Biochemical and genetic characterization of Rbf1p, a putative transcription factor of Candida albicans

Microbiology ◽  
1997 ◽  
Vol 143 (2) ◽  
pp. 429-435 ◽  
Author(s):  
N. Ishii ◽  
M. Yamamoto ◽  
F. Yoshihara ◽  
M. Arisawa ◽  
Y. Aoki
2000 ◽  
Vol 168 (1-2) ◽  
pp. 77-87 ◽  
Author(s):  
Kyle W. Sloop ◽  
Amy McCutchan Schiller ◽  
Timothy P.L. Smith ◽  
John R. Blanton ◽  
Gary A. Rohrer ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1520 ◽  
Author(s):  
Ainara Otamendi ◽  
Eduardo A. Espeso ◽  
Oier Etxebeste

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.


2015 ◽  
Vol 83 ◽  
pp. 45-57 ◽  
Author(s):  
Protiti Maiti ◽  
Priyanka Ghorai ◽  
Sumit Ghosh ◽  
Mohan Kamthan ◽  
Rakesh Kumar Tyagi ◽  
...  

2016 ◽  
pp. AAC.01888-16 ◽  
Author(s):  
Sumanun Suwunnakorn ◽  
Hironao Wakabayashi ◽  
Elena Rustchenko

Candida albicansis an important fungal pathogen with a diploid genome that can adapt to caspofungin, a major drug from the echinocandin class, by a reversible loss of one copy of chromosome 5 (Ch5). Here we explore a hypothesis that more than one gene for negative regulation of echinocandin tolerance is carried on Ch5. We constructedC. albicansstrains that each lacked one of the following Ch5 genes:CHT2for chitinase;PGA4for glucanosyltransferase, andCSU51, a putative transcription factor. We demonstrate that independent deletion of each of these genes increased caspofungin and anidulafungin, another echinocandin, tolerance. Our data indicate that Ch5 carries multiple genes for negative control of echinocandin tolerance, although the final number has yet to be established.


2012 ◽  
Vol 11 (7) ◽  
pp. 916-931 ◽  
Author(s):  
Patrick Vandeputte ◽  
Sylvain Pradervand ◽  
Françoise Ischer ◽  
Alix T. Coste ◽  
Sélène Ferrari ◽  
...  

ABSTRACTThe identification of novel transcription factors associated with antifungal response may allow the discovery of fungus-specific targets for new therapeutic strategies. A collection of 241Candida albicanstranscriptional regulator mutants was screened for altered susceptibility to fluconazole, caspofungin, amphotericin B, and 5-fluorocytosine. Thirteen of these mutants not yet identified in terms of their role in antifungal response were further investigated, and the function of one of them, a mutant of orf19.6102 (RCA1), was characterized by transcriptome analysis. Strand-specific RNA sequencing and phenotypic tests assigned Rca1 as the regulator of hyphal formation through the cyclic AMP/protein kinase A (cAMP/PKA) signaling pathway and the transcription factor Efg1, but also probably through its interaction with a transcriptional repressor, most likely Tup1. The mechanisms responsible for the high level of resistance to caspofungin and fluconazole observed resulting fromRCA1deletion were investigated. From our observations, we propose that caspofungin resistance was the consequence of the deregulation of cell wall gene expression and that fluconazole resistance was linked to the modulation of the cAMP/PKA signaling pathway activity. In conclusion, our large-scale screening of aC. albicanstranscription factor mutant collection allowed the identification of new effectors of the response to antifungals. The functional characterization of Rca1 assigned this transcription factor and its downstream targets as promising candidates for the development of new therapeutic strategies, as Rca1 influences host sensing, hyphal development, and antifungal response.


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