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The Role of Unusual DNA Structures in Chromatin Organization for Transcription

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The structural and mechanical properties of DNA influence nucleosome positioning and the manner in which DNA is organized in chromatin. Curved DNA structures, poly(dA•dT) sequences, and Z-DNA-forming sequences frequently occur near transcription start sites. Many reports have indicated that curved DNA structures play an important role in the formation, stability and positioning of nucleosomes, and consequently in DNA packaging in nuclei. Curved DNA structures and poly(dA•dT) sequences can increase the accessibility of target DNA elements of activators in chromatin to facilitate initiation of transcription. Z-DNA seems to be implicated in gene activation coupled with chromatin remodeling, and eukaryotes may use triplex DNA and cruciform structures to manipulate nucleosome organization in a site-specific manner.

Introduction

DNA is highly compacted in a nucleus. In humans, the genomic DNA measures about a meter if unraveled. Thus, it follows that in the nucleus of a somatic cell, about 1x10-5 m in diameter, our chromosomal DNA must be compacted in length by as much as 200,000-fold. Biologically important DNA regions, such as the origins of replication, regulatory regions of transcription, and recombination loci must also be compacted. A narrow fiber of DNA is first folded into nucleosomes, the most fundamental unit of chromatin. It is generally thought that if nucleosomes assemble over a promoter region, they block initiation of transcription, because they inhibit access and/or assembly of transcription factors.

Histone modifications and ATP-dependent chromatin remodeling play a central role to suppress or amplify the inherently repressive effects of chromatin.1-14 There are several mechanisms to explain how these phenomena participate in gene regulation. One model of transcription initiation is as follows: (i) a transcription factor (activator) binds to its target sequence in chromatin; (ii) the activator recruits a remodeling complex by direct protein-protein interaction; (iii) the complex alters the structure of the surrounding nucleosomes; (iv) the altered chromatin structure allows general transcription factors and RNA polymerase to bind to the promoter; (v) transcription starts.4 Activators can bind to their target DNA elements, even when the target is adjacent to nucleosomes, or actually within a nucleosome.15-19

What chromatin structure is it that activators can bind? At present, we cannot clearly answer this question. This problem is still a “missing link” in the transcription cascade. The structural and mechanical properties of DNA have been often argued in relation to their effects on the nucleosome positioning and their effects on the way DNA is organized in chromatin. In this chapter, I focus on whether unusual DNA structures affect the packaging of genomic DNA into chromatin, and on how transcription is initiated.

Curved DNA and DNA Packaging in Chromatin

Both intrinsic DNA curvature and anisotropic DNA bendability (flexibility) influence the formation, stability and positioning of nucleosomes.20-42 Thus, they may play an important role in the packaging of transcriptional control regions into chromatin.43,44 This section focuses on the role of intrinsic DNA curvature, and considers how the packaged DNA keeps cis elements accessible to transcription factors. The role of DNA bendability is described in the next chapter.

DNA curvature seems to have general significance for DNA packaging. Because DNA has to be bent to fit closely around a histone core, it seems thermodynamically favorable to form nucleosomes on DNA sequences that are already appropriately curved. In fact, it has been experimentally shown that nucleosomes often preferentially associate with curved DNA fragments.26,28-30,35,37,38,41 For example, Widlund et al constructed a library of nucleosome core DNA from the mouse genome, and screened those sequences that form the most stable nucleosomes.37 The identified fragments contained phased runs of three or more consecutive adenines (or thymines), and showed retarded migration in non-denaturing polyacrylamide gel electrophoresis. Thus, curved DNA structure was found to be the most common feature among the screened fragments.

