Characterization of the deficient nodule development of Rhizobium favelukesii LPU83 in Medicago and their transcriptomic profiles.

GONZALO A. TORRES TEJERIZO; JESUS MONTIEL; HANNA BEDNARZ; EVA KONDOROSI; DANIEL WIBBERG; RUI LIMA; ANDREAS SCHLÜTER; KARSTEN NIEHAUS; ANIKA WINKLER; ATTILA FARKAS; ALFRED PÜHLER

Granada

Congreso; 20th International Congress on Nitrogen Fixation; 2017

Leguminous plants from the Inverted Repeat-Lacking Clade (IRLC) developa symbiotic interaction with rhizobia that culminates in the formation of rootnodules, where the rhizobia differentiate to a terminal stage. Previous studieshave suggested that the differentiation process is driven by nodule-specificcysteine-rich (NCRs) peptides (1). More than 600 secreted NCRs, which aretargeted to the bacteria, are encoded in Medicagotruncatula genome. The Medicago-rhizobiasymbiosis is highly specific. Sinorhizobium/Ensifer meliloti and Sinorhizobium/Ensifer medicae are symbionts of various Medicago species. However, otherrhizobia such as Rhizobium favelukesiiare also able to produce nodules in Medicago.Rhizobium favelukesii LPU83Tstrain is more acid tolerant than other Medicago-nodulatingrhizobia and very competitive for nodulating M. sativa (alfalfa) in acidic soils, but inefficient in nitrogenfixation (2). The nodules developed by LPU83 harbor a low number of bacteroids andthe senescence zone is larger compared to those of plants infected by E. meliloti 2011 (3). We investigated the nodule development induced by LPU83 in M. truncatula. Nodule development,differentiation of nodule zones and the fate of bacteroids were investigated bymicroscopic observations. Formation of the infection threads and the release ofthe bacteria were normal, but failure in differentiation started early. LPU83 wasneither elongated nor occupied the nodules in a similar way as the effectivewild type strain E. meliloti 2011. This raised the question whether LPU83 was able to induce the NCR genes onthe same way as the effective wild-type strains. RNAseq analyses ofthe whole nodules revealed that after four weeks of infection, 253 NCRs geneswere downregulated in the LPU83 infected nodules compared to the E. meliloti 2011 infected nodules. In 10days-old nodules, even more, 474 NCRs genes were downregulated. Thus, lack ofcertain NCRs or their perturbed balance could be a reason for the incorrectdifferentiation of LPU83. However, the transcriptomics approach showed that thechanges are not only restricted to NCRs genes. Transcription of more than 5500 geneschanged in nodules infected by LPU83 that collectively could be responsible tothe incomplete differentiation of bacteroids and development of nitrogen-fixingnodules.