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PubMed1999

The abundance of cell cycle regulatory protein Cdc4p is controlled by interactions between its F box and Skp1p.

Posttranslational modification of a protein by ubiquitin usually results in rapid degradation of the ubiquitinated protein by the proteasome. The transfer of ubiquitin to substrate is a multistep process. Cdc4p is a component of a ubiquitin ligase that tethers the ubiquitin-conjugating enzyme Cdc34p to its substrates. Among the domains of Cdc4p that are crucial for function are the F-box, which links Cdc4p to Cdc53p through Skp1p, and the WD-40 repeats, which are required for binding the substrate for Cdc34p. In addition to Cdc4p, other F-box proteins, including Grr1p and Met30p, may similarly act together with Cdc53p and Skp1p to function as ubiquitin ligase complexes. Because the relative abundance of these complexes, known collectively as SCFs, is important for cell viability, we have sought evidence of mechanisms that modulate F-box protein regulation. Here we demonstrate that the abundance of Cdc4p is subject to control by a peptide segment that we term the R-motif (for "reduced abundance"). Furthermore, we show that binding of Skp1p to the F-box of Cdc4p inhibits R-motif-dependent degradation of Cdc4p. These results suggest a general model for control of SCF activities.

Binding Sites↗

PubMed2005

Medical survey of female boxing in Italy in 2002-2003.

BACKGROUND: Female boxing has been permitted in Italy since 2001. According to the latest Italian laws, athletes applying to become boxers have to pass a pre-participation medical examination. OBJECTIVE: To collect novel medical information from the pre-participation visits and mandatory pre-competition and post-competition examinations for all fights involving Italian female boxers in 2002-2003. METHODS: A retrospective study on all official female boxing competitions in Italy from January 2002 to October 2003 was conducted. A prospective study on 28 amateur female boxers was also carried out. RESULTS: Retrospective study: data from 664 examinations were collected. Pre-match examinations were negative. After competitions, 19/645 visits showed some injuries, with mild, soft tissue facial lesions, epistaxis, and hand-wrist problems being the most common. Prospective study: no major lesions were found during the study. One fibroadenoma, one ovarian cyst, and one intramural uterine myoma were found. One boxer was referred to a neurologist because of non-specific electroencephalographic (EEG) abnormalities, which persisted six months later. On a re-admission examination, which was needed because of a contest that was stopped because the referee judged that she was receiving blows to the head that were dangerous, one boxer showed non-specific EEG alterations and nystagmus. A cerebral magnetic resonance imaging scan was normal. She was allowed to participate in competitions again when her EEG returned to normal and clinical signs disappeared. Deviation of the nasal septum was quite common (68%). No major eye injuries were reported. CONCLUSION: Probably because of the correct preventive medical approach, female boxing is much safer than expected, and no major lesions (requiring hospital admission) were reported. Any lesions to the breast and reproductive system could not be considered to be boxing related.

Adult↗

PubMed2005

The risk of chronic traumatic brain injury in professional boxing: change in exposure variables over the past century.

OBJECTIVES: To determine if boxing exposure has changed over time and hence if current professional boxers are at the same risk of developing chronic traumatic brain injury (CTBI) as historical controls. DESIGN: Literature review of published studies and analysis of data of active professional boxers. SUBJECTS: Professional boxers in the United Kingdom and Australia. MAIN OUTCOME MEASURES: Boxing history and participation in sparring and professional bouts. RESULTS: Since the 1930s, the average duration of a professional boxer's career has dropped from 19 years to five years, and the mean number of career bouts has reduced from 336 to 13. This is despite no significant decline in participation rates from 1931 until 2002. CONCLUSIONS: The incidence of boxing related CTBI will diminish in the current era of professional boxing because of the reduction in exposure to repetitive head trauma and increasing medical monitoring of boxers, with preparticipation medical and neuroimaging assessments resulting in the detection of early and potentially pre-symptomatic cases of CTBI.

Australia↗

PubMed2001

Regulation of E-box DNA binding during in vivo and in vitro activation of rat and human hepatic stellate cells.