Curved DNA structures may also stabilize chromatin through their interaction with histone N-terminal tail domains that are the major sites of histone modifications such as acetylation, methylation and phosphorylation.1,5,8,10,12,13 These modifications are implicated in transcription activation and gene silencing. Interactions between N-terminal domains and intrinsic DNA curvature could influence nucleosome positioning and stability.45,46 On rigid, intrinsically curved DNA sequences, interactions between DNA and the histone tails stabilizes the formation of nucleosomes by ca. 250 cal/mol.46

The next question is whether curved DNA structures occur frequently in eukaryotic genomes. There are some clear answers to this. For example, repetitive DNA sequences, including satellite DNAs, very often contain one or more curved DNA structures (Table 1).47-52 Curved DNA structures may be a common feature shared by all satellites, which are universally associated with regions of constitutive heterochromatin and comprise anywhere from a few percent to > 50% of mammalian genomes.53,54 If the hypothesis is correct, then curved DNA structures must contribute significantly to genome packaging. Some satellites, however, do not show the electrophoretic retardation characteristic of curved DNA structures. A fragment from bovine satellite I DNA is one such example. It behaves normally in non-denaturing polyacrylamide gels. Interestingly, an “unseen DNA curvature” was found in the fragment, in which another structural property that causes rapid migration had suppressed the effect of the curved DNA.55 Interestingly, repeatedly occurring curved DNA sites are not restricted to satellite DNA, but are also reported for human ε-, Gγ-Aγ-ψβ-, δ-, and β-globin, c-myc, and immunoglobulin heavy chain μ loci, and in mouse βmajor-globin locus.56-59 Considering that most findings of naturally occurring curved DNA structures have been based on detection of retarded migration, the finding of “unseen curved DNA” strongly suggests that there are many more curved DNA loci on eukaryotic genomes than expected.

Table 1. Repetitive sequences that contain a curved DNA structure in the repeating unit.

Table 1

Repetitive sequences that contain a curved DNA structure in the repeating unit.

Now, let's consider promoter packaging into chromatin. Positioning of nucleosomes on a DNA sequence plays an important role in controlling the access of specific DNA-binding proteins to regulatory DNA elements.60-65 Curved DNA often occurs in transcriptional control regions irrespective of the promoter type (Chapter 5). Thus, curved DNA may regulate positioning of nucleosomes in these regions, so as to allow the binding of activators.44 Logically, the target DNA elements could become accessible by one of two mechanisms: either by positioning the target on a nucleosome and exposing it toward the environment; or by making it free of nucleosomes (fig. 1).

Figure 1. Target DNA elements of transcription activators could become accessible in chromatin, either by making the region free of nucleosomes, or by exposing it toward environment on the nucleosome.

Figure 1

Target DNA elements of transcription activators could become accessible in chromatin, either by making the region free of nucleosomes, or by exposing it toward environment on the nucleosome. In the figure, the rope represents the DNA, and wooden cylinders (more...)

An example of the first mechanism is the nucleosome structure formed on the long terminal repeat of the mouse mammary tumor virus (MMTV-LTR). In this case, four glucocorticoid receptor recognition elements (GREs) are located on the surface of a positioned nucleosome, and the major grooves of two GREs are exposed towards the environment.60 These sites can be recognized by the receptor (a zinc finger protein), which initiates transcription. By what mechanism are these two GREs exposed on the surface of the nucleosome? An early study implicated curved DNA.66 It was subsequently suggested that this curved DNA has a left-handed curved trajectory of its helical axis.44

If the helical axis adopts a left-handed curved trajectory, it will resemble the negatively supercoiled DNA seen on a nucleosome, and thus it may recruit core histones easily. Furthermore, if a cis-DNA element is involved in, or is located near, the curved DNA structure, rotational setting of the element on the histone core (or even in linker DNA region in some cases) would be restricted by the DNA curvature. When its recognition site is displayed toward the environment by the curvature, the recognition step would be facilitated. Recently, this hypothesis was substantiated by using synthetic DNA segments with different conformations.65 When left-handed curved DNA was linked to the herpes simplex virus thymidine kinase (HSV tk) promoter at a specific rotational phase and distance, in COS-7 cells, it activated the promoter approximately 10-fold. Mechanistically, the curved DNA attracted a histone core and the TATA box was thereby left in the linker DNA with its minor groove facing outwards (fig. 2). Neither planar DNA curvature, nor right-handedly curved DNA, nor straight DNA, had this effect.

