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The APSES transcription factor Efg 1 is a global regulator that controls morphogenesis and biofilm formation in C andida parapsilosis
Author(s) -
Connolly Leona A.,
Riccombeni Alessandro,
Grózer Zsuzsana,
Holland Linda M.,
Lynch Denise B.,
Andes David R.,
Gácser Attila,
Butler Geraldine
Publication year - 2013
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12345
Subject(s) - biology , regulator , transcription factor , microbiology and biotechnology , transcription (linguistics) , biofilm , candida parapsilosis , response regulator , genetics , candida albicans , gene , mutant , linguistics , bacteria , philosophy
Summary Efg 1 (a member of the APSES family) is an important regulator of hyphal growth and of the white‐to‐opaque transition in C andida albicans and very closely related species. We show that in C andida parapsilosis Efg 1 is a major regulator of a different morphological switch at the colony level, from a concentric to smooth morphology. The rate of switching is at least 20‐fold increased in an efg1 knockout relative to wild type. Efg1 deletion strains also have reduced biofilm formation, attenuated virulence in an insect model, and increased sensitivity to SDS and caspofungin. Biofilm reduction is more dramatic in in vitro than in in vivo models. An Efg 1 paralogue ( Efh 1) is restricted to C andida species, and does not regulate concentric‐smooth phenotype switching, biofilm formation or stress response. We used ChIP ‐seq to identify the Efg 1 regulon. A total of 931 promoter regions bound by Efg 1 are highly enriched for transcription factors and regulatory proteins. Efg 1 also binds to its own promoter, and negatively regulates its expression. Efg 1 targets are enriched in binding sites for 93 additional transcription factors, including Ndt 80. Our analysis suggests that Efg 1 has an ancient role as regulator of development in fungi, and is central to several regulatory networks.