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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Crop Germplasm Research » Research » Publications at this Location » Publication #323546
Title: TAL effector-mediated susceptibility to bacterial blight of cotton

Author
item COX, KEVIN - Texas A&M University
item MENG, FANHONG - Texas A&M University
item WILKINS, KATIE - Cornell University
item Yu, John
item HE, PING - Texas A&M University
item BOGDANOVE, ADAM - Cornell University
item SHAN, LIBO - Texas A&M University

Submitted to: Plant and Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/13/2015
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Bacterial blight of cotton (BBC) caused by Xanthomonas campestris pv. malvacearum (Xcm) is a destructive disease that has recently re-emerged in the U.S. Xcm injects transcription activator-like (TAL) effectors that directly induce the expression of host susceptibility (S) or resistance (R) genes. Although more than ten Xcm TAL effectors have been characterized, no corresponding S or R genes have been identified in cotton. Avrb6, a key TAL effector in Xcm, plays a major role in promoting pathogenicity in cotton susceptible lines. By using a systems approach combining genome-wide transcriptome profiling and TAL effector binding site (EBE) computational prediction, we found that GhSWEET1, encoding a sugar transporter, is highly induced in cotton by Xcm Avrb6. Importantly, the promoter of GhSWEET1 possesses an EBE site that is specifically activated by Avrb6. Silencing of GhSWEET1 in cotton via virus-induced gene silencing (VIGS) showed reduced susceptibility to the infections by Xcm carrying avrb6, whereas activation of GhSWEET1 by designed TAL effectors enhanced susceptibility of Xcm. Thus, GhSWEET1 is an S gene of Xcm avrb6 for promoting Xcm pathogenicity in cotton. GhSWEET1 contributes to pathogenicity likely via sugar efflux to apoplast to promote Xcm proliferation. We are deploying CRISPR-CAS to engineer the EBE of GhSWEET1 to avoid the induction by Xcm, thereby biologically controlling this important disease.