Figure 2. Synthetic curved DNA with a close resemblance to part of a negative supercoil can activate transcription by modulating local chromatin structure.

Figure 2

Synthetic curved DNA with a close resemblance to part of a negative supercoil can activate transcription by modulating local chromatin structure. The figure shows an example using the HSV tk promoter as a test system. This curved DNA can attract histone (more...)

On the other hand, when a given DNA is dissimilar to the negative supercoil, it would make the region free of nucleosomes (the second mechanism). The adenylate kinase gene promoter of Saccharomyces cerevisiae, which has a curved DNA of this type, seems to be an example of this. This promoter was shown to be free of nucleosomes.67 In the yeast GAL1 promoter and GAL80 promoter, curved DNA may make the UAS (upstream activation sequence) escape from being incorporated into nucleosomes. The underlying mechanisms are, however, different. Under inactivated (non-inducing) conditions, the GAL1 promoter, which has two strong DNA curvatures in the upstream of the TATA box,68 is incorporated into a nucleosome, referred to as nucleosome B. The bend centers lie within the terminal 20 bp or so on each end of the 147 bp sequence bound to the nucleosome B.68 The UASG is located in the non-nucleosomal region just upstream of the nucleosome B. In this case, high nucleosome-forming ability of the two curved DNA structures seems to be used to make the UAS free of nucleosomes. In contrast, in the GAL80 promoter, a single intrinsic DNA curvature which is located close to UASGAL80 seems to exclude nucleosome formation on the UAS.68 It can be imagined that similarity or dissimilarity between a given DNA curvature and the negatively supercoiled DNA seen on a nucleosome determines how easily the curved DNA can be incorporated into nucleosomes.

Besides the mechanism described above, curved DNA may also alter nucleosome structures to make target DNA elements accessible on the surface of nucleosomes. An interesting result was obtained in an experiment using DNA fragments composed of a synthetic DNA bending sequence (the repeated (A/T)3NN(G/C)3NN motifs; TG-motifs) and the binding site for the nuclear factor 1 (NF-1) with an A5 tract on both sides.69 The TG-motifs are anisotropically flexible and have a high nucleosome-forming ability.27 When nucleosomes were reconstituted on the fragments, the NF-1 binding affinity was higher when the flanking A-tracts were out-of-phase with the TG-motifs, than when they were in-phase. An altered nucleosome structure was also formed on a poly(dA•dT) sequence,17 which is described in the next section.

Poly(dA•dT) Sequences and Nucleosome Positioning

DNA sequences of (dA•dT)n also frequently occur in eukaryotic genomes. They are rigid and adopt a unique DNA conformation that has a narrow minor groove.70-72 In Homo sapiens, Caenorhabditis elegans, Arabidopsis thaliana and Saccharomyces cerevisiae, there are more poly(dA•dT) sequences present than would be expected if the DNA sequence were random, while in Escherichia coli and Mycobacterium tuberculosis, no difference is observed between actual and expected occurrences.73 In promoter regions, (dA•dT)n-rich sequences, where several (dA•dT)n sequences are connected by other short sequences, have frequently been found. For example, in yeast, promoters of the genes HIS3, PET56, DED1, CBS2, ARG4, URA3 and ADH2 contain or are flanked by them.74-78 The (dA•dT)n-rich sequences act as upstream promoter elements in HIS3, PET56, DED1, ARG4, and URA3.74,75,77 In the rest of this section, the relationships between poly(dA•dT) sequences, nucleosome formation, and transcription are considered further.

