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At least 19 recordsLinked to original sources
PubMed1988

Transcription of a U6 small nuclear RNA gene in vitro. Transcription of a mouse U6 small nuclear RNA gene in vitro by RNA polymerase III is dependent on transcription factor(s) different from transcription factors IIIA, IIIB, and IIIC.

U6 small nuclear RNA (snRNA), an essential component of the eukaryotic spliceosomes, is unique in that it is synthesized by RNA polymerase III, while all other U-snRNAs are synthesized by RNA polymerase II. U6 genes are notable for functional upstream regulatory elements which resemble RNA polymerase II regulatory sequence motifs. In this study, the optimal conditions for transcription of the U6 snRNA gene in vitro were found to be similar to conditions optimal for transcription of 5S RNA genes. To purify the trans-acting factors necessary for the transcription of the U6 RNA gene, HeLa cell extracts were fractionated on a DEAE-Sephadex column, and three fractions, designated DE-50, DE-175, and DE-500, were obtained by stepwise elution with 50, 175, and 500 mM ammonium sulfate, respectively. DE-175 fraction transcribed tRNA and 5S RNA genes but not a mouse U6 RNA gene. Complementation of the DE-175 fraction with the DE-50 fraction resulted in the transcription of the U6 RNA gene. Experiments in which the transcription factor (TFIIIA) was selectively inactivated indicated that TFIIIA is not required for the transcription of the U6 RNA gene. These results show that the U6 snRNA gene, although transcribed by RNA polymerase III, differs from tRNA and 5S RNA genes in that factors other than TFIIIA, -IIIB, and -IIIC are required for U6 gene transcription in vitro.

Cloning, Molecular↗
PubMed1989

The CD3 delta gene encodes multiple transcripts regulated by transcriptional and post-transcriptional mechanisms.

CD3 is a multi-subunit complex of proteins noncovalently associated with the T cell receptor (TcR) for antigen. Considerable evidence indicates a role for CD3 molecules in the transduction of activation signals in T cells. The murine CD3 delta gene encodes a 0.7-kb transcript present in mature T cells. Here we report the characterization of several additional CD3 delta transcripts; two nuclear transcripts, 4-4.5 kb in size, and two predominamtly cytoplasmic transcripts of 1.5 kb and 2.5 kb. Both T lymphoma cell lines and normal thymocytes express the 1.5-kb and 2.5-kb CD3 delta transcripts. These cytoplasmic transcripts have long 3'-untranslated sequences which extend beyond the polyadenylation site of the predominant 0.7-kb transcript. The protein synthesis inhibitor cycloheximide (CHX) increases the expression of all three cytoplasmic CD3 delta transcripts, indicating that their level of expression may be regulated by a labile inhibitor protein(s). The CHX elicited increase in CD3 delta mRNA appears to result from post-transcriptional events since the rate of CD3 delta gene transcription remains constant. In contrast to CHX, the calcium ionophore A23187 increases the rate of CD3 delta gene transcription and, like CHX, also increases the level of cellular CD3 delta mRNA. The immunosuppressive agent cyclosporin A inhibits A23187-mediated stimulation of transcription, but has no effect on the CHX-mediated induction of CD3 delta mRNA. We conclude that both transcriptional and post-transcriptional mechanisms can regulate the amount of all three cytoplasmic CD3 delta transcripts.

Animals↗
PubMed1989

Transcription of a poxvirus early gene is regulated both by a short promoter element and by a transcriptional termination signal controlling transcriptional interference.

The promoter region of an early gene (38K gene) of cowpox virus has been characterized by deletion and linker scanning mutational analyses. Modified versions of this promoter region were placed into the genome of vaccinia virus, and their transcriptional efficiencies were assessed by quantifying RNAs transcribed from these sequences. These analyses showed that the sequences in the region between 33 and 4 base pairs upstream of the transcriptional start site affect the efficiency of transcription from this promoter. Linker scanning mutations in the -27 to -10 region inhibited transcription. This region contains the sequence 5'-GAAAATATATT-3', which is present in at least two other early genes in the same positions (-21 to -11) relative to the transcriptional start sites of these genes. Elements of this sequence are similarly positioned in the promoter regions of several other poxvirus genes, suggesting that this sequence represents a transcriptional control element of at least a subset of poxvirus genes. The -8 to -2 sequence (5'-TTTTTAT-3') contains a transcriptional termination signal. Mutation of this sequence had two separate effects: (i) it reduced the efficiency of transcription from the promoter by approximately 30%, and (ii) it prevented this sequence from terminating the transcription from upstream genes. When overlapping transcription from upstream genes was not prevented by a termination signal present either within the 38K promoter or upstream of the promoter, transcription from this promoter was reduced by about 30%. This indicates that transcriptional termination has a role in the regulation of viral gene expression by controlling transcriptional interference.

