Plants
are exposed to stresses from a battery of biotic and abiotic agents
resulting in crop losses. Fungi, bacteria, nematodes, insects, and viruses
have all evolved strategies to exploit their hosts. The evolutionary
tug of war between pathogens and their host has led to the development
of polymorphic defense strategies required for resistance. Important
among these is the plant ‘innate immune system’ with a complex
set of genes involved in recognition, signal transduction, and activation
of defense responses. Plants also possess pathogen non-specific broad-spectrum
resistance. Both of those disease resistance responses have received
considerable attention and consequently important components have been
isolated or genetically defined.
However, plant genetic and cellular mechanisms involved in host response
to necrotrophic pathogens such as Botrytis cinerea are poorly understood.
Our research aims at the elucidation of the genetic and molecular control
of plant defense responses to necrotrophic pathogens, their interaction
with other defense and stress response pathways. Our current research
involves the genetic identification of plant loci required for Botrytis
resistance through analysis of mutations that enhance resistance or
susceptibility. We clone genes defined by such mutations and determine
their specific mechanism of function in disease resistance to pathogens
in general and Botrytis in particular. Genetic and molecular studies
will help place these genes in signal transduction pathways.
Why Botrytis?
My research interest with Botrytis is because of its significance as
a crop pathogen. It causes the gray mold disease in a wide range of
crop plants. Host responses to necrotrophs appear to be controlled by
a different set of genes and signaling molecules than those mediating
response to biotrophic pathogens. Genetic variation for resistance to
Botrytis has been documented in plants. However, no genetic resistance
has been identified in any plant species so far. So what defense responses
are triggered by Botrytis? What are the specific patterns associated
with Botrytis infection? What are the genetic regulators of Botrytis
response? What are the signaling molecules that mediate such response?
We use genetic, molecular and genomic approaches to find answers to
those interesting biological questions. Such findings will help design
effective and sustainable crop protection strategies through the breeding
of resistant cultivars. Our research will also contribute to the body
of knowledge on host defense response to fungal pathogens particularly
to necrotrophs.
Botrytis also causes the noble rot. The fungus develops on grapes under
certain environmental conditions and causes the grape to shrivel, concentrating
and intensifying both sugar and flavor. Botrytised grapes make very
elegant, intensely flavored dessert wines.
Zheng
Z, AbuQamar S, Chen Z and Mengiste T. (2006). Arabidopsis WRKY33
transcription factor is required for resistance to necrotrophic fungal
pathogens. The Plant J, doi: 10.1111/j.1365-313X.2006.02901.x
AbuQamar
S, Chen X, Dahwan R, Bluhm B, Salmeron J, Lam S, Dietrich RA
and Mengiste T. (2006). Expression profiling and mutant analysis reveals
complex regulatory networks involved in Arabidopsis response to Botrytis
infection. The Plant J. 48, 28-44.
Veronese
P, Nakagami H, Bluhm B, AbuQamar S, Chen X, Salmeron J, Dietrich
RA, Hirt H, Mengiste T. (2006). Distinct roles of the membrane
anchored Botrytis Induced Kinase 1 in Arabidopsis resistance to
necrotrophic and biotrophic pathogens. Plant Cell 18: 257-273.
Tadele Z, Takeda S, Hofmann I, Angelis KJ, Kaya H, Araki T, Mengiste
T,
Scheid O-M, Probst AV, Shibahara K, Scheel D, and Paszkowski J. (2004).
BRU1, a novel link between genetic/epigenetic inheritance and meristem
development in Arabidopsis. Genes and Development 18(7): 782-793.
Veronese P, Chen X, Bluhm B, Salmeron J, Dietrich R, and Mengiste
T. (2004). The BOS loci of Arabidopsis are required
for resistance to Botrytis cinerea infection. The Plant J. 40: 558-574.
Tesfaye
Mengiste, Chen,
X., Salmeron, J., Dietrich, R. 2003. The BOTRYTIS SUSCEPTIBLE1
gene encodes an R2R3MYB transcription factor protein that is required
for biotic and abiotic stress responses in Arabidopsis. The Plant
Cell 15: 2551-65.
Moez Hanin,
Tesfaye Mengiste, Augustin Bogucki and Jerzy Paszkowski (2000).
Elevated levels of intrachromosomal homologous recombination in Arabidopsis
overexpressing the MIM gene. Plant J. 24 (2), 1983-1989.
Tesfaye Mengiste and Jerzy Paszkowski (2000). The Molecular Genetics
of Homologous Recombination in Plants. pp.47-58. In: Gert E. de Vries
and K. Metzlaff (eds). Phytosfere 99- Highlights in European Plant Biotechnology
Research and Technology Transfer; Proceedings of the Second European
Conference on Plant Biotechnology, 7-9 June 1999, Rome. Elsevier. Amsterdam.
Tesfaye Mengiste, Ekaterina Revenkova, Nicole Bechtold and Jerzy
Paszkowski (1999). An SMC- like protien is required for efficient homologous
recombination in Arabidopsis. EMBO J. 18, 4505-4512.
Tesfaye Mengiste and Jerzy Paszkowski (1999). Prospects for the
precise engineering of plant genomes by homologous recombination. Biol.
Chem. 380 (7-8): 749-58.
Tesfaye Mengiste, Paolo Amedeo and Jerzy Paszkowski (1997). High-efficiency
transformation of Arabidopsis thaliana with a selectable marker gene
regulated by the
T-DNA 1'promoter. Plant J. 12 (4): 945-8.
Faculty