In Vitro Reconstitution of Nucleosomes on Poly(dA•dT) Sequences

It is not yet clear whether poly(dA•dT) sequences always impede nucleosome formation. Earlier studies showed that long poly(dA•dT) sequences resisted nucleosome formation.79-81 It was also shown that nucleosome formation over one member of a young Alu subfamily, which had recently transposed immediately downstream of a T14A11 stretch in the human neurofibromatosis type 1 gene locus, was impeded by the stretch.82 On the other hand, human genomic DNA fragments containing long (dA•dT)n tracts (e.g., n=32, 34, or 41) were successfully incorporated into nucleosome cores.83,84 Furthermore, nucleosomes were reconstituted successfully on the yeast DED1 promoter, containing a T6 tract, two T5 tracts and a T9 tract.85,86 In this case, the characteristic T-tract conformation was lost upon folding into nucleosomes, indicating that the structural constraints in a nucleosome dominate over the intrinsic conformation of the T-tract. Higher temperatures apparently favor reconstitution.87 The length of poly(dA•dT), the number of the poly(dA•dT) sequences, the DNA sequences surrounding poly(dA•dT), and conditions used for reconstitution, all seem to determine whether poly(dA•dT) sequences can form nucleosomes.

Influence of Poly(dA•dT) Sequences on Nucleosome Formation in Vivo

Some promoters carrying one or more poly(dA•dT) sequences are not packaged into stable nucleosomes in vivo,88-90 while others are packaged.78,91 Shimizu et al, found that in the yeast minichromosome, A15TATA16 and A34 tracts disrupt nucleosome formation, whereas a shorter A5TATA4 tract is incorporated into the positioned nucleosome.92 They also reported that the longer A-tracts retained their unique DNA conformation in vivo. Using in vivo UV photofootprinting and DNA repair by photolyase, Suter et al demonstrated that in yeast, poly(dA•dT) sequences in promoters such as HIS3, URA3 and ILV1 were not folded in nucleosomes.89 Like the report by Shimizu et al, this group also suggested that poly(dA•dT) sequences maintain their characteristic DNA structure in vivo. Interestingly, in the Candida glabrata AMT1 gene (encoding copper-metalloregulatory transcription factor), nucleosome formation was allowed but the poly(dA•dT) sequence influenced the resulting nucleosome structure. The promoter harbors a (dA•dT)16 sequence slightly upstream of a metal response element (MRE). These two sequences are packaged into a positioned nucleosome that exhibits the (dA•dT)16—dependent localized distortion (fig. 3). This nucleosome makes the MRE accessible.17,93

Figure 3. A putative nucleosome structure formed on the poly(dA•dT)-containing wild-type AMT1 promoter (left).

Figure 3

A putative nucleosome structure formed on the poly(dA•dT)-containing wild-type AMT1 promoter (left). Also shown is a putative nucleosome structure formed on a mutant promoter (right), which carried “normal” DNA instead of the poly(dA•dT) (more...)

Functional Significance of Poly(dA•dT) Sequences in Transcription

Poly(dA•dT) sequences seem to make target DNA elements in chromatin more accessible, which is essentially the same as the proposed effect of curved DNA. To do this, they either prevent nucleosome formation, or change nucleosome structures. As described above, in some cases, the poly(dA•dT) sequences are incorporated into nucleosomes, with either the original conformation, or with an altered conformation,17,86,92,93 while in other cases they are not incorporated.89,92 Although it is not clear what determines this difference, the lengths of poly(dA•dT) sequences and a slight difference in the conformational and/or mechanical properties of the poly(dA•dT)-containing sequences may be key parameters. In addition, to establish non-nucleosomal regions, or to form distorted nucleosomes, assistance of some factors [e.g., poly(dA•dT)-binding proteins or histone modifying enzymes] may be required. In this sense, the HMG-I(Y) family of “high mobility group” proteins may be important. HMG proteins organize the structure of DNA-protein complexes in the context of chromatin (Chapter 11). HMG-I(Y) can preferentially bind to certain types of poly(dA•dT) sequences on the surface of nucleosomes and alter the local setting of DNA on the nucleosomes.94 Thus, poly(dA•dT) sequences may also function as a signal to introduce structural changes into nucleosomes.