Amino Acid Sequence↗
PubMed1991

Construction of a novel RNA-transcript-trimming plasmid which can be used both in vitro in place of run-off and (G)-free transcriptions and in vivo as multi-sequences transcription vectors.

We have constructed a new transcription system that allows trimming of both 5' and 3'-termini of any RNA transcripts by means of cis-acting ribozyme activities. The vector consists of a promoter, '5' Processing Ribozyme', any DNA template to be transcribed, and '3' Processing Ribozyme' sequences. When the vector possessing T7 promoter was tested in vitro, the transcription efficiency from the circular template was over ten-fold higher than using linearized template (run-off transcription). Further, since uniform RNAs with defined 5'- and 3'-ends can be produced, this strategy complements the conventional run-off transcription. Also the 5'-/3'-trimmed uniform RNA can function as a reporter in elucidating transcription factors and promoter regions in vitro, this strategy can replace the widely used (G)-free transcription (Sawadogo and Roeder (1985) Proc. Natl. Acad. Sci. USA 82, 4394-4398). With this strategy, in addition to the advantage that the template DNA need not be linearized prior to transcription, a cytidine-minus sequence is no longer necessary for quantitative analysis of transcription factors. Since any sequences including those of RNA virus can be inserted between the '5' Processing Ribozyme' and the '3' Processing Ribozyme' sequences, and the entire unit can be inserted into any genes under active transcription, this construct is useful like that of Dzianott and Bujarski ((1989) Proc. Natl. Acad. Sci. USA 86, 4823-4827) for RNA virologists because these strategies provide RNA transcripts without heterologous sequences which may greatly diminish infectivity. Moreover, since the construct can also be used in vivo, multi-transcripts such as trans-acting ribozymes targeted to various sites would be produced by concatenating the entire units in tandem.

Base Sequence↗
PubMed1990

Factors involved in specific transcription by mammalian RNA polymerase II: role of transcription factors IIA, IID, and IIB during formation of a transcription-competent complex.

Human transcription factor TFIID, the TATA-binding protein, was partially purified to a form capable of associating stably with the TATA motif of the adenovirus major late promoter. Binding of the human and yeast TFIID to the TATA motif was stimulated by TFIIA. TFIIA is an integral part of a complex capable of binding other transcription factors. A complex formed with human TFIID and TFIIA (DA complex) was specifically recognized by TFIIB. We found that TFIIB activity was contained in a single polypeptide of 32 kDa and that this polypeptide participated in transcription and was capable of binding to the DA complex to form the DAB complex. Formation of the DAB complex required TFIIA, TFIID, and sequences downstream of the transcriptional start site; however, the DA complex could be formed on an oligonucleotide containing only the adenovirus major late promoter TATA motif. Using anti-TFIIB antibodies and reagents that affect the stability of a transcription-competent complex, we found that yeast and human TFIID yielded DAB complexes with different stabilities.

Base Sequence↗
PubMed1987

Two transcriptional activators, CCAAT-box-binding transcription factor and heat shock transcription factor, interact with a human hsp70 gene promoter.

We characterized the activity of a human hsp70 gene promoter by in vitro transcription. Analysis of 5' deletion and substitution mutants in HeLa nuclear extracts showed that the basal activity of the promoter depends primarily on a CCAAT-box sequence located at -65. A protein factor, CCAAT-box-binding transcription factor (CTF), was isolated from HeLa nuclear extracts and shown to be responsible for stimulation of transcription in a reconstituted in vitro system. DNase I footprinting revealed that CTF interacts with two CCAAT-box elements located at -65 and -147 of the human hsp70 promoter. An additional binding activity, heat shock transcription factor (HSTF), which interacted with the heat shock element, was also identified in HeLa extract fractions. This demonstrates that the promoter of this human hsp70 gene interacts with at least two positive transcriptional activators, CTF, which is required for CCAAT-box-dependent transcription as in other promoters such as those of globin and herpes simplex virus thymidine kinase genes, and HSTF, which is involved in heat inducibility.

