Induction of altered chromatin structures by simian virus 40 enhancer and promoter elements

Jongstra, Jan; Reudelhuber, T L; Oudet, P; Benoist, Christophe; Chae, Chi‐Bom; Jeltsch, Jean‐Marc; Mathis, Diane; Chambon, Pierre

doi:10.1038/307708a0

Cited by 214 publications

(94 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Determinants found in a restricted region of the SV40 genome are sufficient to generate an endonuclease-sensitive region in SV40 chromatin (10,11,17,30). Starting with a viable double-origin mutant, in(Or)1411 (constructed by T. Shenk [24]), we have isolated a collection of deletion mutations which remove segments of DNA at various locations throughout the nuclease-sensitive region.…”

Section: Discussionmentioning

confidence: 99%

“…Genetic elements can act independently within the region of nuclease sensitivity to generate specific hypersensitive sites. A DNA segment containing the 72-bp tandem repeats (and the transcriptional enhancer) creates a DNase I-sensitive site over itself when placed at various positions around the viral genome (10,17). A segment containing the 21-bp tandem repeats forms a DNase I-sensitive site over adjacent sequences even when separated from the 72-bp repeats (10,17 We have investigated the genetic elements responsible for the chromatin structure in this region by analyzing a number of additional mutants.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Role of specific simian virus 40 sequences in the nuclease-sensitive structure in viral chromatin.

Gerard¹,

Montelone²,

Walter³

et al. 1985

Mol. Cell. Biol.

View full text Add to dashboard Cite

A nuclease-sensitive region forms in chromatin containing a 273-base-pair (bp) segment of simian virus 40 DNA encompassing the viral origin of replication and early and late promoters. We have saturated this region with short deletion mutations and compared the nuclease sensitivity of each mutated segment to that of an unaltered segment elsewhere in the partially duplicated mutant. Although no single DNA segment is required for the formation of a nuclease-sensitive region, a deletion mutation (d145) which disrupted both exact copies of the 21-bp repeats substantially reduced nuclease sensitivity. Deletion mutations limited to only one copy of the 21-bp repeats had little, if any, effect. A mutant (d1135) lacking all copies of the 21-and 72-bp repeats, while retaining the origin of replication and the TATA box, did not exhibit a nuclease-sensitive region. Mutants which showed reduced nuclease sensitivity had this effect throughout the nuclease-sensitive region, not just at the site of the deletion, indicating that although multiple determinants must be responsible for the nuclease-sensitive chromatin structure they do not function with complete independence. Mutant d19, which lacks the late portion of the 72-bp segment, showed reduced accessibility to BglI, even though the Bgll site is 146 bp away from the site of the deletion.Simian virus 40 (SV40)-infected cells contain SV40 DNA in a nucleoprotein structure with many similarities to cellular chromatin. The availability of an amplified, homogeneous DNA species in a chromatin-like structure has provided convenient material for the study of specific features of chromatin. Of particular interest is the short region adjacent to the viral origin of replication (ori site) which is hypersensitive to cleavage by endonucleases (23,26,27,29) and which appears as a gap in the nucleosome pattern when visualized in the electron microscope (16,22). This region contains the early and late gene promoters, the transcriptional enhancer sequences, and the viral origin of replication. The distinctive chromatin structure may be relevant to any or all of these functions.To identify which sequences are responsible for the nuclease-sensitive region, partially duplicated SV40 mutants have been studied. All essential information required for the hypersensitive site is contained within a 273-base-pair (bp) segment of DNA spanning the origin of replication (11,30 We have investigated the genetic elements responsible for the chromatin structure in this region by analyzing a number of additional mutants. No single segment is essential for nuclease sensitivity. However, overall accessibility to nuclease was dramatically decreased by a mutant affecting only the two exact copies of the 21-bp repeated sequences. Insertion of a foreign DNA segment into this region also substantially diminished nuclease sensitivity. By contrast, deletion of only one of the two exact copies of the 21-bp repeats had little effect on the pattern of nuclease cleavage.These results imply that the region of the genome e...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Role of specific simian virus 40 sequences in the nuclease-sensitive structure in viral chromatin.

Gerard¹,

Montelone²,

Walter³

et al. 1985

Mol. Cell. Biol.

View full text Add to dashboard Cite

show abstract

“…This was proposed to occur by a nucleosome exclusion mechanism wherein NFI binding simply prevented the binding of nucleosomes over the adjacent elements required for SV40 replication. In its natural context, the SV40 origin is indeed preferentially cleared of nucleosomes and is adjacent to sites with dual roles in transcription and replication (21,27). This model also implies that many transcription factors might have the potential to affect replication when bound near origins.…”

mentioning

confidence: 95%

The replication activation potential of selected RNA polymerase II promoter elements at the simian virus 40 origin.

Hoang¹,

Wang²,

Gralla³

1992

Mol. Cell. Biol.

