Format

Send to

Choose Destination
Proc Natl Acad Sci U S A. 2019 Apr 4. pii: 201818275. doi: 10.1073/pnas.1818275116. [Epub ahead of print]

Biosynthesis and secretion of the microbial sulfated peptide RaxX and binding to the rice XA21 immune receptor.

Author information

1
Department of Plant Pathology, University of California, Davis, CA 95616.
2
The Genome Center, University of California, Davis, CA 95616.
3
Feedstocks Division, Joint Bioenergy Institute, Emeryville, CA 94608.
4
Technology Division, Joint Bioenergy Institute, Emeryville, CA 94608.
5
Gregor Mendel Institute, Austrian Academy of Sciences, 1030 Vienna, Austria.
6
Department of Microbiology & Molecular Genetics, University of California, Davis, CA 95616.
7
Department of Plant Pathology, University of California, Davis, CA 95616; pcronald@ucdavis.edu.

Abstract

The rice immune receptor XA21 is activated by the sulfated microbial peptide required for activation of XA21-mediated immunity X (RaxX) produced by Xanthomonas oryzae pv. oryzae (Xoo). Mutational studies and targeted proteomics revealed that the RaxX precursor peptide (proRaxX) is processed and secreted by the protease/transporter RaxB, the function of which can be partially fulfilled by a noncognate peptidase-containing transporter component B (PctB). proRaxX is cleaved at a Gly-Gly motif, yielding a mature peptide that retains the necessary elements for RaxX function as an immunogen and host peptide hormone mimic. These results indicate that RaxX is a prokaryotic member of a previously unclassified and understudied group of eukaryotic tyrosine sulfated ribosomally synthesized, posttranslationally modified peptides (RiPPs). We further demonstrate that sulfated RaxX directly binds XA21 with high affinity. This work reveals a complete, previously uncharacterized biological process: bacterial RiPP biosynthesis, secretion, binding to a eukaryotic receptor, and triggering of a robust host immune response.

KEYWORDS:

ABC transporter; RIPP; immunogen; peptidase; sulfation

PMID:
30948631
DOI:
10.1073/pnas.1818275116

Conflict of interest statement

The authors declare no conflict of interest.

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center