Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：PUBLIC LIBRARY SCIENCE  

The Drosophila male accessory gland has functions similar to those of the mammalian prostate gland and the seminal vesicle, and secretes accessory gland proteins into the seminal fluid. Each of the two lobes of the accessory gland is composed of two types of binucleate cell: about 1,000 main cells and 40 secondary cells. A well-known accessory gland protein, sex peptide, is secreted from the main cells and induces female postmating response to increase progeny production, whereas little is known about physiological significance of the secondary cells. The homeodomain transcriptional repressor Defective proventriculus (Dve) is strongly expressed in adult secondary cells, and its mutation resulted in loss of secondary cells, mononucleation of main cells, and reduced size of the accessory gland. dve mutant males had low fecundity despite the presence of sex peptide, and failed to induce the female postmating responses of increased egg laying and reduced sexual receptivity. RNAi-mediated dve knockdown males also had low fecundity with normally binucleate main cells. We provide the first evidence that secondary cells are crucial for male fecundity, and also that Dve activity is required for survival of the secondary cells. These findings provide new insights into a mechanism of fertility/fecundity.

DOI： 10.1371/journal.pone.0032302

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Publishing type：Research paper (scientific journal)  

DOI： 10.4172/BSO.1000e101

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

Circadian locomotor rhythms of Drosophila melanogaster are controlled by a neuronal circuit composed of approximately 150 clock neurons that are roughly classified into seven groups. In the circuit, a group of neurons expressing pigment-dispersing factor (PDF) play an important role in organizing the pacemaking system. Recent studies imply that unknown chemical neurotransmitter(s) (UNT) other than PDF is also expressed in the PDF-positive neurons. To explore its role in the circadian pacemaker, we examined the circadian locomotor rhythms of pdf-Gal4/UAS-TNT transgenic flies in which chemical synaptic transmission in PDF-positive neurons was blocked by expressed tetanus toxin light chain (TNT). In constant darkness (DD), the flies showed a free-running rhythm, which was similar to that of wild-type flies but significantly different from pdf null mutants. Under constant light conditions (LL), however, they often showed complex rhythms with a short period and a long period component. The UNT is thus likely involved in the synaptic transmission in the clock network and its release caused by LL leads to arrhythmicity. Immunocytochemistry revealed that LL induced phase separation in TIMELESS (TIM) cycling among some of the PDF-positive and PDF-negative clock neurons in the transgenic flies. These results suggest that both PDF and UNT play important roles in the Drosophila circadian clock, and activation of PDF pathway alone by LL leads to the complex locomotor rhythm through desynchronized oscillation among some of the clock neurons. (C) 2011 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.jinsphys.2011.06.004

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

A pair of the Drosophila eye-antennal disc gives rise to four distinct organs (eyes, antennae, maxillary palps, and ocelli) and surrounding head cuticle. Developmental processes of this imaginal disc provide an excellent model system to study the mechanism of regional specification and subsequent organogenesis. The dorsal head capsule (vertex) of adult Drosophila is divided into three morphologically distinct subdomains: ocellar, frons, and orbital. The homeobox gene orthodenticle (otd) is required for head vertex development, and mutations that reduce or abolish ad expression in the vertex primordium lead to ocelliless flies. The homeodomain-containing transcriptional repressor Engrailed (En) is also involved in ocellar specification, and the En expression is completely lost in otd mutants. However, the molecular mechanism of ocellar specification remains elusive. Here, we provide evidence that the homeobox gene defective proventriculus (dye) is a downstream effector of Otd, and also that the repressor activity of Dye is required for en activation through a relief-of-repression mechanism. Furthermore, the Dye activity is involved in repression of the frons identity in an incoherent feedforward loop of Otd and Dye. (C) 2011 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.ydbio.2011.06.015

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：CELL PRESS  

How complex networks of activators and repressors lead to exquisitely specific cell-type determination during development is poorly understood. In the Drosophila eye, expression patterns of Rhodopsins define at least eight functionally distinct though related subtypes of photoreceptors. Here, we describe a role for the transcription factor gene defective proventriculus (dve) as a critical node in the network regulating Rhodopsin expression. dve is a shared component of two opposing, interlocked feedforward loops (FFLs). Orthodenticle and Dve interact in an incoherent FFL to repress Rhodopsin expression throughout the eye. In R7 and R8 photoreceptors, a coherent FFL relieves repression by Dve while activating Rhodopsin expression. Therefore, this network uses repression to restrict and combinatorial activation to induce cell-type-specific expression. Furthermore, Dve levels are finely tuned to yield cell-type-and region-specific repression or activation outcomes. This interlocked FFL motif may be a general mechanism to control terminal cell-fate specification.

DOI： 10.1016/j.cell.2011.05.003

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

The Drosophila middle midgut cells derived from the endoderm develop into four distinct types of cell. Of these cells, copper cells have invaginated microvillar membranes on their apical surface, and they are involved in two distinct functions, i.e., copper absorption and acid secretion. The homeobox gene defective proventriculus (dve) is expressed in the midgut, and two transcripts, type A (similar to 4.9 kb) and type B (similar to 3.5 kb), have been identified. We isolated the deletion allele dve(E181) that completely removes the first exon for type-A (dve-A) transcript. Dve expression pattern in dve-A mutant background indicates that isoform switching is dynamically regulated in a cell-type specific manner. Using RNAi for dve-A, we examined spatial and temporal requirement of the Dve-A activity. Early Dve-A activity is required to repress isoform switching in copper cells, and for establishment of two gut functions. Late Dve-A activity in copper cells, but not in adjacent interstitial cells, is required for acid secretion, while the activity is redundantly required in both cells for the copper absorptive function. Furthermore, ectopic type-B expression in larval copper cells specifically impaired the copper absorptive function. These results provide insight into molecular mechanisms to establish functional specificity. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.mod.2011.02.003

