Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway

Some <i>Sinorhizobium meliloti</i> mutants in genes involved in isoleucine, valine, and leucine biosynthesis were previously described as being unable to induce nodule formation on host plants. Here, we present a reappraisal of the interconnection between the branched-chain amino acid bi...

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Autores principales: Peltzer, María de las Nieves, Roques, Nicolas, Poinsot, Véréna, Aguilar, Orlando Mario, Batut, Jacques, Capela, Delphine
Formato: Articulo
Lenguaje:Inglés
Publicado: 2008
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Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/84240
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id I19-R120-10915-84240
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Exactas
Sinorhizobium meliloti
spellingShingle Ciencias Exactas
Sinorhizobium meliloti
Peltzer, María de las Nieves
Roques, Nicolas
Poinsot, Véréna
Aguilar, Orlando Mario
Batut, Jacques
Capela, Delphine
Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
topic_facet Ciencias Exactas
Sinorhizobium meliloti
description Some <i>Sinorhizobium meliloti</i> mutants in genes involved in isoleucine, valine, and leucine biosynthesis were previously described as being unable to induce nodule formation on host plants. Here, we present a reappraisal of the interconnection between the branched-chain amino acid biosynthesis pathway and the nodulation process in <i>S. meliloti</i>. We characterized the symbiotic phenotype of seven mutants that are auxotrophic for isoleucine, valine, or leucine in two closely related <i>S. meliloti</i> strains, 1021 and 2011. We showed that all mutants were similarly impaired for nodulation and infection of the <i>Medicago sativa</i> host plant. In most cases, the nodulation phenotype was fully restored by the addition of the missing amino acids to the plant growth medium. This strongly suggests that auxotrophy is the cause of the nodulation defect of these mutants. However, we confirmed previous findings that <i>ilvC</i> and <i>ilvD2</i> mutants in the <i>S. meliloti</i> 1021 genetic background could not be restored to nodulation by supplementation with exogenous amino acids even though their Nod factor production appeared to be normal.
format Articulo
Articulo
author Peltzer, María de las Nieves
Roques, Nicolas
Poinsot, Véréna
Aguilar, Orlando Mario
Batut, Jacques
Capela, Delphine
author_facet Peltzer, María de las Nieves
Roques, Nicolas
Poinsot, Véréna
Aguilar, Orlando Mario
Batut, Jacques
Capela, Delphine
author_sort Peltzer, María de las Nieves
title Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
title_short Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
title_full Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
title_fullStr Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
title_full_unstemmed Auxotrophy accounts for nodulation defect of most Sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
title_sort auxotrophy accounts for nodulation defect of most sinorhizobium meliloti mutants in the branched-chain amino acid biosynthesis pathway
publishDate 2008
url http://sedici.unlp.edu.ar/handle/10915/84240
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