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Plant cells respond to invading
pathogens via complex signaling networks. Both positive and
negative signaling pathways interplay to coordinate the
development of the appropriate amplitude and duration of a
resistance response. We are employing a combination of
genetic, molecular, biochemical, and functional genomics
tools to dissect the signaling pathways that lead to
development of efficient defense mechanisms in the model
plant Arabidopsis. We have identified several
Arabidopsis genes whose mutations cause alteration in
basal resistance to the bacterial pathogen Pseudomonas
syringae. The loss of function of MODULATION OF
PATHOGEN RESPONSE 1 (MPR1), which encodes an
enzyme that hydrolyzes nucleotide derivatives including
NAD(P)H, results in enhanced resistance to the bacterial
pathogen. The mpr1 mutation causes
hyper-responsiveness to infection by a wide range of
pathogens including non-host pathogens that do not pose a
threat to the Arabidopsis plants (Figure 1). Our
preliminary results indicate that MPR1 may function as a
redox regulator by modulating cellular levels of NAD(P)/NAD(P)H.
In addition to MPR1, we are characterizing two positive
regulators of the plant innate immune response initially
identified by a functional genomics approach.
We have
also been taking a multidisciplinary approach to determine
the biological functions of the aspartic protease genes in
Arabidopsis. Aspartic protease is one of five classes
of endopeptidases that carry out limited proteolytic
processing of their substrates in cells. Proteolytic
processing results in a specific change of protein function
and is another common mechanism for achieving precise
cellular control of biological processes. The Arabidopsis
genome encodes at least 60 putative aspartic proteases (AtASPs).
Activation of one AtASPs (CDR1), which was found to
accumulate in the apoplast during pathogen infection,
results in activation of the defense response. We have
recently found that another AtASP (PCS1), which is localized
in the ER, plays an important role in regulating cell death
and cell survival. Loss of PCS1 function causes excessive
cell death of developing embryos and gametophytes, whereas
its ectopic over-expression leads to a failure in anther
dehiscence by blocking normal cell death required for the
dehiscence process (Figure 2). The study indicates that PCS1
functions as an anti-cell death component in some
developmental processes in plants.
Figure
1.
The mpr1 mutation causes hyper-responsiveness
to both the virulent Pseudomonas syringae
strain Pst and the non-host stain Psp
as indicated by remarkably stronger and more rapid
activation of the pathogenesis-related gene PR2
following infection.
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Figure 2.
PCS1 regulates the cell fates. Loss of the PCS1
function causes degeneration of embryonic cells (B),
whereas its ectopic overexpression leads to blockage
of anther dehiscence (D). Shown in (A) and (C) are a
wild-type embryo and a wild-type flower, respectively.
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