BACKGROUND: Activation of hepatic stellate cells (HSCs) to a myofibroblastic phenotype is a key event in liver fibrosis. Identification of transcription factors with activities that are modulated during HSC activation will improve our understanding of the molecular events controlling HSC activation. AIMS: To determine if changes in E-box DNA binding activity occur during in vitro and in vivo activation of rat and human HSCs and to investigate mechanisms underlying any observed changes. METHODS: Nuclear extracts were prepared from rat HSCs isolated and cultured from normal and carbon tetrachloride injured rat livers and from HSCs isolated from human liver. EMSA analysis of E-box DNA binding activity was performed on nuclear extracts to determine changes during HSC activation. Western and northern blot analysis of MyoD and Id1 basic helix-loop-helix (bHLH) proteins was performed to confirm expression in HSC. RESULTS: HSC activation was associated with inducible expression of two low mobility E-box binding complexes that were immunoreactive with an anti-MyoD antibody. MyoD mRNA expression was found at similar levels in freshly isolated and activated HSCs; in contrast, MyoD protein expression was elevated in activated HSCs. Activation of rat HSCs was accompanied by reduced expression of the inhibitory bHLH protein Id1. CONCLUSIONS: In vitro and in vivo activation of rat and human HSCs is accompanied by induction of MyoD binding to E-box DNA sequences which appears to be mechanistically associated with elevated MyoD protein expression and reduced expression of the inhibitory Id1 protein. Clarification of the role of MyoD and Id1 proteins in HSC activation and liver fibrogenesis is now required.

Adult↗

PubMed2004

Correlation between the UDP-glucuronosyltransferase (UGT1A1) TATAA box polymorphism and carcinogen detoxification phenotype: significantly decreased glucuronidating activity against benzo(a)pyrene-7,8-dihydrodiol(-) in liver microsomes from subjects with the UGT1A1*28 variant.

Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide. The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)>(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert's syndrome. To determine whether the UGT1A1 TATAA box polymorphism may play a role in the overall glucuronidation of BPD(-) in humans, we compared UGT1A1 TATAA box genotype with BPD(-) glucuronidating activity in normal liver microsomes. Significant decreases in UGT1A1 protein (P < 0.005) and bilirubin conjugation activity (P < 0.001) were observed in liver microsomes from subjects homozygous for the UGT1A1*28 allelic variant compared with subjects homozygous for the wild-type UGT1A1*1 allele. Significant decreases in BPD(-) glucuronidation activity (P < 0.02) were observed in subjects with the UGT1A1(*28/*28) genotype compared with subjects having the wild-type UGT1A1(*1/*1) genotype in assays of liver microsomes that included 0.1 mM alpha-naphthylamine, a competitive inhibitor of UGT1A9 and not UGT1A1. Similar phenotype:genotype correlations were observed when we compared subjects with the UGT1A1(*28/*28) genotype with subjects having the UGT1A1(*1/*28) genotype. In assays with alpha-naphthylamine, the K(m) of liver microsomes against BPD(-) was similar to that reported for UGT1A1-overexpressing baculosomes (319 micro M versus 290 micro M; Fang et al., Cancer Res., 62: 1978-1986, 2002). These data suggest that the UGT1A1 TATAA box polymorphism plays a role in an individual's overall ability to detoxify benzo(a)pyrene and in cancer risk.

Dihydroxydihydrobenzopyrenes↗

PubMed2000

Thrombin activates a Y box-binding protein (DNA-binding protein B) in endothelial cells.

Thrombin stimulates the expression of multiple genes in endothelial cells (ECs), but the trans-acting factors responsible for this induction remain undefined. We have previously described a thrombin-inducible nuclear factor (TINF), which binds to an element in the PDGF B promoter and is responsible for the thrombin inducibility of this gene. Inactive cytoplasmic TINF is rapidly activated and translocated to nuclei of ECs upon stimulation with thrombin. We have now purified TINF from thrombin-treated ECs. Amino acid sequencing revealed it to be a member of the Y-box protein family, and the sole Y-box protein-encoding cDNA we detected in human or bovine ECs corresponded to DNA-binding protein B (dbpB). DbpB translocated to the nucleus after thrombin stimulation of ECs as shown by FACS analysis of nuclei from ECs expressing GFP-dbpB fusion proteins. During thrombin activation, dbpB was found to be cleaved, yielding a 30-kDa NH(2)-terminal fragment that recognized the thrombin-response element sequence, but not the Y-box consensus sequence. Preincubation of ECs with protein tyrosine phosphatase inhibitors completely blocked dbpB activation by thrombin and blocked induction of endogenous PDGF B-chain mRNA and promoter activation by thrombin. Y-box proteins are known to act constitutively to regulate the expression of several genes. Activation of this class of transcription factors in response to thrombin or any other agonist represents a novel signaling pathway.

