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Eukaryotic Cell doi:10.1128/EC.00380-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Temporal and spatial control of HGC1 expression results in Hgc1 localization to the apical cell of hyphae in Candida albicans

Department of Biological Chemistry, University of California, Irvine, CA 92697-1700, USA; Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel

^* To whom correspondence should be addressed. Email: h4liu{at}uci.edu.

	Abstract

The human fungal pathogen Candida albicans can undergo a morphological transition from a unicellular yeast growth form to a multicellular hyphal growth form. During hyphal growth, cell division is asymmetric. Only the apical cell divides whereas subapical cells remain in G₁, and cell surface growth is highly restricted to the tip of the apical cell. Hgc1, a hypha-specific G₁ cyclin-like protein, is essential for hyphal development. Here we report, using indirect immunofluorescence, that Hgc1 is preferentially localized to the dividing apical cells of hyphae. Hgc1 protein is rapidly degraded in a cell cycle independent manner, and the protein turnover likely occurs both in the apical and subapical cells of hyphae. In addition to rapid protein turnover, the HGC1 transcript is also dynamically regulated during cell cycle progression in hyphal growth. It is induced upon germ tube formation in early G₁; the transcript level is reduced during the G₁/S transition, and peaks again around the G₂/M phase in the subsequent cell cycles. Transcription from the HGC1 promoter is essential for its apical cell localization, as Hgc1 no longer exhibits preferential apical localization when expressed under the MAL2 promoter. Using fluorescence in situ hybridization, the HGC1 transcript is detected only in the apical cells of hyphae, suggesting that HGC1 is transcribed in the apical cell. Therefore, the preferential localization of Hgc1 to the apical cells of hyphae results from the dynamic temporal and spatial control of HGC1 expression.