期刊
PLOS ONE
卷 15, 期 10, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0235446
关键词
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资金
- Post-doctoral AGREENSKILLS fellowship
- ANR [ANR-15-CE20-0004-01]
- CSC PhD scholarship
- INRA SPE post-doctoral fellowship
- French Ministere de l'Enseignement superieur et de la Recherche
- ANR RhizocAMP [ANR-10-BLAN-1719]
- ANR AOl [ANR-15-CE20-0004-01]
- Pole de Competitivite Agri Sud Ouest Innovation
- Laboratoire d'Excellence (LABEX) entitled TULIP [ANR-10-LABX-41]
- European funds (Fonds Europeens de DEveloppement Regional, FEDER)
- Toulouse Metropole
- French Ministry of Research [ANR-10-INBS-08]
- Region Occitanie
- Agence Nationale de la Recherche (ANR) [ANR-10-BLAN-1719, ANR-15-CE20-0004] Funding Source: Agence Nationale de la Recherche (ANR)
We recently described a regulatory loop, which we termed autoregulation of infection (AOI), by which Sinorhizobium meliloti, a Medicago endosymbiont, down regulates the root susceptibility to secondary infection events via ethylene. AOI is initially triggered by so-far unidentified Medicago nodule signals named signal 1 and signal 1' whose transduction in bacteroids requires the S. melilotiouter-membrane-associated NsrA receptor protein and the cognate inner-membrane-associated adenylate cyclases, CyaK and CyaD1/D2, respectively. Here, we report on advances in signal 1 identification. Signal 1 activity is widespread as we robustly detected it in Medicago nodule extracts as well as in yeast and bacteria cell extracts. Biochemical analyses indicated a peptidic nature for signal 1 and, together with proteomic analyses, a universally conserved Medicago ribosomal protein of the uL2 family was identified as a candidate signal 1. Specifically, MtRPuL2A (MtrunA17Chr7g0247311) displays a strong signal activity that requires S. meliloti NsrA and CyaK, as endogenous signal 1. We have shown that MtRPuL2A is active in signaling only in a non-ribosomal form. A Medicago truncatula mutant in the major symbiotic transcriptional regulator MtNF-YA1 lacked most signal 1 activity, suggesting that signal 1 is under developmental control. Altogether, our results point to the MtRPuL2A ribosomal protein as the candidate for signal 1. Based on the Mtnf-yal mutant, we suggest a link between root infectiveness and nodule development. We discuss our findings in the context of ribosomal protein moonlighting.
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