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Saccharomyces forkhead protein Fkh1 regulates donor preference during mating-type switching through the recombination enhancer
Gespeichert in:
Zeitschriftentitel: | Genes & Development |
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Personen und Körperschaften: | , , , , |
In: | Genes & Development, 16, 2002, 16, S. 2085-2096 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Cold Spring Harbor Laboratory
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Schlagwörter: |
Zusammenfassung: | <jats:p><jats:italic>Saccharomyces</jats:italic> mating-type switching results from replacement by gene conversion of the <jats:italic>MAT</jats:italic> locus with sequences copied from one of two unexpressed donor loci, <jats:italic>HML</jats:italic> or <jats:italic>HMR. MAT</jats:italic>a cells recombine with <jats:italic>HML</jats:italic>α ∼90% of the time, whereas <jats:italic>MAT</jats:italic>α cells choose <jats:italic>HMR</jats:italic>a 80%–90% of the time. <jats:italic>HML</jats:italic> preference in <jats:italic>MAT</jats:italic>a is controlled by the cis-acting recombination enhancer (RE) that regulates recombination along the entire left arm of chromosome III. Comparison of RE sequences between <jats:italic>S. cerevisiae</jats:italic>, <jats:italic>S. carlsbergensis</jats:italic>, and <jats:italic>S. bayanus</jats:italic> defines four highly conserved regions (A, B, C, and D) within a 270-bp minimum RE. An adjacent E region enhances RE activity. Multimers of region A, D, or E are sufficient to promote selective use of <jats:italic>HML</jats:italic>. Regions A, D, and E each bind in vivo the transcription activator forkhead proteins Fkh1p and Fkh2p and their associated Ndd1p, although there are no adjacent open reading frames (ORFs). Deletion of <jats:italic>FKH1</jats:italic>significantly reduces <jats:italic>MAT</jats:italic>a's use of <jats:italic>HML</jats:italic>, as does mutation of the Fkh1/Fkh2-binding sites in a multimer of region A. We conclude that Fkh1p regulates <jats:italic>MAT</jats:italic>a donor preference through direct interaction with RE.</jats:p> |
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Umfang: | 2085-2096 |
ISSN: |
0890-9369
1549-5477 |
DOI: | 10.1101/gad.994902 |