Effector-triggered immunity against Pseudomonas syringae pv. actinidiae in nonhost plants : thesis submitted to the Massey University for the degree of Doctor of Philosophy
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Date
2017
DOI
Open Access Location
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Massey University
Rights
The Author
Abstract
Pseudomonas
syringae
pv.
actinidiae
(Psa)
is
a
virulent
and
highly
damaging
pathogen
causing
bacterial
canker
in
all
currently
commercially
important
cultivars
of
kiwifruit
(Actinidia
spp.).
Arabidopsis
and
Nicotiana
spp.
plants,
however,
are
nonhosts
to
Psa.
In
our
course
of
investigating
the
various
nonhost
resistance
mechanisms
in
play
against
Psa,
we
identified
several
sources
of
resistance
against
several
Psa
strains
as
well
as
a
possible
novel
virulence
mechanism
used
by
Psa
and
Hyaloperonospora
arabidopsidis
(Hpa),
a
biotrophic
pathogen
of
Arabidopsis.
Firstly,
we
discovered
that
the
highly
virulent
strain,
Psa
V13,
triggers
hypersensitive
response
(HR)
in
Arabidopsis
in
an
accession-‐specific
manner
and
that
HopZ5PsaV13,
a
member
of
the
YopJ
family
of
putative
acetyltransferases,
confers
this
bacterial
avirulence.
We
also
show
that
the
immunity
triggered
by
HopZ5
is
independent
from
HR
in
the
Arabidopsis
accession
Col-‐0.
Through
mutagenesis,
we
show
that
key
amino
acid
residues
predicted
for
acetyltransferase
activity
are
vital
to
HopZ5-‐triggered
immunity
and
HR,
phenotypes
reproduced
in
Nicotiana
spp.
Secondly,
we
identified
multiple
sources
of
avirulence
for
the
kiwifruit
low-‐
virulence
strain,
Psa
LV5,
in
Arabidopsis
and
Nicotiana
benthamiana,
namely
homologs
of
previously
characterized
effectors,
HopAR1
and
HopAB3,
respectively.
We
additionally
show
that
HopAB3
can
trigger
resistance
in
cultivated
tomato
putatively
due
to
a
novel
recognition
by
a
cultivated
tomato
homolog
(SlPtoB)
of
the
resistance
gene
Fen.
Finally,
we
identified
several
nuclear-‐localized
effectors
from
Psa
and
Hpa
that
interact
with
Arabidopsis
WRKY
transcription
factors,
different
to
WRKYs
targeted
by
previously
identified
AvrRps4
and
PopP2.
We
show
that
some
WRKYs
can
trigger
a
cell
death
response
in
N.
benthamiana
when
overexpressed
and
that
coexpression
of
AvrRps4
or
PopP2
is
able
to
suppress
this
cell
death
response
for
the
WRKYs
they
interact
with.
We
show
that
this
suppression
is
associated
with
suppression
of
transcriptional
activation
ability
of
the
WRKY
and
7
propose
that
this
mechanism
of
transcription
suppression
may
be
utilized
by
other
Psa
and
Hpa
effectors
identified
in
this
study.
Description
Keywords
Arabidopsis, Nicotiana, Disease and pest resistance, Pseudomonas syringae, Research Subject Categories::NATURAL SCIENCES::Biology::Organism biology::Plant physiology