Amino Acid Sequence↗

PubMed1999

Activation of the insulin-like growth factor-binding protein-5 promoter in osteoblasts by cooperative E box, CCAAT enhancer-binding protein, and nuclear factor-1 deoxyribonucleic acid-binding sequences.

Insulin-like growth factor (IGF)-binding protein-5 (IGFBP-5) has IGF-dependent and -independent actions. PGE2 rapidly increases IGFBP-5 expression by osteoblasts through cAMP-dependent processes. A minimal DNA sequence required for basal and PGE2-stimulated IGFBP-5 promoter activity spans -69 to -35 bp. This region adjoins a functional TATA box and contains E box, CCAAT enhancer-binding protein (C/EBP), nuclear factor-1 (NF-1), and activator protein-2 (AP-2) transcription factor related binding motifs. In this study we compared minimal promoter sequences of -74 to +120 bp, without or with mutations in each potential regulatory element, by reporter gene expression and electrophoretic mobility shift assays. Mutation of the E box-related element reduced basal promoter activity by 50% and eliminated the 2-fold stimulatory effect of PGE2. In contrast, mutations in the C/EBP- or NF-1-related elements also reduced basal promoter activity without fully eliminating the PGE2 effect. Overexpression of C/EBPdelta stimulated basal IGFBP-5 promoter activity, and this effect was eliminated by mutating the C/EBP-binding site. However, mutation of the AP-2-binding site or overexpression of AP-2 did not correlate with basal or PGE2-induced promoter activation. By electrophoretic mobility shift assay, prominent gel shift complexes occurred with osteoblast nuclear extracts and 32P-labeled probes spanning the E box-, C/EBP-, and NF-1-related motifs. These gel shift complexes were depleted by specific binding site mutations and were enhanced by PGE2. Increased binding by extracts from PGE2-treated cultures was blocked by cycloheximide treatment. These results identify several elements as integral binding sequences for both basal and PGE2-stimulated IGFBP-5 promoter activity. They further reveal that multiple sequences within this cluster form a basic transcription unit where nuclear factors can accumulate in a protein synthesis-dependent way and enhance IGFBP-5 expression by osteoblasts in response to PGE2.

Animals↗

PubMed2004

Regulation of the human secretin gene is controlled by the combined effects of CpG methylation, Sp1/Sp3 ratio, and the E-box element.

To unravel the mechanisms that regulate the human secretin gene expression, in this study, we have used secretin-expressing (HuTu-80 cells, human duodenal adenocarcinoma) and non-secretin-expressing [PANC-1 (human pancreatic ductile carcinoma) and HepG2 (human hepatocellular carcinoma) cells] cell models for in vitro and in vivo analyses. By transient transfection assays, within the promoter region (-11 to -341 from ATG, relative to the ATG initiation codon), we have initially identified several functional motifs including an E-box and 2 GC-boxes. Results from gel mobility shift and chromatin immunoprecipitation assays confirmed further that NeuroD, E2A, Sp1, and Sp3 bind to these E- and GC-boxes in HuTu-80 cells in vitro and in vivo, whereas only high levels of Sp3 is observed to bind the promoter in HepG2 cells. In addition, overexpression of Sp3 resulted in a dose-dependent repression of the Sp1-mediated transactivation. Collectively, these data suggest that the Sp1/Sp3 ratio is instrumental to controlling secretin gene expression in secretin-producing and non-secretin-producing cells. The functions of GC-box and Sp proteins prompted us to investigate the possible involvement of DNA methylation in regulating this gene. Consistent with this idea, we found a putative CpG island (-336 to 262 from ATG) that overlaps with the human secretin gene promoter. By methylation-specific PCR, all the CpG dinucleo-tides (26 of them) within the CpG island in HuTu-80 cells are unmethylated, whereas all these sites are methylated in PANC-1 and HepG2 cells. The expressions of secretin in PANC-1 and HepG2 cells were subsequently found to be significantly activated by a demethylation agent, 5'-Aza-2' deoxycytidine. Taken together, our data indicate that the human secretin gene is controlled by the in vivo Sp1/Sp3 ratio and the methylation status of the promoter.

