ArticleInternational microbiology : the official journal of the Spanish Society for Microbiology2022
Tec1, a member of the TEA transcription factors family, is involved in virulence and basidiocarp development in Ustilago maydis.
Article in International microbiology : the official journal of the Spanish Society for Microbiology, 2022. 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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4 citing papers in PubMed, 5 citations in OpenAlex.
- MAPK Signaling Pathway May Directly Regulate the Expression of Hydrophobin Genes inJournal of fungi (Basel, Switzerland) · 2026Article
- Conserved signaling modules regulate filamentous growth in fungi: a model for eukaryotic cell differentiation.Genetics · 2024Review
- Transcription Factors Tec1 and Tec2 Play Key Roles in the Hyphal Growth and Virulence of Mucor lusitanicus Through Increased Mitochondrial Oxidative Metabolism.Journal of microbiology (Seoul, Korea) · 2023Article
- Global Gene Expression of Post-Senescent Telomerase-NegativeJournal of fungi (Basel, Switzerland) · 2023Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The life cycle of Ustilago maydis involves alternation of a haploid saprophytic yeast-like stage and a dikaryotic hyphal virulent form. Under in vitro conditions, basidiocarps are formed. Analysis of the transcriptional network of basidiocarp formation revealed the possible involvement of a Tec transcription factor (Tec1, UMAG_02835) in the process. In some Ascomycota, Tec factors are involved in mycelial formation, pathogenesis, and interaction with other regulatory elements, but their role in Basidiomycota species is almost unknown. Accordingly, we proceeded to determine the role of this gene in U. maydis by its mutation. Tec1 was found to be a crucial factor for normal mating, basidiocarp development, and virulence, all of the functions related to the dikaryotic stage dependent of the b genes, whereas dimorphism and resistance to different stress conditions occurring in the haploid stage were not affected in tec1 mutants. The observation that mutants showed a low residual wild-type phenotype suggests the presence of a secondary mechanism that partially compensates the loss of Tec1.
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