COMPARING AND CONTRASTING TWO PLANT PATHOGENS PROVIDE A UNIQUE WINDOW INTO THE DIFFERENCES IN THE INNATE IMMUNE RESPONSES BETWEEN DICOTS AND MONOCOTS 公开
Liu, Yue (2012)
Published
Abstract
iv
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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