Natural loss‐of‐function mutation of EDR1 conferring resistance to tomato powdery mildew in A rabidopsis thaliana accession C24
To screen for potentially novel types of resistance to tomato powdery mildew O idium neolycopersici , a disease assay was performed on 123 A rabidopsis thaliana accessions. Forty accessions were fully resistant, and one, C24 , was analysed in detail. By quantitative trait locus ( QTL ) analysis of a...
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Veröffentlicht in: | Molecular plant pathology 2015-01, Vol.16 (1), p.71-82 |
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Sprache: | eng |
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Zusammenfassung: | To screen for potentially novel types of resistance to tomato powdery mildew
O
idium neolycopersici
, a disease assay was performed on 123
A
rabidopsis thaliana
accessions. Forty accessions were fully resistant, and one,
C24
, was analysed in detail. By quantitative trait locus (
QTL
) analysis of an
F
2
population derived from
C24
×
S
ha (susceptible accession), two
QTL
s associated with resistance were identified in
C24
. Fine mapping of
QTL
‐1 on chromosome 1 delimited the region to an interval of 58 kb encompassing 15 candidate genes. One of these was
Enhanced Disease Resistance 1
(
EDR1
). Evaluation of the previously obtained
edr1
mutant of Arabidopsis accession Col‐0, which was identified because of its resistance to powdery mildew
G
olovinomyces cichoracearum
, showed that it also displayed resistance to
O
. neolycopersici
. Sequencing of
EDR1
in our
C24
germplasm (referred to as
C24
‐
W
) revealed two missing nucleotides in the second exon of
EDR1
resulting in a premature stop codon. Remarkably,
C24
obtained from other laboratories does not contain the
EDR1
mutation. To verify the identity of
C24
‐
W
, a
DNA
region containing a single nucleotide polymorphism (
SNP
) unique to
C24
was sequenced showing that
C24
‐
W
contains the
C24
‐specific nucleotide.
C24
‐
W
showed enhanced resistance to
O
. neolycopersici
compared with
C24
not containing the
edr1
mutation. Furthermore,
C24
‐
W
displayed a dwarf phenotype, which was not associated with the mutation in
EDR1
and was not caused by the differential accumulation of pathogenesis‐related genes. In conclusion, we identified a natural
edr1
mutant in the background of
C24
. |
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ISSN: | 1464-6722 1364-3703 |
DOI: | 10.1111/mpp.12165 |