Identification and characterization of aspergillus nidulans mutants impaired in asexual development under phosphate stress
| Autor: | Ainara Otamendi, Eduardo A. Espeso, Oier Etxebeste |
|---|---|
| Přispěvatelé: | Universidad del País Vasco, Agencia Estatal de Investigación (España), Eusko Jaurlaritza, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España) |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Filamentous fungi biology 030106 microbiology Mutant fungi Conidiation General Medicine Signal transduction biology.organism_classification protein O-mannosylation Phenotype Conidium Cell biology 03 medical and health sciences 030104 developmental biology Transcriptional regulation Aspergillus nidulans Mutagenesis Asexual development Protein O-mannosylation Genomic library Gene Transcription factor |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname Cells Volume 8 Issue 12 |
| Popis: | © The Author(s). The transcription factor BrlA plays a central role in the production of asexual spores (conidia) in the fungus Aspergillus nidulans. BrlA levels are controlled by signal transducers known collectively as UDAs. Furthermore, it governs the expression of CDP regulators, which control most of the morphological transitions leading to the production of conidia. In response to the emergence of fungal cells in the air, the main stimulus triggering conidiation, UDA mutants such as the flbB deletant fail to induce brlA expression. Nevertheless, ΔflbB colonies conidiate profusely when they are cultured on a medium containing high H2PO4− concentrations, suggesting that the need for FlbB activity is bypassed. We used this phenotypic trait and an UV-mutagenesis procedure to isolate ΔflbB mutants unable to conidiate under these stress conditions. Transformation of mutant FLIP166 with a wild-type genomic library led to the identification of the putative transcription factor SocA as a multicopy suppressor of the FLIP (Fluffy, aconidial, In Phosphate) phenotype. Deregulation of socA altered both growth and developmental patterns. Sequencing of the FLIP166 genome enabled the identification and characterization of PmtCP282L as the recessive mutant form responsible for the FLIP phenotype. Overall, results validate this strategy for identifying genes/mutations related to the control of conidiation Work at the UPV/EHU lab was funded by UPV/EHU (grants EHUA15/08 and PPGA19/08 to O.E) and the Basque Government (grant IT599-13 to Prof. Unai Ugalde and grant Elkartek19/72 to Prof. María Teresa Dueñas). Work at CIB-CSIC was funded by MINECO (BFU2015-66806-R) and MICIU (RTI2018-094263-B-100) to E.A.E (both partially supported by FEDER, EU). A.O held a predoctoral fellowship from the Basque Government. |
| Databáze: | OpenAIRE |
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