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Differences in Behavior During Early Nectarine Infection Among Main Monilinia spp. Causing Brown Rot
Juan Diego Astacio1,2, Silvia Rodríguez-Pires3, Paloma Melgarejo1
1Grupo de Hongos Fitopatógenos, Departamento de Protección Vegetal, Centro Nacional INIA-CSIC, 28040 Madrid, Spain.
Abstract:
Brown rot is a disease that affects stone and pome fruit crops worldwide. It is caused by fungal members of the genus Monilinia, mainly M. fructicola, M. laxa, and M. fructigena. This study presents evidence that, despite having a very similar battery of cell wall-degrading enzymes, the three species behave differently during the early stages of infection, suggesting differences at the regulatory level, which could also explain the differences in host preference among the three species. We have shown that M. fructicola infection is accelerated by red light, and the first symptoms appear much earlier than in darkness or in the other two species. The overexpression of genes encoding for CAZymes, such as pme3, pme2, pg1, cel1, pnl1, and pnl2, as well as the necrosis factor nep2, can be associated with the etiology of Monilinia spp. In addition, we found that nep2 in M. fructigena lacks binding sites in its promoter sequence for the white-collar complex, which is the major transcription factor responsible for regulating photoreception processes in fungi. Finally, we found that AlphaFold models of the NEP1-like proteins present on the three Monilinia species predict proteins with a very high degree of similarity.
Insights
Brown rot fungi show distinct infection behaviors despite similar enzymes. Red light accelerates Monilinia fructicola infection, indicating regulatory differences in these important plant pathogens.
Area of Science:
- Plant Pathology
- Mycology
- Molecular Biology
Background:
- Brown rot, caused by Monilinia fungi, impacts stone and pome fruits globally.
- Three main species (M. fructicola, M. laxa, M. fructigena) exhibit varying infection patterns and host preferences.
Purpose of the Study:
- Investigate regulatory differences in early infection stages among Monilinia species.
- Determine the role of environmental factors like light in Monilinia pathogenesis.
- Identify key genes and proteins involved in Monilinia spp. infection.
Main Methods:
- Comparative analysis of cell wall-degrading enzyme gene expression.
- Assessment of infection progression under different light conditions (red light vs. darkness).
- Bioinformatic analysis of gene promoter regions and protein structure prediction (AlphaFold).
Main Results:
- Monilinia fructicola infection is accelerated by red light, with earlier symptom development compared to other species or darkness.
- Overexpression of specific cell wall-associated enzymes (CAZymes) and necrosis factor Nep2 correlates with Monilinia etiology.
- M. fructigena's nep2 gene lacks white-collar complex binding sites, suggesting altered photoreception regulation.
- AlphaFold modeling indicates high similarity among NEP1-like proteins across the three Monilinia species.
Conclusions:
- Differential gene regulation, potentially influenced by light, contributes to varied infection strategies and host specificity in Monilinia species.
- The NEP1-like protein family and Nep2 function are important in Monilinia pathogenesis.
- Understanding these regulatory mechanisms can inform strategies to manage brown rot disease.
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