Base Sequence↗
PubMed1989

Transcription factor IIIA gene expression in Xenopus oocytes utilizes a transcription factor similar to the major late transcription factor.

Xenopus transcription factor IIIA (TFIIIA) gene expression is stringently regulated during development. The steady-state level of TFIIIA mRNA in a somatic cell is approximately 10(6) times less than in an immature oocyte. We have undertaken studies designed to identify differences in how the TFIIIA gene is transcribed in oocytes and somatic cells. In this regard, we have localized an upstream transcriptional control element in the TFIIIA promoter that stimulates transcription from the TFIIIA promoter approximately threefold in microinjected oocytes. The upstream element, in cis. does not stimulate transcription from the TFIIIA promoter in somatic cells. Thus, the element appears to be oocyte specific in the context of the TFIIIA promoter. However, both oocytes and somatic cells contain a protein (or a related protein) that binds the upstream element. We have termed this protein from oocytes the TFIIIA distal element factor. The sequence of the upstream element is similar to the sequence of the upstream element found in the adenovirus major late promoter that is a binding site for the major late transcription factor. By gel shift analysis, chemical footprinting, methylation intereference, and point mutation analysis, we demonstrate that the TFIIIA distal element factor and major late transcription factor have similar DNA-binding properties.

Animals↗
PubMed1991

Concerted stimulation of transcription by glucocorticoid receptors and basal transcription factors: limited transcriptional synergism suggests mediation by coactivators/adaptors.

Steroid receptors have been reported to stimulate transcription in a manner synergistic with other transcription factors. We have examined this synergism or functional cooperativity between glucocorticoid receptors and basal transcription factors in a variety of promoter and reporter gene contexts. A fragment containing a hormone response element from mouse mammary tumor virus was fused to well characterized promoters from the herpes virus thymidine kinase and mouse beta-globin genes and to related mutant promoters altered by inactivation of transcription factor-binding sites through point mutagenesis or deletion. These constructs were transfected into glucocorticoid-sensitive fibroblasts, and reporter gene activity was assessed with or without hormonal stimulation. In contrast to previous studies, we found little indication of synergistic interaction between elements mediating a hormone response and adjacent basal promoters. In fact, we observed that inactivating basal factor-binding sites, thereby decreasing promoter strength, actually increased hormone inducibility. We suggest that the inverse relationship between basal promoter strength and the induction ratio attained upon hormonal stimulation may be due to limitation of a common factor, an "adaptor" through which glucocorticoid receptor and basal transcription factors interact with the components of the RNA polymerase II complex to stimulate rates of transcription.

Animals↗
PubMed1991

Transcription initiated by RNA polymerase II and transcription factors from liver. Structure and action of transcription factors epsilon and tau.

We have fractionated rat liver and identified a set of transcription factors that are essential for accurate initiation by RNA polymerase II. These factors were resolved into five distinct enzyme fractions designated alpha, beta gamma, delta, epsilon, and tau. Four of these fractions can now be replaced with purified proteins. alpha and beta gamma were previously purified to apparent homogeneity (Conaway, J. W., and Conaway, R. C. (1989) J. Biol. Chem. 264, 2357-2362). Here, we report purification to near homogeneity of transcription factor epsilon. Epsilon has a native molecular mass of approximately 90 kDa and is composed of 34- and 58-kDa polypeptides. Both the 34- and 58-kDa polypeptides are required for runoff transcription. In addition, we show that transcription factor tau is a rat liver homologue of the TATA factor (TFIID or BTF1) that can be efficiently replaced in transcription in vitro by recombinant yeast TFIID. Comparison of the two factors reveals, however, that they differ significantly in their abilities to direct the transcription system to discriminate between promoters of different sequences.

Animals↗
PubMed1990

The transcription complex of the 5 S RNA gene, but not transcription factor IIIA alone, prevents nucleosomal repression of transcription.

