Differential positive control by Oct-1 and Oct-2: activation of a transcriptionally silent motif through Oct-1 and VP16 corecruitment.

Cleary, Michele A.; Stern, Seth; Tanaka, Masafumi; Herr, Winship

doi:10.1101/gad.7.1.72

Cited by 85 publications

(75 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the case of the VP16-induced complex, a single subunit of the complex, the octamer-binding protein Oct-l, has been shown to bind specifically to the sequence ATGCTAAT that comprises a portion of the AT-GCTAATGARAT sequence recognized by the VP16-induced complex (Kristie and Sharp 1990;Stern and Herr 1991). The interaction between Oct-l, VP16, and a host cell factor (HCF) aids in the recruitment of Oct-1 to the ATGCTAATGARAT sequence (Cleary et al 1993) located in the upstream promoter regions of the immediate early genes of HSV-1 (O' Hare and Goding 1988;Preston et al 1988). In the case of ISGF-3, the 48-kD subunit has been shown to bind specifically to the IFN-stimulated response element (ISRE) in the absence of the other subunits, StatloL, Statl~, and Stat2; however, the presence of the Stat subunits increases the affinity of this DNAprotein interaction Kessler et al 1990).…”

Section: Discussionmentioning

confidence: 99%

Cloning of yeast HAP5: a novel subunit of a heterotrimeric complex required for CCAAT binding.

McNabb¹,

Xing²,

Guarente³

1995

Genes Dev.

262

244

View full text Add to dashboard Cite

The CCAAT-binding factor is a conserved heteromeric transcription factor that binds to CCAAT box-containing upstream activation sites (UASs) within the promoters of numerous eukaryotic genes. The The transcriptional activation of gene expression is mediated by the binding of distinct regulatory factors to specific cis-acting DNA sequence elements, referred to as enhancers or upstream activation sites (UASs), located within the promoters of eukaryotic genes. Many of these transcription factors are composed of multiple polypeptides that interact in a specific manner to form an oligomeric complex that is capable of recognizing specific cisacting DNA sequence elements. Several families of hetero-oligomeric transcription factors have been identified in eukaryotes (McKnight et al. 1987;Olesen et al. 1987;

show abstract

Section: Discussionmentioning

confidence: 99%

Cloning of yeast HAP5: a novel subunit of a heterotrimeric complex required for CCAAT binding.

McNabb¹,

Xing²,

Guarente³

1995

Genes Dev.

262

244

View full text Add to dashboard Cite

show abstract

“…Cells were washed with Ix PBS/1 mM EGTA 24 hr post-transfection and collected 12 hr later. To measure reporter and internal reference transcripts, cytoplasmic RNA was prepared by the NP-40 lysis method and probed with radiolabeled antisense 3-globin (P134) and a-globin (a98) probes (Cleary et al 1993). Unprotected RNA was digested with RNase A and Tj, and the resulting protected RNAs separated on a 6% denaturing polyacrylamide gel.…”

Section: Transient Expression Assaymentioning

confidence: 99%

“…Immediately after seeding, the cells were placed at the assay temperature (either 33.5°C or 39.5°C) and then transfected 24 hr later by calcium phosphate coprecipitation essentially as described by Cleary et al (1993). Briefly, each plate was transfected with 4 pg of the VP16-responsive (3-globin-related reporter plasmid pU2/3 6xTAAT, along with 200 ng of the internal reference plasmid pa4x(A+C), 80 ng of a wild-type VP16 expression plasmid (pC-GNVP16) where appropriate, and pUC119 carrier DNA to a total of 20 pg DNA.…”

Section: Transient Expression Assaymentioning

confidence: 99%

A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function.

Goto¹,

Motomura²,

Wilson³

et al. 1997

Genes Dev.

