​Plant Cell | Zhang Yuelin/Ivo Feussner collaborates to reveal the mechanism by which the glycosyltransferase UGT76B1 regulates plant immunity

Responsible Editor | Wang Yi plant needs to strictly regulate its own immune response to maintain the balance between growth and defense.

Studies have shown that when plants are infected by pathogenic bacteria, they can adjust the defense response of remote tissues through signals that can move between tissues, and obtain systemic acquired resistance (SAR).

SAR is essential for plant immunity, and N-hydroxy-pipecolic acid (NHP) has been identified as one of the main signals [1].

The biosynthetic pathway formed by NHP is basically clear (Figure 1): First, L-lysine is converted to ε-amino-α-ketohexanoic acid by ALD1 (AGD2-LIKE DEFENSE RESPONSE PROTEIN 1); this compound cyclizes spontaneously It is Δ1-piperidine-2-carboxylic acid (P2C) and reduced to piperonic acid (Pip) by SARD4 (SAR DEFICIENT 4), and FMO1 (FLAVIN-DEPENDENT MONOOXYGENASE 1) further hydroxylates Pip to form NHP [2].

In addition, recent studies have discovered glycosylated NHP (NHP-OGlc) in the SAR process [3], but the enzyme that catalyzes the formation of NHP-OGlc and its mode of action are still unclear.

Figure 1 Biosynthesis of NHP-OGlc Recently, Zhang Yuelin's research group from the University of British Columbia and Ivo Feussner's research group from the University of Goettingen in Germany jointly published an online article entitled The glycosyltransferase UGT76B1 modulates N-hydroxy-pipecolic acid in The Plant Cell.
The research paper of homeostasis and plant immunity clarified the function of the glycosyltransferase UGT76B1 in catalyzing the formation of NHP from NHP-OGlc, and revealed its mechanism of action in plant immunity.

Based on previous studies, this study first used UGT76B1 as a candidate gene for catalyzing the synthesis of NHP-OGlc, and found that UGT76B1 was co-expressed with FMO1.

Through targeted and non-target metabolomics analysis, it was found that mutant strains with loss of UGT76B1 function did not accumulate NHP-OGlc, but NHP increased significantly.

In vitro experiments show that UGT76B1 has strong catalytic activity for NHP.

Further studies have found that the ugt76b1 mutant strain has a dwarfed phenotype and enhanced defense response, and the loss of FMO1 can inhibit this phenotype, which indicates that UGT76B1 plays a role in the downstream of FMO1 and NHP is a plant immune and dwarfed phenotype of ugt76b1 Necessary.

Interestingly, exogenous application of NHP can move to the distal tissues of ugt76b1 mutant plants, and the long-distance movement of NHP during SAR does not require self-glycosylation.

The above studies show that NHP is an active mobile signal that triggers SAR after the plant feels pathogen infection, and UGT76B1 causes NHP inactivation through NHP glycosylation, thereby inhibiting immune response.

UGT76B1 glycosylates N-hydroxy-pipecolic acid (NHP) to suppress immune responses In summary, this study shows that UGT76B1 plays a key role in NPH glycosylation, and reveals that UGT76B1 regulates NPH metabolism in maintaining the balance of plant growth and defense responses.
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Original link: https://academic.
oup.
com/plcell/advance-article /doi/10.
1093/plcell/koaa045/6080805