area: Maize Molecular Genetics and Pathology - molecular and genetic basis of maize's interaction with fungal pathogens; disease lesion mimic mutants and programmed cell death in maize.

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.