ArticleBMC microbiology2015
Transcriptome changes in Fusarium verticillioides caused by mutation in the transporter-like gene FST1.
Article in BMC microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Transcriptomic Analysis ofMicroorganisms · 2026Article
- Genome Sequences of Three Isolates of Fusarium verticillioides.Microbiology resource announcements · 2018Article
- Involvement of FST1 from Fusarium verticillioides in virulence and transport of inositol.Molecular plant pathology · 2017Article
- Transcription factor ART1 mediates starch hydrolysis and mycotoxin production in Fusarium graminearum and F. verticillioides.Molecular plant pathology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFusarium verticillioides causes an important seed disease on maize and produces the fumonisin group of mycotoxins, which are toxic to humans and livestock. A previous study discovered that a gene (FST1) in the pathogen affects fumonisin production and virulence. Although the predicted amino acid sequence of FST1 is similar to hexose transporters, previous experimental evidence failed to prove function.
resultsThree new phenotypes were identified that are associated with the FST1 mutant of F. verticillioides (Δfst1), namely reduction in macroconidia production, increased sensitivity to hydrogen peroxide, and reduced mycelial hydrophobicity. A transcriptome comparison of the wild type and strain Δfst1 grown on autoclaved maize kernels for six days identified 2677 genes that were differentially expressed. Through gene ontology analysis, 961 genes were assigned to one of 12 molecular function categories. Sets of down-regulated genes in strain Δfst1 were identified that could account for each of the mutant phenotypes.
conclusionThe study provides evidence that disruption of FST1 causes several metabolic and developmental defects in F. verticillioides. FST1 appears to connect the expression of several gene networks, including those involved in secondary metabolism, cell wall structure, conidiogenesis, virulence, and resistance to reactive oxygen species. The results support our hypothesis that FST1 functions within the framework of environmental sensing.
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