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Boron deficiency affects N-glycosilation in legume symbiotic nodules

    1. [1] Universidad Autónoma de Madrid

      Universidad Autónoma de Madrid

      Madrid, España

  • Localización: SEFV 2011: programa de sesiones y resúmenes de conferencias plenarias e invitadas / coord. por Vicent Arbona Mengual, Rosa María Pérez Clemente, María Fernanda López Climent, Aurelio Gómez Cadenas, 2011, ISBN 978-84-8021-805-4, pág. 50
  • Idioma: inglés
  • Texto completo no disponible (Saber más ...)
  • Resumen
    • Legume symbioses require a complex molecular dialogue between the host rhizobia and thelegume in which glycoconjugates from both symbionts are essential. Because of the capacity ofboron (B) to react as boric acid or borate with cis-diol groups, alterations in theseglycoconjugates under B deficiency are expected. This could be an important clue to explain theabnormal plant-microbe interaction and the aberrant nodule development under low Bconditions. Using biochemical and immunological methods to detect N-glycosilation and othersglycosil-modifications we have been able to detect an abnormal glycosilation pattern duringdevelopment of B-deficient nodules. Particularly, by using protein electrophoresis followed byaffinity detection with the Concanavalin A lectin, we have detected an accumulation of highmannose type N-glycans, synthesized in the endoplasmic reticulum. By using antibodies againstxylose and fucose we have detected also an accumulation of complex N-glycans, which aresynthesized in the Golgi apparatus. Moreover, we have used specific antibodies againstglycoproteins involved in the nodule organogenesis and symbiosome/cell differentiationprocesses. In these experiments, we confirmed that B deficiency resulted in lack or incorrectglycosilation of some of them, as the lectin-like PsNLEC1 or membrane glycoproteins sharingantigenicity with rhamnogalacturonan II (RGII-glycoproteins). Overall results support a role ofboron in N-glycosilation pathway, and although the precise relationship of boron withglycosylation still remains unknown, these results may link our previous reports that B-deficientnodules develop as tumour-like structures, and bacteroids inside them remain undifferentiated.These new data also support the hypothesis that B is more than a cell wall stabilizer and that, byensuring a correct glycosylation, the micronutriente is involved in cell signalling duringorganogenesis.


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