Abstract
BTF3 is a human protein that is thought to be involved in transcription by RNA polymerase II [Zheng et al., Cell 50, 361-368, 1987]. A yeast homologue of BTF3, Egd1p, has been identified by its ability to enhance DNA binding of the Gal4p activator [Parthun et al., Mol. Cell. Biol. 12, 5683-5689, 1992]. We have cloned a second yeast gene, BTT1, which also encodes a BTF3 homologue. Btt1p and Egd1p are highly similar in sequence, which suggests that they are duplicated proteins with similar functions. Gene disruptions were used to investigate the function of the two proteins. Consistent with published results, we found that loss of EGD1 causes a minor defect in GAL gene induction. Loss of BTT1 has little if any effect. Surprisingly, we found that cells which lack both genes instead express the GAL1 and GAL10 mRNAs at much higher levels than wild type cells. This suggests that BTF3 really plays a negative role in GAL gene expression. Further experiments revealed that expression of the ACT1 and SSO1 genes also is elevated in cells that lack EGD1 and BTT1. In contrast, expression of rRNA and tRNA was not affected. We conclude that Btt1p and Egd1p have redundant functions in vivo, and that they exert a negative effect on the expression of several genes that are transcribed by RNA polymerase II.
MeSH Terms
Amino Acid Sequence
Base Sequence
Blotting, Northern
DNA-Binding Proteins/genetics,metabolism
Gene Expression Regulation, Fungal
Genes, Fungal
Humans
Kinetics
Molecular Sequence Data
Multigene Family
Nuclear Proteins
Oligodeoxyribonucleotides
RNA, Messenger/biosynthesis
Saccharomyces cerevisiae/genetics,metabolism
Saccharomyces cerevisiae Proteins
Sequence Homology, Amino Acid
Transcription Factors/genetics,metabolism
Transcriptional Activation
Chemicals
DNA-Binding Proteins
EGD1 protein, S cerevisiae
Nuclear Proteins
Oligodeoxyribonucleotides
RNA, Messenger
Saccharomyces cerevisiae Proteins
Transcription Factors
transcription factor BTF3
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hu G Z
Ludwig Institute for Cancer Research, Uppsala Biomedical Center, Sweden.
Ronne H
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