View full text Add to dashboard Cite

Binding sites for cellular transcription factors were placed near the simian virus 40 origin of replication, and their effect on replication and TATA-dependent transcription was measured in COS cells. The hierarchy of transcriptional stimulation changed when the plasmids replicated. Only one of seven inserted sequences, a moderately weak transcription element, stimulated replication detectably. However, when two nonstimulatory sites were present in multiple copies they did activate replication. Multiple sites for the chimeric activator GAL4-VP16 did not stimulate replication even though transcription was stimulated strongly. The results indicate that the ability of a binding site to stimulate replication from the simian virus 40 ori is not based on its transcriptional activation potential but is instead related to a separate replication activation potential that can be increased by having multiple sites.The interrelationship between control of cellular replication and transcription has been the subject of extensive experimentation and discussion (10,11,19,38). Because of the uncertainty concerning what constitutes a cellular origin of replication, information has come mostly from viral systems where the origins are defined genetically (6,10,21). Among the papova-and adenoviruses, the involvement of transcription regulatory elements in replication control is very well documented (12,25,31). Conversely, template replication is typically required for late gene transcription (9,19). Thus, there is important communication between control of replication and transcription.The elements jointly controlling DNA and RNA synthesis are generally located near the replication origin in these viruses (5,12,22). These are binding sites for different factors in the different viruses, demonstrating that a variety of factors may play dual regulatory roles. These factors can be derived from the host or encoded by the virus. The host proteins are known to function as transcription factors for cellular genes and include, for example, NFI/CTF, used by BK virus and adenovirus, GC box binding factors such as Spl, used by simian virus 40 (SV40), and a variety of cellular proteins that bind viral enhancer regions (14,25,26,28). Some proteins that influence both processes appear to have separate domains for transcription and replication stimulation (18,32,33,37 to stimulate both replication and transcription was demonstrated. Stimulation of either process required the fused transcription activation domain. There was also a correlation between the strength of transcription activation and that of replication activation (2). This raised the possibility that nearly any transcription factor might have the capacity to stimulate replication when bound near an origin. A potential mechanism for this was that the factor activation domain might interact with a common mediating factor required for both transcription and replication.A different mechanism was suggested by experiments with the host NFI factor used in BK transcription (7). Those results sh...

show abstract

“…We propose that the formation of the LCR HSs is a multistep process and that the first step is the binding of non-erythroid factors such as Sp1 to the core-forming element. Supporting data for this function of Sp1 come from in vitro studies from Workman and co-workers (58) showing that Sp1 is able to bind to nucleosome-associated DNA and from Jongstra et al (59) and Widlak et al (60), who demonstrated that Sp1 participates in the formation of the nuclease HSs of the SV40 early gene promoter and human immunodeficiency virus, type I LTR. Data from Pondel et al (61) indicate that Sp1 is critical for the chromatin-dependent expression of the human ␣-globin gene, and work from Marin et al (62) shows that embryonic globin genes were expressed at reduced levels in Sp1 homozygous knockout mice.…”

Section: ␤-Globin Lcr Hs Core Formationmentioning

confidence: 99%

In Vivo Formation of a Human β-Globin Locus Control Region Core Element Requires Binding Sites for Multiple Factors Including GATA-1, NF-E2, Erythroid Kruppel-like Factor, and Sp1

Goodwin

McInerney

Glander

et al. 2001

Journal of Biological Chemistry

View full text Add to dashboard Cite

The active elements of the ␤-globin locus control region (LCR) are located within domains of unique chromatin structure. These nuclease hypersensitive sites (HSs) are characterized by high DNase I sensitivity, erythroid specificity, similar nucleosomal structure, and evolutionarily conserved clusters of cis-acting elements that are required for the formation and function of the core elements. To determine the requirements for HS core formation in the setting of nuclear chromatin, we constructed a series of artificial HS cores containing binding sites for GATA-1, NF-E2, and Sp1. In contrast to the results of previous in vitro experiments, we found that when constructs were stably integrated in mouse erythroleukemia cells the binding sites for NF-E2, GATA-1, or Sp1 alone or in any combination were unable to form core HS structures. We subsequently identified two new cis-acting elements from the LCR HS4 core that, when combined with the NF-E2, Sp1, and tandem inverted GATA elements, result in core structure formation. Both new cis-acting elements bind Sp1, and one binds erythroid Kruppel-like factor (EKLF). We conclude that in vivo ␤-globin LCR HS core formation is more complex than previously thought and that several factors are required for this process to occur.

show abstract

Induction of altered chromatin structures by simian virus 40 enhancer and promoter elements

Cited by 214 publications

References 39 publications

Role of specific simian virus 40 sequences in the nuclease-sensitive structure in viral chromatin.

Role of specific simian virus 40 sequences in the nuclease-sensitive structure in viral chromatin.

The replication activation potential of selected RNA polymerase II promoter elements at the simian virus 40 origin.

In Vivo Formation of a Human β-Globin Locus Control Region Core Element Requires Binding Sites for Multiple Factors Including GATA-1, NF-E2, Erythroid Kruppel-like Factor, and Sp1

Contact Info

Product

Resources

About