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Characterization of Endoglucanase (GH9) Gene Family in Tomato and Its Expression in Response to Rhizophagus irregularis and Sclerotinia sclerotiorum

Summary

This study examined how tomato plants regulate genes that break down and remodel cellulose in cell walls during interactions with beneficial fungi and harmful pathogens. Beneficial mycorrhizal fungi boost the expression of these genes, leading to larger leaves and better plant growth. When pathogens attack, these genes are turned down to strengthen the cell wall defense. This demonstrates how plants balance growth and defense depending on their microbial environment.

Background

Plant cell walls are crucial in plant-microbe interactions and contain cellulose as the main load-bearing polymer. Endoglucanases (GH9 family) play roles in cell wall remodeling and degradation, but their regulation during beneficial mycorrhizal symbiosis and pathogenic infections is poorly understood.

Objective

To characterize the endoglucanase GH9 gene family in tomato using the SL5.0 genome and determine the transcriptional regulation of SlGH9 genes in leaves and roots during interactions with the mutualistic fungus Rhizophagus irregularis and the pathogen Sclerotinia sclerotiorum.

Results

Nineteen SlGH9 genes were identified and classified into classes A, B, and C. Several SlGH9 genes were upregulated in leaves of mycorrhizal plants, suggesting involvement in cellulose remodeling for cell expansion and increased foliar area. Pathogen infection downregulated some SlGH9 genes, particularly in mycorrhizal plants, potentially maintaining cell wall integrity and enhancing resistance.

Conclusion

Endoglucanase genes are differentially regulated during plant-microbe interactions, with mycorrhizal colonization promoting leaf expansion through upregulation of SlGH9 genes, while pathogen infection triggers downregulation to enhance defense. This pattern reflects a growth-defense trade-off mechanism in tomato plants.
  • Published in:Plants (Basel),
  • Study Type:Experimental Study,
  • Source: 41304609
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