COMPARING AND CONTRASTING TWO PLANT PATHOGENS PROVIDE A UNIQUE WINDOW INTO THE DIFFERENCES IN THE INNATE IMMUNE RESPONSES BETWEEN DICOTS AND MONOCOTS Open Access

Liu, Yue (2012)

Permanent URL: https://etd.library.emory.edu/concern/etds/9306t0196?locale=en
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Abstract

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ABSTRACT

COMPARING AND CONTRASTING TWO PLANT PATHOGENS PROVIDE A
UNIQUE WINDOW INTO THE DIFFERENCES IN THE INNATE IMMUNE
RESPONSES BETWEEN DICOTS AND MONOCOTS
The eukaryotic parasitic plant Striga asiatica and the prokaryotic Agrobacterium
tumefaciens
are both plant pathogens that cue on host-derived phenylpropanoids for host
recognition. The onset of virulence in both pathogens is regulated by a wounding event,
but one manifested in slightly different ways. S. asiatica mimics a partial wounding
response by producing reactive oxygen species on host contact, whereas A. tumefaciens
depends on the wounding response of host plants to generate susceptible plant cells for
transformation. Despite the similarity in their chemical strategy for host recognition, A.
tumefaciens
and S. asiatica pathogenize non-overlapping host ranges; monocotyledonous
grasses are resistant to A. tumefaciens, but susceptible to S. asiatica. These two plant
pathogens then provide a unique window into the differences in the innate immunity of
dicots and monocots. The engineering potential of A. tumefaciens further provides an
opportunity to map the signaling landscape at the host-pathogen interface. This study
represents the first example of mapping systemically the virulence inducing signal
landscape in vivo and in real time. I quantified not only the concentration of wound-
induced phenol and sugar signals separately, but the duration of exudation. These results
demonstrated that the fundamental difference in the wounding response between dicots
and grasses is communicated via their wound-induced phenol exudation. A. tumefaciens
recognizes dicots by the high level and extended exudation of wound-induced phenols,
whereas grasses remain invisible to A. tumefaciens by not inducing phenol exudation.
The modular nature of the subterranean development of S. asiatica further provides a
valuable opportunity to study genetic regulation of development via differential
expression libraries. The immune response genes and phenylpropanoid biosynthetic
genes found in the differential libraries highlighted again the critical roles that the
wounding response and phenol production play in plant pathogenesis. Our study on the
phenylpropanoid biosynthetic genes further indicated that phenolpropanoids play a most
critical role in regulating plant development beyond lignin biosynthesis. Lastly, the
interaction between quinolic haustorial inducers and auxin/cytokinin signaling pathways
suggest a possible evolutionary route for the parasitic plants in Scrophulariaceae and
Orobanchaceae to have emerged.

v
COMPARING AND CONTRASTING TWO PLANT PATHOGENS PROVIDE A
UNIQUE WINDOW INTO THE DIFFERENCES IN THE INNATE IMMUNE
RESPONSES BETWEEN DICOTS AND MONOCOTS
B. S., Beijing University, 2003
Advisor: David G. Lynn, PhD.
A dissertation submitted to the Faculty of the
James T. Laney School of Graduate Studies of Emory University
in partial fulfillment of the requirements for the degree of
Doctor of Philosophy
Department of Chemistry
2012

Table of Contents

ix

Table of Contents

Chapter 1 Introduction…………………………………………………………………........................1
Bibliography ....................................................................................................................8
Chapter 2 Dissecting the genetic regulation of haustorium development and shoot
initiation of Striga asiatica by differential expression libraries……………………...................11
2.1 Introduction .............................................................................................................11
2.2 Results ....................................................................................................................14
2.3 Discussion ................................................................................................................32
2.4 Methods ..................................................................................................................37
Bibliography ...................................................................................................................40
Chapter 3 Phenylpropanoids and the regulation of plant growth and
development ……………………………………………………………………………........................44
3.1 Introduction .............................................................................................................44
3.2 Results ....................................................................................................................46
3.3 Discussion ................................................................................................................53
3.4 Methods ..................................................................................................................56
Bibliography ...................................................................................................................60
Chapter 4 Haustorium inducing benzoquinone signals interact with auxin/cytokinin
signaling pathways to mediate haustorial development in Striga asiatica …………..............65
4.1 Introduction .............................................................................................................65
4.2 Results ....................................................................................................................67

x

4.3 Discussion ................................................................................................................80
4.4 Methods ..................................................................................................................85
Bibliography .................................................................................................................. 90
Chapter 5 Mapping the signaling landscape with a plant pathogen Agrobacterium
tumefaciens ……………………………………………………………............................................97
5.1 Introduction ..............................................................................................................97
5.2 Results ...................................................................................................................101
5.3 Discussion ...............................................................................................................133
5.4 Methods .................................................................................................................136
Bibliography ..................................................................................................................140
Chapter 6 Conclusion…………………………………………………………………........................151
Bibliography ..................................................................................................................157

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