5' Flanking Region↗

PubMed2006

1Alpha,25(OH)2D3-induced transrepression by vitamin D receptor through E-box-type elements in the human parathyroid hormone gene promoter.

Although transactivation by the liganded vitamin D receptor (VDR) is well described at the molecular level, the precise molecular mechanism of negative regulation by the liganded VDR remains to be elucidated. We have previously reported a novel class of negative vitamin D response element (nVDRE) called 1alphanVDRE in the human 25(OH)D31alpha-hydroxylase [1alpha(OH)ase] gene by 1alpha,25(OH)2D3-bound VDR. This element was composed of two E-box-type motifs that bound to VDIR for transactivation, which was attenuated by liganded VDR. Here, we explore the possible functions of VDIR and E-box motifs in the human (h) PTH and hPTHrP gene promoters. Functional mapping of the hPTH and hPTHrP promoters identified E-box-type elements acting as nVDREs in both the hPTH promoter (hPTHnVDRE; -87 to -60 bp) and in the hPTHrP promoter (hPTHrPnVDRE; -850 to -600 bp; -463 to -104 bp) in a mouse renal tubule cell line. The hPTHnVDRE alone was enough to direct ligand-induced transrepression mediated through VDR/retinoid X receptor and VDIR. Direct DNA binding of hPTHnVDRE to VDIR, but not VDR/retinoid X receptor, was observed and ligand-induced transrepression was coupled with recruitment of VDR and histone deacetylase 2 (HDAC2) to the hPTH promoter. These results suggest that negative regulation of the hPTH gene by liganded VDR is mediated by VDIR directly binding to the E-box-type nVDRE at the promoter, together with recruitment of an HDAC corepressor for ligand-induced transrepression.

Animals↗

PubMed2005

Concussion in professional football: comparison with boxing head impacts--part 10.

OBJECTIVE: This study addresses impact biomechanics from boxing punches causing translational and rotational head acceleration. Olympic boxers threw four different punches at an instrumented Hybrid III dummy and responses were compared with laboratory-reconstructed NFL concussions. METHODS: Eleven Olympic boxers weighing 51 to 130 kg (112-285 lb) delivered 78 blows to the head of the Hybrid III dummy, including hooks, uppercuts and straight punches to the forehead and jaw. Instrumentation included translational and rotational head acceleration and neck loads in the dummy. Biaxial acceleration was measured in the boxer's hand to determine punch force. High-speed video recorded each blow. Hybrid III head responses and finite element (FE) brain modeling were compared to similarly determined responses from reconstructed NFL concussions. RESULTS: The hook produced the highest change in hand velocity (11.0 +/- 3.4 m/s) and greatest punch force (4405 +/- 2318 N) with average neck load of 855 +/- 537 N. It caused head translational and rotational accelerations of 71.2 +/- 32.2 g and 9306 +/- 4485 r/s. These levels are consistent with those causing concussion in NFL impacts. However, the head injury criterion (HIC) for boxing punches was lower than for NFL concussions because of shorter duration acceleration. Boxers deliver punches with proportionately more rotational than translational acceleration than in football concussion. Boxing punches have a 65 mm effective radius from the head cg, which is almost double the 34 mm in football. A smaller radius in football prevents the helmets from sliding off each other in a tackle. CONCLUSION: Olympic boxers deliver punches with high impact velocity but lower HIC and translational acceleration than in football impacts because of a lower effective punch mass. They cause proportionately more rotational acceleration than in football. Modeling shows that the greatest strain is in the midbrain late in the exposure, after the primary impact acceleration in boxing and football.

Acceleration↗

PubMed2005

T-box transcription factors and their roles in regulatory hierarchies in the developing heart.

T-box transcription factors are important players in the molecular circuitry that generates lineage diversity and form in the developing embryo. At least seven family members are expressed in the developing mammalian heart, and the human T-box genes TBX1 and TBX5 are mutated in cardiac congenital anomaly syndromes. Here, we review T-box gene function during mammalian heart development in the light of new insights into heart morphogenesis. We see for the first time how hierarchies of transcriptional activation and repression involving multiple T-box factors play out in three-dimensional space to establish the cardiac progenitors fields, to define their subservient lineages, and to generate heart form and function.

