RT Journal Article
SR Electronic
T1 <em>Arabidopsis</em> UGT76B1 glycosylates <em>N</em>-hydroxy-pipecolic acid and inactivates systemic acquired resistance in tomato
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.07.06.189894
DO 10.1101/2020.07.06.189894
A1 Eric C. Holmes
A1 Yun-Chu Chen
A1 Mary Beth Mudgett
A1 Elizabeth S. Sattely
YR 2020
UL http://biorxiv.org/content/early/2020/07/07/2020.07.06.189894.abstract
AB Systemic acquired resistance (SAR) is a mechanism that plants utilize to connect a local pathogen infection to global defense responses. N-hydroxy-pipecolic acid (NHP) and a glycosylated derivative are produced during SAR, yet their individual roles in the response have not yet been elucidated. Here we report that Arabidopsis thaliana UGT76B1 can generate glycosylated NHP (NHP-Glc) in vitro and when transiently expressed alongside Arabidopsis NHP biosynthetic genes in two Solanaceous plants. During infection, Arabidopsis ugt76b1 mutants do not accumulate NHP-Glc and accumulate less glycosylated salicylic acid (SA-Glc) than wild type plants. The metabolic changes in ugt76b1 mutant plants are accompanied by enhanced defense to the bacterial pathogen Pseudomonas syringae, suggesting that glycosylation of SAR molecules NHP and SA by UGT76B1 plays an important role in defense modulation. Transient expression of Arabidopsis UGT76B1 with the Arabidopsis NHP biosynthesis genes ALD1 and FMO1 in tomato increases NHP-Glc production and reduces NHP accumulation in local tissue, and abolishes the systemic resistance seen when expressing NHP-biosynthetic genes alone. These findings reveal that the glycosylation of NHP by UGT76B1 alters defense priming in systemic tissue and provide further evidence for the role of the NHP aglycone as the active metabolite in SAR signaling.