Abstract
Nodule senescence in barrel medic (Medicago truncatula) can occur as a natural, developmentally regulated process or be triggered prematurely by environmental stress or ineffective symbiotic interactions. In this study, we examined five M. truncatula Fix⁻ mutants (dnf4, dnf7-2, TR183, TRV36 and TR36) that fail to fix nitrogen to determine whether they share common senescence-related traits. Our findings reveal that, despite distinct genetic defects, all mutants exhibit similar hallmarks of premature senescence: a rapid decline in the transcription of nitrogen-fixation-related genes (as indicated by DINITROGENASE REDUCTASE (NifH) expression), early degradation of bacteroids and symbiotic cells, recolonization of nodules by saprophytic rhizobia, premature closure of the nodule endodermis, impaired post-mitotic differentiation of the symbiotic cells, and upregulation of senescence marker genes (CYSTEINE PROTEASE 2 (CP2), CYSTEINE PROTEASE 6 (CP6), CHITINASE 2 and PURPLE ACID PHOSPHATASE 22 (PAP22). Neither symbiotic maintenance genes (DEFECTIVE IN NITROGEN FIXATION 2 (DNF2), Symbiotic CYSTEINE-RICH RECEPTOR-LIKE KINASE (SymCRK) and REGULATOR OF SYMBIOSOME DIFFERENTIATION (RSD) that inhibit plant defense responses nor the defense-related gene PATHOGENESIS-RELATED PROTEIN 10.1 (PR10.1) were upregulated, suggesting that premature senescence in these mutants is driven primarily by proteolytic activities rather than immune responses. These results indicate that early nodule senescence is a common feature of ineffective M. truncatula-Sinorhizobium medicae interactions, independent of the specific genetic mutation. Understanding nodule longevity and functionality may contribute to the development of strategies to enhance symbiotic efficiency in legumes for sustainable agriculture. © The Author(s) 2025. Published by Oxford University Press on behalf of American Society of Plant Biologists.
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Claims 11
Claim · model-written summary
All five Fix⁻ mutants showed a rapid decline in NifH expression.
- Taxon
- Medicago truncatula
Medicago truncatulat0 - Material
- mutantse0
- Gene
- DINITROGENASE REDUCTASE (NifH)e0
- Outcome
- DINITROGENASE REDUCTASE (NifH) expressione0
- Direction
- rapid declinee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“all mutants exhibit similar hallmarks of premature senescence: a rapid decline in the transcription of nitrogen-fixation-related genes (as indicated by DINITROGENASE REDUCTASE (NifH) expression)”
t0“Medicago truncatula”
Claim · model-written summary
All Fix⁻ mutants showed early degradation of bacteroids and symbiotic cells.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Organ / stage
- symbiotic cellse0
- Outcome
- early degradation of bacteroids and symbiotic cellse0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“early degradation of bacteroids and symbiotic cells”
t0“Medicago truncatula”
Claim · model-written summary
Saprophytic rhizobia recolonized nodules in the mutants.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Interactor
- saprophytic rhizobiae0symbiont
- Outcome
- recolonization of nodulese0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“recolonization of nodules by saprophytic rhizobia”
t0“Medicago truncatula”
Claim · model-written summary
The mutant nodules had premature endodermis closure.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Organ / stage
- nodule endodermise0
- Outcome
- premature closure of the nodule endodermise0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“premature closure of the nodule endodermis”
t0“Medicago truncatula”
Claim · model-written summary
Post-mitotic differentiation of symbiotic cells was impaired in the mutants.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Outcome
- post-mitotic differentiation of the symbiotic cellse0
- Direction
- impairede0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“impaired post-mitotic differentiation of the symbiotic cells”
t0“Medicago truncatula”
Claim · model-written summary
Senescence marker genes CP2, CP6 and CHITINASE 2 were upregulated in the mutants.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Gene
- CYSTEINE PROTEASE 2 (CP2), CYSTEINE PROTEASE 6 (CP6), CHITINASE 2e0
- Outcome
- upregulation of senescence marker genese0
- Direction
- upregulatione0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“upregulation of senescence marker genes (CYSTEINE PROTEASE 2 (CP2), CYSTEINE PROTEASE 6 (CP6), CHITINASE 2 and PURPLE ACID PHOSPHATASE 22 (PAP22)”
t0“Medicago truncatula”
Claim · model-written summary
The senescence marker PAP22 was upregulated in the mutants.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Gene
- PURPLE ACID PHOSPHATASE 22 (PAP22)e0
- Outcome
- upregulation of senescence marker genese0
- Direction
- upregulatione0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“upregulation of senescence marker genes (CYSTEINE PROTEASE 2 (CP2), CYSTEINE PROTEASE 6 (CP6), CHITINASE 2 and PURPLE ACID PHOSPHATASE 22 (PAP22)”
t0“Medicago truncatula”
Claim · model-written summary
Symbiotic maintenance genes DNF2, SymCRK and RSD were not upregulated.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Gene
- DEFECTIVE IN NITROGEN FIXATION 2 (DNF2), Symbiotic CYSTEINE-RICH RECEPTOR-LIKE KINASE (SymCRK) and REGULATOR OF SYMBIOSOME DIFFERENTIATION (RSD)e0
- Outcome
- symbiotic maintenance genese0
- Direction
- Neithere0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Neither symbiotic maintenance genes (DEFECTIVE IN NITROGEN FIXATION 2 (DNF2), Symbiotic CYSTEINE-RICH RECEPTOR-LIKE KINASE (SymCRK) and REGULATOR OF SYMBIOSOME DIFFERENTIATION (RSD) that inhibit plant defense responses nor the defense-related gene PATHOGENESIS-RELATED PROTEIN 10.1 (PR10.1) were upregulated”
t0“Medicago truncatula”
Claim · model-written summary
Defense-related PR10.1 was not upregulated.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Gene
- PATHOGENESIS-RELATED PROTEIN 10.1 (PR10.1)e0
- Outcome
- defense-related gene PATHOGENESIS-RELATED PROTEIN 10.1 (PR10.1)e0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“nor the defense-related gene PATHOGENESIS-RELATED PROTEIN 10.1 (PR10.1) were upregulated”
t0“Medicago truncatula”
Claim · model-written summary
The authors infer that proteolytic activity, rather than immune response, primarily drives premature senescence.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Outcome
- premature senescencee0
- Qualifier
- proteolytic activities rather than immune responsese0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“premature senescence in these mutants is driven primarily by proteolytic activities rather than immune responses”
t0“Medicago truncatula”
Claim · model-written summary
Early nodule senescence was common across ineffective Medicago truncatula-Sinorhizobium medicae interactions despite different mutations.
- Taxon
- Medicago truncatulaMedicago truncatulat0
- Interactor
- Sinorhizobium medicae
Sinorhizobium medicaee0symbiont - Outcome
- early nodule senescencee0
- Qualifier
- independent of the specific genetic mutatione0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“early nodule senescence is a common feature of ineffective M. truncatula-Sinorhizobium medicae interactions, independent of the specific genetic mutation”
t0“Medicago truncatula”