Activation of three targets by a TAL effector confers susceptibility to bacterial blight of cotton

Brendan W. Mormile, Yan Yan, Taran Bauer, Li Wang, Rachel C. Rivero, Sara C. D. Carpenter, Catherine Danmaigona Clement, Kevin L. Cox, Lin Zhang, Xiyu Ma, Terry A. Wheeler, Jane K. Dever, Ping He, Adam J. Bogdanove () and Libo Shan ()
Additional contact information
Brendan W. Mormile: University of Michigan
Yan Yan: University of Michigan
Taran Bauer: Cornell University
Li Wang: Cornell University
Rachel C. Rivero: University of Michigan
Sara C. D. Carpenter: Cornell University
Catherine Danmaigona Clement: Texas A&M University
Kevin L. Cox: Texas A&M University
Lin Zhang: Texas A&M University
Xiyu Ma: Texas A&M University
Terry A. Wheeler: Texas A&M AgriLife Research
Jane K. Dever: Texas A&M AgriLife Research
Ping He: University of Michigan
Adam J. Bogdanove: Cornell University
Libo Shan: University of Michigan

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Bacterial transcription activator-like effectors (TALEs) promote pathogenicity by activating host susceptibility (S) genes. To understand the pathogenicity and host adaptation of Xanthomonas citri pv. malvacearum (Xcm), we assemble the genome and the TALE repertoire of three recent Xcm Texas isolates. A newly evolved TALE, Tal7b, activates GhSWEET14a and GhSWEET14b, different from GhSWEET10 targeted by a TALE in an early Xcm isolate. Activation of GhSWEET14a and GhSWEET14b results in water-soaked lesions. Transcriptome profiling coupled with TALE-binding element prediction identify a pectin lyase gene as an additional Tal7b target, quantitatively contributing to Xcm virulence alongside GhSWEET14a/b. CRISPR-Cas9 gene editing supports the function of GhSWEETs in cotton bacterial blight and the promise of disrupting the TALE-binding site in S genes for disease management. Collectively, our findings elucidate the rapid evolution of TALEs in Xanthomonas field isolates and highlight the virulence mechanism wherein TALEs induce multiple S genes to promote pathogenicity.

Date: 2025
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-025-55926-7 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-55926-7

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-025-55926-7

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().