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Summary
The soil‐borne pathogen
R
alstonia solanacearum
causes bacterial wilt in a broad range of plants. The main virulence determinants of
R
. solanacearum
are the type
III
secretion system (
T3SS
) and its associated type
III
effectors (
T3E
s), translocated into the host cells. Of the conserved
T3E
s among
R
. solanacearum
strains, the
F
box protein RipG7 is required for
R
. solanacearum
pathogenesis on
M
edicago truncatula
. In this work, we describe the natural
rip
G
7
variability existing in the
R
. solanacearum
species complex. We show that eight representative
rip
G
7
orthologues have different contributions to pathogenicity on
M
. truncatula
: only
rip
G
7
from Asian or African strains can complement the absence of
rip
G
7
in
GMI
1000 (
A
sian reference strain). Nonetheless,
RipG
7 proteins from American and Indonesian strains can still interact with
M
. truncatula
SKP
1‐like/
MSKa
protein, essential for the function of
RipG
7 in virulence. This indicates that the absence of complementation is most likely a result of the variability in the leucine‐rich repeat (
LRR
) domain of
RipG
7. We identified 11 sites under positive selection in the
LRR
domains of
RipG
7. By studying the functional impact of these 11 sites, we show the contribution of five positively selected sites for the function of
RipG
7
CMR15
in
M
. truncatula
colonization. This work reveals the genetic and functional variation of the essential core
T3E RipG
7 from
R
. solanacearum
. This analysis is the first of its kind on an essential disease‐controlling
T3E
, and sheds light on the co‐evolutionary arms race between the bacterium and its hosts.
Sprache
Englisch
Identifikatoren
ISSN: 1464-6722
eISSN: 1364-3703
DOI: 10.1111/mpp.12302
Titel-ID: cdi_crossref_primary_10_1111_mpp_12302
Format
–
Weiterführende Literatur
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