Assembly of nucleosomes on a 5 S DNA plasmid with histone H3.H4-N1 complex and histone H2A-H2B dimers causes a marked, 30-300-fold repression of 5 S RNA transcription. This repression is a time-dependent process that parallels the process of nucleosome formation. At physiological histone levels, DNA plasmids carrying nucleosomes with only histones H3 and H4 are transcriptionally permissive. The histone H3-H4 chromatin becomes transcriptionally nonpermissive when histone H2A-H2B dimers complement the nucleosome assembly reaction. H3-H4-H2A-H2B nucleosomes, but not H3-H4 nucleosomes, displace a DNA-bound transcription factor IIIA. In contrast, a preassembled 5 S RNA transcription complex is refractory to inactivation by nucleosomes.

Animals↗
PubMed1990

Transcription initiated by RNA polymerase II and purified transcription factors from liver. Cooperative action of transcription factors tau and epsilon in initial complex formation.

Synthesis of accurately initiated transcripts has been reconstituted with RNA polymerase II and a set of five transcription factors purified from rat liver. In addition to three previously identified factors alpha, beta gamma, and delta (Conaway, R. C., and Conaway, J. W. (1989) Proc. Natl. Acad. Sci. U. S. A. 86, 7356-7360), transcription in the reconstituted liver system requires two novel factors designated tau and epsilon. These five transcription factors comprise two functional classes: (i) promoter recognition factors (tau and epsilon), which interact with template DNA to facilitate formation of a stable initial complex that is subsequently recognized and bound by RNA polymerase II, and (ii) RNA chain initiation factors (alpha, beta gamma, and delta), which do not participate in formation of the initial complex, but which are essential for transcription initiation.

Animals↗
PubMed1992

Factors involved in specific transcription by mammalian RNA polymerase II: purification and analysis of transcription factor IIA and identification of transcription factor IIJ.

The previously described transcription factor IIA (TFIIA) protein fraction was separated into two factors that affect transcription, TFIIA and TFIIJ. TFIIA was found to have a stimulatory effect, and TFIIJ was found to be required for transcription. The requirement of TFIIJ was observed when bacterially produced purified human or yeast (Saccharomyces cerevisiae) TATA-binding protein (TBP) was used in lieu of the endogenous HeLa cell TFIID complex, suggesting that TFIIJ may be part of the TFIID complex. The stimulatory activity of TFIIA was found also to be dependent on the source of the TBP. Transcription reactions reconstituted with TFIID were stimulated by TFIIA; however, when human or yeast TBP was used instead of TFIID, TFIIA had no effect. TFIIA was found to interact with the TBP and was extensively purified by the use of affinity chromatography on columns containing immobilized recombinant yeast TBP. TFIIA is a heterotrimer composed of polypeptides of 34, 19, and 14 kDa. These three polypeptides were required to isolate, by using the gel mobility shift assay, a stable complex between TBP and the TATA box sequence.

Chromatography↗
PubMed1992

Mechanism of coronavirus transcription: duration of primary transcription initiation activity and effects of subgenomic RNA transcription on RNA replication.

Previously, we established a system whereby an intergenic region from mouse hepatitis virus (MHV) inserted into an MHV defective interfering (DI) RNA led to transcription of a subgenomic DI RNA in helper virus-infected cells. By using this system, the duration of a primary transcription initiation activity which transcribes subgenomic-size RNAs from the genomic-size RNA template in MHV-infected cells was examined. Efficient DI genomic and subgenomic RNA synthesis was observed when the DI RNA was transfected at 1, 3, 3.5, 5, and 6 h postinfection, indicating that all activities which are necessary for MHV RNA synthesis are present continuously during the first 6 h of infection. The effect of subgenomic DI RNA synthesis on DI genomic RNA replication was then examined. Replication efficiency of the DI genomic RNA which synthesized the subgenomic RNA was approximately 70% lower than that of DI genomic RNA which did not synthesize the subgenomic DI RNA in MHV-infected cells. Cotransfection of two different-size DI RNAs demonstrated that replication of the larger DI RNA was strongly inhibited by replication of the smaller genomic DI RNA. Cotransfection of two DI RNA species of the same length into MHV-infected cells demonstrated that reduced replication of the genomic DI RNA which synthesizes the subgenomic RNA did not affect the replication of cotransfected DI RNA, demonstrating that the reduction in DI genomic RNA replication works only in cis, not in trans. Therefore, the previously proposed hypothesis that coronavirus, subgenomic RNA synthesis may inhibit the replication of genomic RNA by competing for a limited amount of virus-derived factors seems unlikely. Possible mechanisms of coronavirus transcription are discussed.

