ArticleFEBS open bio2011
Expressing the Erwinia amylovora type III effector DspA/E in the yeast Saccharomyces cerevisiae strongly alters cellular trafficking.
Article in FEBS open bio, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Pathogenicity and virulence ofVirulence · 2026Review
- The conserved AvrE family of bacterial effectors: functions and targets during pathogenesis.Trends in microbiology · 2025Review
- Comparative sequence analysis of pPATH pathogenicity plasmids inFrontiers in plant science · 2023Article
- Yeast as a Heterologous Model System to Uncover Type III Effector Function.PLoS pathogens · 2016Review
- The AvrE superfamily: ancestral type III effectors involved in suppression of pathogen-associated molecular pattern-triggered immunity.Molecular plant pathology · 2015Review
- Article
- Virulence Factors of Erwinia amylovora: A Review.International journal of molecular sciences · 2015Review
- Expression of the bacterial type III effector DspA/E in Saccharomyces cerevisiae down-regulates the sphingolipid biosynthetic pathway leading to growth arrest.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Erwinia amylovora is responsible for fire blight, a necrotic disease of apples and pears. E. amylovora relies on a type III secretion system (T3SS) to induce disease on host plants. DspA/E belongs to the AvrE family of type III effector. Effectors of the AvrE family are injected via the T3SS in plant cell and are important to promote bacterial growth following infection and to suppress plant defense responses. Their mode of action in the plant cells is unknown. Here we study the physiological effects induced by dspA/E expression in the yeast Saccharomyces cerevisiae. Expression of dspA/E in the yeast inhibits cell growth. This growth inhibition is associated with perturbations of the actin cytoskeleton and endocytosis.
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Registered trials
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