Binding and bending of the lambda replication origin by the phage O protein.

Zahn, Kenneth; Blattner, F. R.

doi:10.1002/j.1460-2075.1985.tb04124.x

Cited by 88 publications

(47 citation statements)

References 38 publications

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“…Although increased DNA flexibility might be expected to aid longdistance enhancer-promoter interactions, it is also possible that by facilitating the appropriate protein-protein interactions, increased flexibility could assist formation of a structure that antagonizes enhancer-promoter interactions. Increased flexibility could assist structure formation by bringing DNAbound proteins and sites on DNA into contact with each other, similar to the way DNA bends aid initiation of DNA replication (21,24,38), site-specific recombination (12,28), and transcription activation (reviewed in reference 35). Increased DNA flexibility could also help SUHW interact and interfere with factors that assist long-distance enhancer-promoter interactions.…”

Section: Discussionmentioning

confidence: 99%

The enhancer-blocking suppressor of Hairy-wing zinc finger protein of Drosophila melanogaster alters DNA structure.

Shen¹,

Kim²,

Dorsett³

1994

Mol. Cell. Biol.

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(6,10,11,13,14). The SUHW-binding sites are the only part of gypsy required for enhancer blocking. For example, heat shock transcription is repressed when SUHW-binding sites are inserted in the hsp70 promoter between the two heat shock elements or between the heat shock elements and the TATA box (13). Similarly, insertion of SUHW-binding sites at various positions in the yellow gene prevents different enhancers from activating gene expression (10).The mechanism of enhancer blocking by SUHW is unknown but is likely to provide insight into how enhancers activate transcription over long distances. SUHW blocks an enhancer only when positioned between the enhancer and promoter, yet enhancer blocking is also distance independent, even for distances approaching 100 kb (6). Thus, SUHW bound just upstream of an embryonic enhancer in the cut locus does not interfere with that enhancer, yet it effectively blocks all upstream enhancers, including an enhancer nearly 50 kb further upstream (6,14). Furthermore, the embryonic enhancer is effectively blocked when SUHW is bound 40 kb downstream. Therefore, it is extremely unlikely that SUHW blocks by interacting with the transcription-activating proteins that bind to enhancers. SUHW enhancer blocking is also immediate and reversible (6), indicating that blocking does not result from formation of quasi-stable heterochromatin-like structures.An additional clue to the mechanism of enhancer blocking is the inability of SUHW to effectively block activation by the GAL4 protein in the yeast Saccharomyces cerevisiae when bound between GAL4 and the promoter (19). SUHW produced in yeast is indistinguishable from Drosophila SUHW and is present in the yeast nucleus at high levels. The GAL4 protein activates transcription in D. melanogaster (8) and is blocked by bacterial LexA protein in yeast cells (4), indicating that the failure of SUHW to block GAILA in yeast cells is not because GAIA activates through an unusual mechanism or because GAL4 is refractory to blocking. A key difference between enhancer-promoter interactions between S. cerevisiae and higher eukaryotes is that activator proteins do not function when more than a few hundred base pairs away from the promoter in yeast cells. Therefore, it is plausible that SUHW blocks enhancers by interfering with proteins or chromatin structures found only in higher eukaryotes, which allows enhancers to function several kilobases away from the promoter. For example, it is possible that SUHW disturbs a processive mechanism whereby enhancers find promoters by tracking along the chromatin fiber.The problem in long-distance activation is to bring the enhancer physically close to the promoter to allow interactions between the proteins bound to them. We considered the 5645 Vol.

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Section: Discussionmentioning

confidence: 99%

The enhancer-blocking suppressor of Hairy-wing zinc finger protein of Drosophila melanogaster alters DNA structure.

Shen¹,

Kim²,

Dorsett³

1994

Mol. Cell. Biol.

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“…Deletions of one or more A tracts alter the degree of net bending. Furthermore, binding of the lambda 0 protein to lambda origin sites containing a central A tract increases the bending of the DNA (27). Ryder et al (17) found that intrinsic bending is a prerequisite for the binding of SV40 T antigen to a high-affinity site outside of the core origin.…”

Section: C T T a T C S A S T C T C C C G C T C C S C C S S A S C C mentioning

confidence: 99%

The adenine-thymine domain of the simian virus 40 core origin directs DNA bending and coordinately regulates DNA replication.

Deb¹,

DeLucia²,

Koff³

et al. 1986

Mol. Cell. Biol.