Chromatin and Z-DNA, Triple-Stranded DNA, and Cruciform DNA

The bulk of the eukaryotic genome is believed not to be torsionally stressed, even though it is negatively supercoiled, because such supercoilings are largely accommodated by the DNA writhing in nucleosomes. Unconstrained negative supercoils, however, can be still generated. For example, they are generated behind an RNA polymerase transcribing a DNA template (Chapter 10).95 The negative supercoils stabilize non-B DNA structures such as Z-DNA, triplex DNA and cruciform DNA. DNA elements with sequences suitable for the formation of Z-DNA are found at various positions in genomes. An early study estimated that the human genome contains approximately 100,000 copies of potential Z-DNA-forming sequences.96 Interestingly, similar to curved DNA and poly(dA•dT) sequences, Z-DNA-forming sequences occur more frequently near transcription start sites.97 Do they function to position nucleosomes or to inhibit nucleosome formation? It is thought that the actual Z-DNA structure lies in non-nucleosomal regions in chromatin.98 However, we do not yet know whether Z-DNA can regulate nucleosome position.

An interesting study has been reported recently. Z-DNA seems to be implicated in gene activation coupled with chromatin remodeling (fig. 4). The promoter of the human colony-stimulating factor 1 (CSF1) gene is flanked by TG repeats (Z-DNA forming sequence), which were converted to Z-DNA upon activation by the SWI/SNF-like BRG1-associated factor (BAF) complex in vivo. Furthermore, the in vitro data showed that the BAF complex facilitates Z-DNA formation in a nucleosomal template.99 These data suggest that at the CSF1 promoter, BAF-induced Z-DNA formation stabilizes an open chromatin structure. This illustrates why promoters sometimes contain, or are flanked by, Z-DNA forming sequences.

Figure 4. A model depicting NFI- and Z-DNA-facilitated chromatin remodeling by the BAF complex, at the CSF1 promoter.

Figure 4

A model depicting NFI- and Z-DNA-facilitated chromatin remodeling by the BAF complex, at the CSF1 promoter. Prior binding of NFI/CTF to its target site in the CSF1 promoter is required for the recruitment of the BAF complex. Activation of the promoter (more...)

Triple-stranded DNA seems unable to be accommodated within nucleosomes.100 This conclusion is strengthened by the report by Espinas et al, who performed in vitro assembly of mono-nucleosomes onto 180 bp DNA fragments containing (GA•TC)22, or onto 190 bp fragments with (GA•TC)10.101 Although the repeated sequences themselves had no influence on nucleosome positioning, nucleosome assembly was strongly inhibited when the triple-stranded DNA was formed at the (GA•TC)n site. On the other hand, triplex formation was difficult when the (GA•TC)n site was incorporated into a nucleosome. Thus, nucleosome assembly and triplex formation are presumably competing processes. In conclusion, triplexes seem unable to determine the position of nucleosomes by recruiting histone cores.

Cruciform structures are located mainly on internucleosomal DNA,102 perhaps because they cannot associate with histone cores103 and as a result, they could induce an alternative positioning of nucleosomes. The cruciform structures could also act over a distance to destabilize adjacent nucleosomes.104 Thus, cruciforms are probably not used to recruit histone octamers to form positioned nucleosomes. However, eukaryotes may use triplex structures and cruciforms to form open chromatin structures.

Linker histones are probably implicated in transcriptional regulation.105,106 However, the interaction between unusual DNA structures and linker histones has not been studied adequately. Interestingly, H1 seems to bind preferentially to curved DNA structures that are flanked with specific sequences.107 It is evident that more information is needed, on the interaction between linker histones and DNA of various conformations.

Conclusion

Curved DNA and poly(dA•dT) structures can enhance the accessibility of cis-DNA elements in chromatin by exposing them to the milieu while on the nucleosome (curved DNA), or by preventing nucleosome formation [both curved DNA and poly(dA•dT)], or in some cases by forming altered nucleosomal structures [poly(dA•dT)]. Z-DNA seems to be implicated in gene activation coupled with chromatin remodeling, and triplex DNA and cruciform structures may be used to form open chromatin structures.

Acknowledgements

The author would like to acknowledge the contributions of Jun-ichi Nishikawa, Yoshiro Fukue, and Junko Ohyama. The studies reported from my laboratory were supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan.

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