TAL effector driven induction of a SWEET gene confers susceptibility to bacterial blight of cotton
Transcription activator-like (TAL) effectors from Xanthomonas citri subsp. malvacearum ( Xcm ) are essential for bacterial blight of cotton (BBC). Here, by combining transcriptome profiling with TAL effector-binding element (EBE) prediction, we show that GhSWEET10 , encoding a functional sucrose tra...
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Published in | Nature communications Vol. 8; no. 1; pp. 15588 - 14 |
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Main Authors | , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
24.05.2017
Nature Publishing Group Nature Portfolio |
Subjects | |
Online Access | Get full text |
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Summary: | Transcription activator-like (TAL) effectors from
Xanthomonas citri
subsp.
malvacearum
(
Xcm
) are essential for bacterial blight of cotton (BBC). Here, by combining transcriptome profiling with TAL effector-binding element (EBE) prediction, we show that
GhSWEET10
, encoding a functional sucrose transporter, is induced by Avrb6, a TAL effector determining
Xcm
pathogenicity. Activation of
GhSWEET10
by designer TAL effectors (dTALEs) restores virulence of
Xcm avrb6
deletion strains, whereas silencing of
GhSWEET10
compromises cotton susceptibility to infections. A BBC-resistant line carrying an unknown recessive
b6
gene bears the same EBE as the susceptible line, but Avrb6-mediated induction of
GhSWEET10
is reduced, suggesting a unique mechanism underlying
b6
-mediated resistance. We show via an extensive survey of
GhSWEET
transcriptional responsiveness to different
Xcm
field isolates that additional
GhSWEETs
may also be involved in BBC. These findings advance our understanding of the disease and resistance in cotton and may facilitate the development cotton with improved resistance to BBC.
Transcription activator-like effectors contribute to virulence of the
Xanthomonas
strain responsible for bacterial blight in cotton. Here Cox
et al
. show that the
Xanthomonas
Avrb6 effector induces expression of the cotton SWEET10 sugar transporter and that this induction promotes disease. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this work. Present address: Institute of Molecular Physiology, Heinrich Heine University Düsseldorf and Max Planck Institute for Plant Breeding Research, 50829 Köln, Germany |
ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/ncomms15588 |