Animals↗

PubMed1996

The Xenopus T-box gene, Antipodean, encodes a vegetally localised maternal mRNA and can trigger mesoderm formation.

We have used differential display to identify genes inducible by activin and isolated a novel member of the T-box gene family that includes the Xenopus genes Xbrachyury and Eomesodermin. Here we show that this novel gene is unique within the T-box family because it is maternally expressed at a high level. Furthermore, it belongs to a rare class of maternal mRNAs in Xenopus that are localised to the vegetal hemisphere of the egg and we have therefore named it Antipodean. We show here that low amounts of Antipodean injected into ectoderm (animal cap cells) strongly induce pan mesodermal genes such as Xbrachyury and ventral mesodermal genes such as Xwnt-8. Overexpression of Antipodean generates mesoderm of ventral character, and induces muscle only weakly. This property is consistent with the observed late zygotic Antipodean mRNA expression in the posterior paraxial mesoderm and ventral blastopore, and its exclusion from the most dorsal mesodermal structure, the notochord. Antipodean is induced by several molecules of the TGF-beta class, but in contrast to Xbrachyury, not by bFGF. This result suggests that the expression of these T-box genes may be under the control of different regulatory pathways. Finally, we demonstrate that Antipodean and Eomesodermin induce each other and both are able to induce Xbrachyury. The early zygotic expression of Antipodean is not induced by Xbrachyury, though later it is to some extent. Considering its maternal content, Antipodean could initiate a cascade of T-box gene activations. The expression of these genes may, in turn, sustain each other's expression to define and maintain the mesoderm identity in Xenopus.

Amino Acid Sequence↗

PubMed1998

Molecular identification of spadetail: regulation of zebrafish trunk and tail mesoderm formation by T-box genes.

Inhibition of fibroblast growth factor (FGF) signaling prevents trunk and tail formation in Xenopus and zebrafish embryos. While the T-box transcription factor Brachyury (called No Tail in zebrafish) is a key mediator of FGF signaling in the notochord and tail, the pathways activated by FGF in non-notochordal trunk mesoderm have been uncertain. Previous studies have shown that the spadetail gene is required for non-notochordal trunk mesoderm formation; spadetail mutant embryos have major trunk mesoderm deficiencies, but relatively normal tail and notochord development. We demonstrate here that spadetail encodes a T-box transcription factor with homologues in Xenopus and chick. Spadetail is likely to be a key mediator of FGF signaling in trunk non-notochordal mesoderm, since spadetail expression is regulated by FGF signaling. Trunk and tail development are therefore dependent upon the complementary actions of two T-box genes, spadetail and no tail. We show that the regulatory hierarchy among spadetail, no tail and a third T-box gene, tbx6, are substantially different during trunk and tail mesoderm formation, and propose a genetic model that accounts for the regional phenotypes of spadetail and no tail mutants.

Amino Acid Sequence↗

PubMed1995

Activation functions of transcription factor Sp1 at U2 snRNA and TATA box promoters.

To localize regions in the human transcription factor Sp1, which are involved in activating transcription of the U2 snRNA gene promoter and of a TATA box gene promoter, the activation potentials of GAL4/Sp1 chimeras were analyzed in mammalian cells. In vitro mutagenesis analysis of Sp1 showed that mutation of a hydrophobic amino acid residue in glutamine-rich activation domain A impairs stimulation of transcription from the TATA box promoter, but not from the U2 promoter. Furthermore, we found that similar parts of Sp1 are involved in synergistic activation of transcription together with the SV40 enhancer and with an enhancer which binds a single type of transcription factor. This suggests that the activating mechanism of Sp1 is the same with both enhancers. Interestingly, we found that the glutamine-rich domains A and B, that stimulate transcription from the TATA box promoter were not sufficient for U2 gene activation. Stimulation of U2 transcription required amino acid residues 231-485 of Sp1, which contain the glutamine-rich domain B and a serine/threonine-rich part. Since overlapping, but non-identical parts of Sp1 are required for activation of the two promoter types, we conclude that Sp1 activates the U2 snRNA and TATA box promoters by different mechanisms.

Base Sequence↗

PubMed1995

The neuropsychiatric aspects of boxing.

