Auxotrophy Accounts for Nodulation Defect of Most Sinorhizobium meliloti Mutants in the Branched-Chain Amino Acid Biosynthesis Pathway

Some Sinorhizobium meliloti 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...

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Main Authors: Maria de las Nieves Peltzer, Nicolas Roques, Véréna Poinsot, O. Mario Aguilar, Jacques Batut, Delphine Capela
Format: Article
Language:English
Published: The American Phytopathological Society 2008-09-01
Series:Molecular Plant-Microbe Interactions
Online Access:https://apsjournals.apsnet.org/doi/10.1094/MPMI-21-9-1232
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author Maria de las Nieves Peltzer
Nicolas Roques
Véréna Poinsot
O. Mario Aguilar
Jacques Batut
Delphine Capela
author_facet Maria de las Nieves Peltzer
Nicolas Roques
Véréna Poinsot
O. Mario Aguilar
Jacques Batut
Delphine Capela
author_sort Maria de las Nieves Peltzer
collection DOAJ
description Some Sinorhizobium meliloti 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 S. meliloti. We characterized the symbiotic phenotype of seven mutants that are auxotrophic for isoleucine, valine, or leucine in two closely related S. meliloti strains, 1021 and 2011. We showed that all mutants were similarly impaired for nodulation and infection of the Medicago sativa 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 ilvC and ilvD2 mutants in the S. meliloti 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.
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spelling doaj.art-6ad33585c8d54671b0fac47444869e1a2022-12-21T18:51:59ZengThe American Phytopathological SocietyMolecular Plant-Microbe Interactions0894-02821943-77062008-09-012191232124110.1094/MPMI-21-9-1232Auxotrophy Accounts for Nodulation Defect of Most Sinorhizobium meliloti Mutants in the Branched-Chain Amino Acid Biosynthesis PathwayMaria de las Nieves PeltzerNicolas RoquesVéréna PoinsotO. Mario AguilarJacques BatutDelphine CapelaSome Sinorhizobium meliloti 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 S. meliloti. We characterized the symbiotic phenotype of seven mutants that are auxotrophic for isoleucine, valine, or leucine in two closely related S. meliloti strains, 1021 and 2011. We showed that all mutants were similarly impaired for nodulation and infection of the Medicago sativa 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 ilvC and ilvD2 mutants in the S. meliloti 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.https://apsjournals.apsnet.org/doi/10.1094/MPMI-21-9-1232
spellingShingle Maria de las Nieves Peltzer
Nicolas Roques
Véréna Poinsot
O. Mario Aguilar
Jacques Batut
Delphine Capela
Auxotrophy Accounts for Nodulation Defect of Most Sinorhizobium meliloti Mutants in the Branched-Chain Amino Acid Biosynthesis Pathway
Molecular Plant-Microbe Interactions
title 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_short 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
url https://apsjournals.apsnet.org/doi/10.1094/MPMI-21-9-1232
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