Animals↗
PubMed1990

Transcription initiated by RNA polymerase II and purified transcription factors from liver. Transcription factors alpha, beta gamma, and delta promote formation of intermediates in assembly of the functional preinitiation complex.

Accurate initiation at promoters by RNA polymerase II in a highly purified transcription system from rat liver depends on five accessory factors, which comprise two functional classes: (i) "promoter recognition" factors, designated tau and epsilon, which interact with template DNA to form an initial complex that serves as a recognition site for binding by RNA polymerase II and (ii) "RNA chain initiation" factors, designated alpha, beta gamma, and delta, which do not participate in initial complex formation, but which are essential for initiation (Conaway, J. W., Reines, D., and Conaway, R. C. (1990) J. Biol. Chem. 265, 7552-7558). Here we investigate the roles of alpha, beta gamma, and delta in accurate initiation. Kinetic evidence indicates that all three factors act in a stage prior to RNA synthesis to facilitate formation of a functional preinitiation complex. Moreover, results of "template challenge" experiments argue that all three factors become stably associated with the preinitiation complex during this stage. Neither alpha, beta gamma, nor delta functions catalytically in this process; instead, each factor appears to interact directly and stoichiometrically with intermediates in assembly of the preinitiation complex. Order of addition experiments reveal that transcription factors alpha and beta gamma assemble into the preinitiation complex by an "ordered" mechanism. We discuss two recently proposed models for assembly of the functional preinitiation complex and argue that our findings provide a plausible means of reconciling them.

Animals↗
PubMed2026

Transcription Start Regions in PTU-intergenic regions drive cell cycle-dependent transcriptional activation events in Leishmania donovani.

Leishmania displays an unconventional mode of transcription, with long clusters of genes being transcribed polycistronically from Transcription Start Regions (TSRs), being processed into monocistronic units prior to translation. It has long been believed that transcription is constitutive: failure to identify consensus sequences across TSRs (except a GT-rich motif supporting transcription in Trypanosoma brucei) and absence of canonical eukaryotic transcription factors led to the conclusion that regulation is primarily post-transcriptional, with epigenetics playing a role in triggering transcription initiation. This study stems from our previous findings identifying a few genes to be activated in a cell cycle-dependent manner. Using nuclear run-on assays to analyze nascent transcripts of two chromosomes, chromosomes 2 and 14, we find that while most genes are constitutively transcribed, a subset of genes gets activated at specific cell cycle stages. Reporter assays reveal that this transcriptional activation is driven by the regions immediately upstream of the genes. Sequence analyses of these TSRs lying in polycistronic intergenic regions (PIRs) uncovered a 10-mer GT-rich motif, in synchrony with earlier findings in T. brucei identifying a GT-rich motif at bidirectional TSRs. We also identify a second 25-mer motif at these TSRs, and deletion analyses find this motif to be critical for regulating gene expression. The findings of this study reveal that transcriptional events in these unicellular parasites are more complex than believed thus far: not all transcriptional events are constitutive, polycistronic transcription is not the only mode of transcription, and cis-acting sequence elements regulate at least some transcriptional events in these parasites.IMPORTANCEEndemic to 90 countries, Leishmania parasites cause a spectrum of diseases called Leishmaniases. No vaccines for human use are available to date, and the drugs currently used to treat the disease are expensive, have toxic side effects, and have complex administration regimens, with emerging drug resistance compounding problems. Researchers continue to investigate Leishmania cellular processes, with the hope of uncovering new therapeutic target sites. Gene regulation in these parasites is unusual, being modulated by various mechanisms, including epigenetic modifications, gene dosage, and post-transcriptional processing. Transcription is typically polycistronic and constitutive, initiating from Transcription Start Regions (TSRs) lying upstream of the first gene in the polycistronic transcription unit (PTU). The work presented here reveals that a subset of genes is transcribed monocistronically in a cell cycle-dependent manner from Transcription Start Regions lying in the PTU-intergenic regions (PIRs), underscoring the complexities of gene regulation in these parasites.

Leishmania donovani↗
PubMed1991

Poliovirus proteinase 3C converts an active form of transcription factor IIIC to an inactive form: a mechanism for inhibition of host cell polymerase III transcription by poliovirus.

