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Interaction of TFIID in the minor groove of the TATA element. 总被引:32,自引:0,他引:32
TFIID binding in the minor groove of DNA at the TATA element was demonstrated by methylation interference and hydroxyl radical footprinting assays, and by binding studies with thymine analog substituted oligonucleotides. These results provide an explanation for TFIID-dependent DNA bending at the TATA element. TFIID binding shows phosphate contacts with the same residues that were found to be essential for TFIID interactions by methylation and thymine-specific modification interference assays. Based on previous studies implicating residues conserved between the direct repeats in DNA binding, as well as models of prokaryotic DNA binding proteins, these results also suggest a model in which the direct repeats of TFIID form two basic antiparallel beta ribbon arms that could contact DNA through the minor groove. 相似文献
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TFIIA induces conformational changes in TFIID via interactions with the basic repeat. 总被引:5,自引:0,他引:5
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D K Lee J DeJong S Hashimoto M Horikoshi R G Roeder 《Molecular and cellular biology》1992,12(11):5189-5196
DNA-binding studies with Saccharomyces cerevisiae TFIID point mutants indicated that TFIIA interacts with the basic repeat region of TFIID and induces structural changes. The latter was shown by the ability of TFIIA to compensate for TFIID point mutants defective for DNA binding. Interaction with TFIIA also rendered TFIID binding temperature independent, thus mimicking the effect of removing the nonconserved N terminus of TFIID. In addition, N-terminal truncation of the TFIID point mutants defective for DNA binding mimicked the ability of TFIIA to restore DNA binding of those mutants. Taken together, these results suggest that TFIIA enhances TFIID binding to DNA by eliminating an otherwise inhibitory effect of the nonconserved N terminus of TFIID. Furthermore, analyses of TFIID contact points on DNA and binding studies with TATA-containing oligonucleotide probes showed that TFIIA decreases the effect of sequences flanking the adenovirus major late TATA element on TFIID binding to DNA, suggesting a possible role of TFIIA in allowing TFIID to recognize a wider variety of promoters. 相似文献
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Novel and recurrent COMP (cartilage oligomeric matrix protein) mutations in pseudoachondroplasia and multiple epiphyseal dysplasia 总被引:2,自引:0,他引:2
S. Ikegawa Hirofumi Ohashi Gen Nishimura Kyoung Chang Kim Akio Sannohe Mamori Kimizuka Yoshimitsu Fukushima Toshiro Nagai Yusuke Nakamura 《Human genetics》1998,103(6):633-638
Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are common skeletal dysplasias with impaired enchondral
ossification and premature degenerative joint disease. The two disorders were in the past considered to be distinct clinical
entities; however, recent studies have proven that both diseases can result from mutations of the gene encoding cartilage
oligomeric matrix protein (COMP). To characterize further COMP mutations and investigate phenotype-genotype relationships, we screened this gene in 15 patients with PSACH or MED by directly
sequencing polymerase chain reaction products from genomic DNA. We identified ten mutations involving conserved residues among
the eight calmodulin-like repeats of the gene product: seven were novel missense mutations in exons 9, 10, 11, 13 or 14, and
the other three resulted from deletion of one of the five GAC repeats in exon 13. We have found that the GAC repeats in the
7th calmodulin-like repeat in exon 13 represent a hot-spot for mutation, and that mutations in the 7th calmodulin-like repeat
produce severe PSACH phenotypes while mutations elsewhere in the gene exhibit mild PSACH or MED phenotypes. These genotype-phenotype
correlations may facilitate molecular diagnosis and classification of PSACH and MED, and provide insight into the relationship
between structure and function of the COMP gene product.
Received: 1 June 1998 / Accepted: 22 October 1998 相似文献
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