131

132

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The simian virus 40 origin of replication contains a 20-base-pair adenine-thymine-rich segment with the sequence 5'-TGCATAAATAAAAAAAATTA-3'. The continuous tract of eight adenines is highly conserved among polyomaviruses. We used single-base substitutions to map structural and functional features of this DNA. Mutations in the AAA and AAAAAAAATT sequences significantly reduce DNA replication and thus identify two sequence-specific functional domains or a single domain with two parts. The AAAAAAAATT sequence also determines a DNA conformation that is characteristic of DNA bending. Single-base mutations in this domain change the degree of net bending, presumably by altering the length and location of the bending sequence. Thus, DNA bending in the correct conformation and location may be a structural signal for replication in polyomavirus origins and perhaps in other origins of replication with consecutive runs of adenines. The first five base pairs (TGCAT) of the 20-base-pair segment and the T between the AAA and AAAAAAAATT domains serve a sequence-independent function that may establish proper spacing within the core origin.Adenine-thymine (AT) tracts are a common feature of a wide variety of replication origins in both procaryotes and eucaryotes (7,12,13,20,23,26). The relatively weak base pairing of these tracts would facilitate strand separation, an early and indispensable step in the initiation of DNA replication. The AT segments also contain continuous runs of adenine residues of various lengths. These runs may encode an additional signal common to the initiation process. Replication origins of polyomaviruses conform to this general sequence pattern (4). The viruses control their own replication through the interaction of the virus-encoded T antigen with a distinct viral origin of replication. Immediately adjacent to the T-antigen binding site is an AT segment of 15 to 20 base pairs (bp) (4). The AT segment of each virus contains a continuous run of at least six adenine residues at an equivalent position relative to the T-antigen recognition site. Thus, this viral AT domain provides an excellent opportunity to probe the importance and nature of adenine tracts in DNA replication. Because polyomaviruses are highly dependent on host replication factors, their AT segments may resemble components of cellular origins.The origin of the polyomavirus simian virus 40 (SV40) consists of multiple distinct elements. Although flanking regulatory regions of the early promoter-operator facilitate replication, an essential core origin is sufficient to initiate replication (6,15,19). We have shown that the core origin consists of nucleotides 5211 through 31 (4). These 64 bp contain multiple functional domains with strict sequence requirements and spacer regions with relaxed sequence specificity but precise positional constraints. The central domain is the T-antigen binding site (5, 21). We have recently mapped a 10-bp sequence-specific, functional domain and a 9-bp spacer DNA to the early side of the T-antigen binding site (4)...

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“…The locally curved DNA possibly is a sequencedependent feature recognized by some proteins (2,3,4). Proteins that induce or stabilize bends in specific DNA sequences are involved in a variety of cellular processes including site-specific recombination (5), DNA replication (6,7,8), chromatin organization (1) and gene regulation (9). Since the electrophoretic mobility of DNA fragments gels is dependent on their average shape, a curved DNA molecule migrates at a different rate than a linear fragment with the same number of base pairs; bent protein-DNA complexes behave in a analogous manner.…”

Section: Introductionmentioning

confidence: 99%

DNA curvature in front of the human mitochondrial L-strand replication origin with specific protein binding

et al. 1989

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DNA bending has been suggested to play a role in the regulation of gene expression, initiation of DNA-replication, site specific recombination, and DNA packaging. In the human mitochondrial DNA we have found a DNA curvature structure within the 3'-region of ther URF2 sequence in front of the L-strand origin of replication. This structure interacts specifically with a protein factor isolated from mitochondria. Based on the localization of this DNA curvature structure and the known function of such structures the data suggest a model in which this DNA signal sequence and its specific protein binding is involved in the regulatory initiation event of L-strand replication. INTRODUCTIONRecent studies have provided increasing evidence that certain DNA regions show a curved structure and that this curvature correlates with the periodical distribution of some dinucleotides along these molecules. The term 'curved DNA' refers to molecules which are curvilinear rather than straight without application of any external forces, as opposed to 'bent DNA', forcibly deformed (1). The locally curved DNA possibly is a sequencedependent feature recognized by some proteins (2,3,4). Proteins that induce or stabilize bends in specific DNA sequences are involved in a variety of cellular processes including site-specific recombination (5), DNA replication (6,7,8), chromatin organization (1) and gene regulation (9). Since the electrophoretic mobility of DNA fragments gels is dependent on their average shape, a curved DNA molecule migrates at a different rate than a linear fragment with the same number of base pairs; bent protein-DNA complexes behave in a analogous manner. A number of duplex DNA molecules obtained as restriction fragments from both, prokaryotic and eukaryotic sources, display distinctly anomalous electrophoretic behavior. The behavior is characterized by reduced electrophoretic mobilities of the restriction fragments on polyacrylamide gels. It is thought that the fragment's curvature hinders its mobility through a gel. This striking similarity between all the known curved fragments of DNA is constituted by the periodic presence of short adenine residues runs. In a few cases, the curved site has been shown to be within these periodic runs of A's (8,9,10).Our present data suggest such a natural DNA curvature in human mitochondrial genome.

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Binding and bending of the lambda replication origin by the phage O protein.

Cited by 88 publications

References 38 publications

The enhancer-blocking suppressor of Hairy-wing zinc finger protein of Drosophila melanogaster alters DNA structure.

The enhancer-blocking suppressor of Hairy-wing zinc finger protein of Drosophila melanogaster alters DNA structure.

The adenine-thymine domain of the simian virus 40 core origin directs DNA bending and coordinately regulates DNA replication.

DNA curvature in front of the human mitochondrial L-strand replication origin with specific protein binding

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