Self Cite

137

192

View full text Add to dashboard Cite

The temperature-sensitive BHK21 hamster cell line tsBN67 ceases to proliferate at the nonpermissive temperature after a lag of one to a few cell divisions, and the arrested cells display a gene expression pattern similar to that of serum-starved cells. The temperature-sensitive phenotype is reversible and results from a single missense mutation-proline to serine at position 134-in HCF, a cellular protein that, together with the viral protein VP16, activates transcription of herpes simplex virus (HSV) immediate-early genes. The tsBN67 HCF mutation also prevents VP16 activation of transcription at the nonpermissive temperature. The finding that the same point mutation in HCF disrupts both VP16 function and the cell cycle suggests that HCF plays a role in cell-cycle progression in addition to VP16-dependent transcription.[Key Words: tsBN67; HCF protein,-VP16 function,-GQ/GI cell cycle arrest; transcription] Received November 14, 1996; accepted in revised form February 7, 1997.Conditional mutations, particularly temperature-sensitive mutations, have been valuable tools for clarifying cell-cycle regulation in yeast as well as mammalian cells (for review, see Marcus et al. 1985). Previously, we have isolated a series of temperature-sensitive cell-proliferation mutants from the hamster BHK21 cell line (Nishimoto and Basilico 1978;Nishimoto et al. 1982). Following mutagenesis with N-methyl-N'-nitro-JV-nitrosoguanidine, mutants that proliferate at the permissive temperature of 33.5°C but not at the nonpermissive temperature of 39.5°C were concentrated through multiple rounds of negative selection with the cytotoxic base analog 5-fluoro-2-deoxyuridine to eliminate proliferating cells at the elevated temperature. Based on the ability of hybrid cells created by the fusion of different mutant lines to grow at the nonpermissive temperature, these temperature-sensitive lines have been classified into 25 complementation groups (Nishimoto and Basilico 1978;Nishimoto et al. 1982).To identify the genes affected by these mutations, human DNA has been used to complement the hamsterPresent address:

show abstract

“…Oct-1 binds independently to TAATGARAT elements and directs the recruitment of VP16 via determinants present in the POU homeodomain (17)(18)(19)(20)(21). The prior binding of Oct-1 to TAATGARAT elements is a prerequisite to the formation of VIC; however, the efficient incorporation of VP16 into the complex requires the auxiliary component VCAF-1, a large cellular factor which can interact directly with VP16 in the absence of Oct-1 and DNA (5,7,8,13,14,17).…”

mentioning

confidence: 99%

Amino Acid Substitutions in the Herpes Simplex Virus Transactivator VP16 Uncouple Direct Protein-Protein Interaction and DNA Binding from Complex Assembly and Transactivation

Shaw¹,

Knez²,

Capone³

1995

Journal of Biological Chemistry

View full text Add to dashboard Cite

The herpes simplex virus transactivator VP16 directs the assembly of a multicomponent protein-DNA complex that requires the participation of two cellular factors, the POU homeodomain protein Oct-1, which binds independently to response elements, and VCAF-1 (VP16 complex assembly factor; also called HCF, C1), a factor that binds directly to VP16. A number of distinct properties of VP16 have been implicated in the assembly of the VP16-induced complex (VIC). These include its independent association with VCAF-1 and, under appropriate conditions, its ability to bind to DNA or to DNAbound Oct-1 in the absence of VCAF-1. In order to probe the requirements of these individual interactions in the functional asembly of VIC, we mutated selected charged amino acids in two subdomains of VP16 previously shown to be important in protein-DNA complex formation. Purified VP16 proteins were analyzed for their ability to direct protein-DNA complex formation and to interact directly with VCAF-1. Several classes of mutants that were differentially compromised in VCAF-1 interaction, direct DNA binding, and/or association with DNA-bound Oct-1 were obtained. Interestingly, all of the derivatives were still capable of generating the VIC complex in vitro and activating transcription in vivo. Our findings indicate that the cooperative assembly of functional VP16-containing complexes can occur by pathways that do not necessarily require the prior interaction of VP16 with VCAF-1 or the ability of VP16 to bind directly to DNA or associate with DNA-bound Oct-1.

show abstract

Differential positive control by Oct-1 and Oct-2: activation of a transcriptionally silent motif through Oct-1 and VP16 corecruitment.

Cited by 85 publications

References 64 publications

Cloning of yeast HAP5: a novel subunit of a heterotrimeric complex required for CCAAT binding.

Cloning of yeast HAP5: a novel subunit of a heterotrimeric complex required for CCAAT binding.

A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function.

Amino Acid Substitutions in the Herpes Simplex Virus Transactivator VP16 Uncouple Direct Protein-Protein Interaction and DNA Binding from Complex Assembly and Transactivation

Contact Info

Product

Resources

About