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Peer-reviewedCC BY-NC-ND 4.0Plant Physiology

A Xanthomonas effector increases virulence quantitatively by inducing at least three minor susceptibility genes

Abstract

The transcription activator-like effector Tal12a is widely conserved among Xanthomonas campestris pv. campestris strains that cause black rot in Brassica crops. However, its role in disease remains unclear. To investigate how Tal12a contributes to pathogenesis, we combined transcriptomic profiling of cauliflower leaves infected with Tal12a-expressing strains, prediction of TALE-binding elements, and heterologous expression assays in Nicotiana benthamiana. The aim of this approach was to identify candidate susceptibility genes. Artificial TALEs were further employed to validate the contribution of these candidate targets to disease development. Tal12a enhanced both virulence and bacterial growth in cauliflower. Transcriptome analysis revealed 380 genes that were induced upon infection, nine of which were prioritised as candidates. Seven of these were confirmed as direct Tal12a targets, while the induction of the sugar transporter genes BoSWEET13 and BoSWEET14c likely occurred indirectly. Functional assays demonstrated that these two SWEET genes and the BoIAA7c gene, which encodes auxin-dependent transcriptional regulator, contribute to disease development. These findings identify the first susceptibility genes in cauliflower and reveal that Tal12a promotes disease through a complex transcriptional reprogramming, involving direct and indirect target induction, with several genes functioning as minor susceptibility factors.

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BibTeX
@article{charleux2026xanthomonas,
  title = {{A Xanthomonas effector increases virulence quantitatively by inducing at least three minor susceptibility genes}},
  author = {Brice Charleux and Carine Gris and Sébastien Carrère and Alvaro Pérez-Quintero and Aurélie Le Ru and Caroline Bellenot and Ivanna Fuentes and Zoë Dubrow and Adam Bogdanove and Laurent Noël and Corinne Audran},
  journal = {Plant Physiology},
  year = {2026},
  month = sep,
  doi = {10.1093/plphys/kiag665},
  url = {https://hal.science/hal-05747137v1},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - A Xanthomonas effector increases virulence quantitatively by inducing at least three minor susceptibility genes
AU  - Brice Charleux
AU  - Carine Gris
AU  - Sébastien Carrère
AU  - Alvaro Pérez-Quintero
AU  - Aurélie Le Ru
AU  - Caroline Bellenot
AU  - Ivanna Fuentes
AU  - Zoë Dubrow
AU  - Adam Bogdanove
AU  - Laurent Noël
AU  - Corinne Audran
PY  - 2026
DA  - 2026/09/05
JO  - Plant Physiology
DO  - 10.1093/plphys/kiag665
UR  - https://hal.science/hal-05747137v1
AB  - The transcription activator-like effector Tal12a is widely conserved among Xanthomonas campestris pv. campestris strains that cause black rot in Brassica crops. However, its role in disease remains unclear. To investigate how Tal12a contributes to pathogenesis, we combined transcriptomic profiling of cauliflower leaves infected with Tal12a-expressing strains, prediction of TALE-binding elements, and heterologous expression assays in Nicotiana benthamiana. The aim of this approach was to identify candidate susceptibility genes. Artificial TALEs were further employed to validate the contribution of these candidate targets to disease development. Tal12a enhanced both virulence and bacterial growth in cauliflower. Transcriptome analysis revealed 380 genes that were induced upon infection, nine of which were prioritised as candidates. Seven of these were confirmed as direct Tal12a targets, while the induction of the sugar transporter genes BoSWEET13 and BoSWEET14c likely occurred indirectly. Functional assays demonstrated that these two SWEET genes and the BoIAA7c gene, which encodes auxin-dependent transcriptional regulator, contribute to disease development. These findings identify the first susceptibility genes in cauliflower and reveal that Tal12a promotes disease through a complex transcriptional reprogramming, involving direct and indirect target induction, with several genes functioning as minor susceptibility factors.
SN  - 0032-0889
SN  - 1532-2548
ER  -