Eukaryotic Cell
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EC Accepts, published online ahead of print on 9 November 2007
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Eukaryotic Cell doi:10.1128/EC.00207-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The bZIP-type transcription factor FlbB controls asexual development in Aspergillus nidulans

Oier Etxebeste, Min Ni, Aitor Garzia, Nak-Jung Kwon, Reinhard Fischer, Jae-Hyuk Yu, Eduardo A. Espeso, and Unai Ugalde*

Department of Applied Chemistry, Faculty of Chemistry, University of The Basque Country, San Sebastian 20018 San Sebastian, Spain; Centro de Investigaciones Biológicas (CSIC), Ramiro de Maeztu, 9, 28040 Madrid, Spain; Departments of Bacteriology and Genetics, University of Wisconsin, Madison WI 53706, USA.; Institute for Applied Biosciences. Department of Applied Microbiology. Univ. of Karlsruhe, Hertzstrasse 16, Karlsruhe, D-76187 Germany

* To whom correspondence should be addressed. Email: qppugmau{at}ehu.es.


   Abstract

The fungal colony is a complex multicellular unit consisting of various cell types and functions. Asexual spore formation, conidiation, is integrated into the general morphogenetic plan through sensory and regulatory elements of which the activation of the transcription factor BrlA is the first determining step. A number of early regulatory elements acting upstream of BrlA (fluG and flbA-E genes) have been identified, but their functional relations remain to be further investigated.

In this report we describe FlbB as a putative basic-zipper type transcription factor restricted to filamentous fungi. FlbB accumulates at the hyphal apex during early vegetative growth, but is later found in apical nuclei, suggesting that an activating modification triggers nuclear import. Moreover, proper temporal and quantitative expression of FlbB is a prerequisite for brlA transcription and miss-scheduled overexpression inhibits conidiation. We also present evidence that FlbB activation results in the production of a second diffusible signal, acting downstream from the FluG factor, to induce conidiation.







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