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Eukaryotic Cell, August 2004, p. 984-991, Vol. 3, No. 4
1535-9778/04/$08.00+0 DOI: 10.1128/EC.3.4.984-991.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
and Ken Shirasu1*
The Sainsbury Laboratory,1 Department of Cell and Developmental Biology, John Innes Centre,3 Norwich NR4 7UH, and Institute of Biomedical and Lifesciences, University of Glasgow, Glasgow G12 8QQ,United Kingdom2
Received 10 November 2003/ Accepted 7 May 2004
The alternation of eukaryotic life cycles between haploid and diploid phases is crucial for maintaining genetic diversity. In some organisms, the growth and development of haploid and diploid phases are nearly identical, and one might suppose that all genes required for one phase are likely to be critical for the other phase. Here, we show that targeted disruption of the chpA (cysteine- and histidine-rich-domain- [CHORD]-containing protein A) gene in haploid Aspergillus nidulans strains gives rise to chpA knockout haploids and heterozygous diploids but no chpA knockout diploids. A. nidulans chpA heterozygous diploids showed impaired conidiophore development and reduced conidiation. Deletion of chpA from diploid A. nidulans resulted in genome instability and reversion to a haploid state. Thus, our data suggest a vital role for chpA in maintenance of the diploid phase in A. nidulans. Furthermore, the human chpA homolog, Chp-1, was able to complement haploinsufficiency in A. nidulans chpA heterozygotes, suggesting that the function of CHORD-containing proteins is highly conserved in eukaryotes.
Present address: Max-Planck-Institut für Zuechtungsforschung, D-50829 Cologne, Germany.
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