In HeLa cells, RNA polymerase III (pol III)-mediated transcription is severely inhibited by poliovirus infection. This is due primarily to a reduction in the transcriptional activity of TFIIIC, a transcription factor which binds in a sequence specific manner to the internal promoter of pol III genes. Using gel retardation assays, we have shown previously that inhibition of pol III transcription by poliovirus is correlated with disappearance of a transcriptionally active form of TFIIIC (complex I) concomitant with the appearance of a faster mobility, transcriptionally inactive form of TFIIIC (complex III). We show here that a poliovirus with a point mutation in the proteinase 3C (3Cpro) region failed to produce complex III and is limited in its ability to inhibit pol III transcription compared with the wild-type virus. Incubation of purified 3Cpro, expressed in Escherichia coli, with transcriptionally active TFIIIC (complex I) in vitro resulted in generation of the transcriptionally inactive complex III form of TFIIIC. In an in vitro transcription assay, treatment of the complex I form of TFIIIC with 3Cpro almost completely inhibited pol III transcription. Finally expression of the 3Cpro gene in transfected HeLa cells resulted in significant inhibition of pol III-mediated transcription. The results presented here suggest that proteolysis of the transcriptionally active form of TFIIIC by poliovirus 3Cpro is a mechanism by which poliovirus inhibits host cell RNA pol III transcription.

3C Viral Proteases↗
PubMed1990

Analysis of Saccharomyces cerevisiae his3 transcription in vitro: biochemical support for multiple mechanisms of transcription.

The promoter region of the Saccharomyces cerevisiae his3 gene contains two TATA elements, TC and TR, that direct transcription initiation to two sites designated +1 and +13. On the basis of differences between their nucleotide sequences and their responsiveness to upstream promoter elements, it has previously been proposed that TC and TR promote transcription by different molecular mechanisms. To begin a study of his3 transcription in vitro, we used S. cerevisiae nuclear extracts together with various DNA templates and transcriptional activator proteins that have been characterized in vivo. We demonstrated accurate transcription initiation in vitro at the sites used in vivo, transcriptional activation by GCN4, and activation by a GAL4 derivative on various gal-his3 hybrid promoters. In all cases, transcription stimulation was dependent on the presence of an acidic activation region in the activator protein. In addition, analysis of promoters containing a variety of TR derivatives indicated that the level of transcription in vitro was directly related to the level achieved in vivo. The results demonstrated that the in vitro system accurately reproduced all known aspects of in vivo his3 transcription that depend on the TR element. However, in striking contrast to his3 transcription in vivo, transcription in vitro yielded approximately 20 times more of the +13 transcript than the +1 transcript. This result was not due to inability of the +1 initiation site to be efficiently utilized in vitro, but rather it reflects the lack of TC function in vitro. The results support the idea that TC and TR mediate transcription from the wild-type promoter by distinct mechanisms.

Base Sequence↗
PubMed1989

Transcription elongation factor SII (TFIIS) enables RNA polymerase II to elongate through a block to transcription in a human gene in vitro.

Elongation and termination by RNA polymerase II are important regulatory steps for eukaryotic gene expression. We have previously studied the transcription of linear DNA templates where specific initiation of transcription by highly purified RNA polymerase II can be achieved in the absence of promoters and promoter-specific factors. Using these templates we have shown that a human histone gene, H3.3, contains sequences (intrinsic terminators) within which purified RNA polymerase II will efficiently terminate transcription (Reines, D., Wells, D., Chamberlin, M.J., and Kane, C. M. (1987) J. Mol. Biol. 196, 299-312). Curiously, these signals were found within an intron, 3'-untranslated, and protein-encoding regions of the gene suggesting that they might act to attenuate transcription of H3.3 in vivo. Here we show that intrinsic terminator sequences from an H3.3 gene intron also block in vitro transcript elongation by RNA polymerase II when the enzyme has initiated transcription from a promoter using highly purified transcription initiation factors. However, under the conditions used for promoter-specific transcription there is little transcript release. Instead the polymerase can pause at these sites for periods exceeding 60 min. We have identified and partially purified an activity from HeLa cells that causes the transcription complex to read through this block to transcription elongation. This readthrough activity fractionates with a previously characterized elongation factor (SII) over three chromatographic columns. A homogeneous preparation of calf thymus SII can also provide this activity in trans. This factor may facilitate passage of the RNA polymerase II transcription complex through such intragenic sites in cellular genes in vivo.

Animals↗