Ash1 protein, an asymmetrically localized transcriptional regulator, controls filamentous growth and virulence of Candida albicans.
In response to a number of distinct environmental conditions, the fungal pathogen Candida albicans undergoes a morphological transition from a round, yeast form to a series of elongated, filamentous forms. This transition is believed to be critical for virulence in a mouse model of disseminated candidiasis. Here we describe the characterization of C. albicans ASH1, a gene that encodes an asymmetrically localized transcriptional regulatory protein involved in this response. We show that C. albicans ash1 mutants are defective in responding to some filament-inducing conditions. We also show that Ash1p is preferentially localized to daughter cell nuclei in the budding-yeast form of C. albicans cell growth and to the hyphal tip cells in growing filaments. Thus, Ash1p "marks" newly formed cells and presumably directs a specialized transcriptional program in these cells. Finally, we show that ASH1 is required for full virulence of C. albicans in a mouse model of disseminated candidiasis.
Inglis
Diane O
DO
Department of Biochemistry and Biophysics, University of California-San Francisco, San Francisco, California 94143, USA.
Johnson
Alexander D
AD
D000595:Amino Acid Sequence; D000818:Animals; D002176:Candida albicans / Q000166:cytology / Q000235:genetics / Q000254:growth & development* / Q000472:pathogenicity*; D002177:Candidiasis / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005656:Fungal Proteins / Q000378:metabolism; D015966:Gene Expression Regulation, Fungal; D018390:Gene Targeting; D025301:Hyphae / Q000166:cytology / Q000378:metabolism; D007668:Kidney / Q000166:cytology / Q000382:microbiology; D051379:Mice; D008807:Mice, Inbred BALB C; D008969:Molecular Sequence Data; D009154:Mutation; D011401:Promoter Regions, Genetic; D016415:Sequence Alignment; D014157:Transcription Factors / Q000378:metabolism*; D014158:Transcription, Genetic
D005656:Fungal Proteins; D014157:Transcription Factors