OBJECTIVE: To review the neuropsychiatry of boxing. METHOD: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. RESULTS: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy (CTE). Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. CTE includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for CTE. CONCLUSIONS: Boxing results in a spectrum of CTE ranging from mild, nonprogressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for CTE. For this reason, there is an active movement to ban boxing.

Athletic Injuries↗

PubMedDate not supplied

Expression of Y box-binding protein-1 correlates with DNA topoisomerase IIalpha and proliferating cell nuclear antigen expression in lung cancer.

Y box-binding protein-1 (YB-1), a member of the DNA binding protein family, interacts with inverted CCAAT boxes (Y-boxes). Y-boxes are located on the promoter of numerous genes, such as DNA topoisomerase IIalpha (Topo IIalpha), proliferating cell nuclear antigen (PCNA) and multidrug resistance 1 (MDR1). In this study, we used immunohistochemical (IHC) staining to detect YB-1 expression in 59 lung cancer tissues and to evaluate whether YB-1 expression was associated with the expression of YB-1 target genes such as Topo IIalpha, PCNA and MDR1 in human lung carcinoma. Twenty-eight out of 59 cases (47.5%) were stained positive for YB-1 in the cytoplasm, while 30 out of 59 cases (50.8%) were positive for PCNA in the nuclei. Topo IIalpha-positive cells were detected in 16 out of 59 cases (27.1%). Eight out of 59 cases (13.6%) had greater than 5% P-gp positive cells expression. There was a significant correlation between the YB-1 and Topo IIalpha expression in small cell lung cancer (SCLC) (p=0.0242). YB-1 expression also correlated with PCNA expression in non-small cell lung cancer (NSCLC) (p=0.0001). Higher levels of YB-1 expression were associated with T3-4 and Stage III-IV tumors in adenocarcinomas (p=0.0072; p=0.0168). In contrast, no relationship was found between YB-1 expression and P-gp expression. Our study suggests that YB-1 expression correlates with Topo IIalpha and PCNA expression in lung cancer.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2002

cDNA cloning and expression analysis of a novel human F-box only protein.

F-box proteins are an expanding family of eukaryotic proteins that are characterized by an approximately 40 amino acid motif. Some F-box proteins are critical for the controlled degradation of cellular regulatory proteins. During a large-scale sequencing analysis of a human fetal brain cDNA library, we isolated a cDNA clone that encodes a novel F-box protein. It showed a 90.0% identity with the previously isolated mouse F-box protein16 at the amino acid level. Northern blot analysis showed no detectable expression, while reverse transcription-polymerase chain reaction analysis indicated that FBXO16 was expressed in the heart, spleen, and colon. By mapping, we localized the FBXO16 gene to the human chromosome 8p12. The FBXO16 gene consisted of 9 exons that spanned 67,816 bp of human genomic DNA.

Amino Acid Sequence↗

PubMed1992

TATA box-mediated polymerase III transcription in vitro.

We have defined conditions whereby a functional TATA box can mediate efficient in vitro transcription by RNA polymerase III. A TATA box is absolutely required for this reaction as a single-point mutation in this sequence completely abolishes transcription. Two protein components are also required: a HeLa cell phosphocellulose fraction (fraction B) and at least one other factor that can be supplied by various crude nuclear extracts or by HeLa cell phosphocellulose fractions C and D. The order of addition is critical; fraction B must be preincubated with the template DNA for TATA box-dependent polymerase III transcription to occur. Various TATA sequences are quite similar in their ability to mediate transcription by polymerases II and III. Despite the similarity in sequence requirements, fraction B does not appear to contain any detectable transcription factor (TF) IID activity, and TATA box-mediated polymerase III transcription does not appear to require TFIID in the form contained in phosphocellulose fraction D. It was recently reported that TFIID is required TFIID in the form contained in phosphocellulose fraction D. It was recently reported that TFIID is required for polymerase III transcription of the yeast and human U6 genes (Margottin, F., Dujardin, G., Gerard, M., Egly, J.-M., Huet, J., and Sentenac, A. (1991) Science 251, 424-426; Simmen, K. A., Bernues, J., Parry, H. D., Stunnenberg, H. G., Berkenstam, A., Cavallini, B., Egly, J.-M., and Mattaj, I. W. (1991) EMBO J. 10, 1853-1862). We propose that fraction B may contain TFIID in a modified form that is not functional for polymerase II transcription.

Base Sequence↗