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Segmentation plays crucial roles during morphogenesis. Drosophila legs are divided into segments along the proximal-distal axis by flexible structures called joints. Notch signaling is necessary and sufficient to promote leg growth and joint fort-nation, and is activated in distal cells of each segment in everting prepupal leg discs. The homeobox gene defective proventriculus (dve) is expressed in regions both proximal and distal to the intersegmental folds at 4 h after puparium formation (APF). Dve-expressing region partly overlaps with the Notch-activated region, and they become a complementary pattern at 6 It APF. Interestingly, dve mutant legs resulted in extra joint formation at the center of each tarsal segment, and the forced expression of dve caused a jointless phenotype. We present evidence that Dve suppresses the potential joint-forming activity, and that Notch signaling represses Dve expression to form joints. (C) 2007 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.ydbio.2007.09.003

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

The mechanisms for cell fate determination have been extensively studied whereas little is known about the mechanism through which functional specificity is established. In the Drosophila midgut, copper cells provide an excellent model system to examine this mechanism. Copper is an essential element for the activity of a number of physiologically important enzymes including Cu/Zn-superoxide dismutase, cytochrome c oxidase, and dopamine-beta-hydroxylase. Drosophila copper cells are involved in two distinct functions, i.e., copper absorption and acid secretion, which are visualized as a fluorescent signal and a color change of a pH indicator dye, respectively. Here we show that the absorptive function is established through two independent pathways, the Notch signaling pathway in adjacent interstitial cells and the Wingless signaling pathway in copper cells. Furthermore, the other function, acid secretion, is regulated through the Decapentaplegic and Wingless signaling pathways in interstitial cells. Our results clearly indicate that normal morphological development is insufficient for functional maturation, and that subsequent functional specification is achieved through several independent pathways. These results provide valuable insights into the molecular mechanism underlying functional specification. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.ydbio.2006.12.018

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING  

The discovery of homeobox gene clusters led us to realize that the mechanisms for body patterning and other developmental programs are evolutionally-conserved in vertebrates and invertebrates. The endoderm contributes to the lining of the gut and associated organs such as the liver and pancreas, which are critical for physiological functions. Our knowledge of endoderm development is limited; however, recent studies suggest that cooperation between the HNF3/Fork head and GATA transcription factors is crucial for endoderm specification. It is necessary to further understand the mechanism through which cells become functionally organized. Molecular genetic analyses of the Drosophila endoderm would provide insights into this issue. During proventriculus morphogenesis, a simple epithelial tube is folded into a functional multilayered structure, while two functions of midgut copper cells (i.e. copper absorption and acid secretion) can be easily visualized. The homeobox gene defective proventriculus (dve) plays key roles in these functional specifications.

DOI： 10.1111/j.1440-169X.2005.00811.x

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

A homeobox gene, defective proventriculus (dve), is expressed in various tissues including the ventral ectoderm and midgut. Here, we show the expression pattern of due in the ventral ectoderm, in which dve expression is induced by Spitz, a ligand for Drosophila epidermal growth factor receptor (EGFR). In spitz mutants, due expression is only lost in the ventral ectoderm and overexpression of Spitz induces ectopic due activation in the ventral ectoderm. Dve expression in the middle midgut depends on Decapentaplegic (Dpp) signaling, while expression of a dominant-negative form of Drosophila EGFR (DERDN) also causes a marked decrease in due expression in the middle midgut. Furthermore, heterozygous mutation of thick veins (tkv), a Dpp receptor, strongly enhances the effect of DERDN. These results indicate that EGFR signaling is crucial for dve expression in the ventral ectoderm and is required in the middle midgut where it cooperates with Dpp signaling. (C) 2003 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2003.10.017

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER-VERLAG  

Transgenic flies that can drive GAL4 expression under the control of the 7 kb 5'-region of the Drosophila Ca2+/calmodulin-dependent protein kinase II (dCaMKII) gene (dCaMKII-GAL4) were established. Characteristic features of this dCaMKII-GAL4 driven reporter expression were compatible with the endogenous dCaMKII expression pattern: The dCaMKII-GAL4 driven reporter gene was expressed preferentially in the central nervous system of the embryo and larvae. Reporter expression was also observed in the brain, thoracic ganglion, and gut of the adult. The whole-brain distribution and projections of dCaMKII-GAL4-expressing cells in the adults were visualized three-dimensionally by using UAS-linked reporter genes. Prominent signals of nuclear-localized beta-Gal reporter gene expression were found in extensive brain regions, especially in the Kenyon cells of the mushroom body (MB), cells in the pars intercerebralis, and subesophageal ganglion (SOG). tau reporter gene expression highlighting neurite projections was detected in the MB lobes, median bundle, antennal lobe glomeruli, and fibers of clusters in the SOG, ventrolateral protocerebrum and superior lateral protocerebrum. These observations agree with those of a previous study mapping the dCaMKII-dependent memory circuits in courtship conditioning. Interestingly, green fluorescent protein reporter gene expression in adult MB lobes was predominantly observed in the alpha and beta lobes with a core-deficient pattern, but not in the alpha' and beta' lobes, similar to Fasciclin II immunoreactivity.

DOI： 10.1007/s00441-002-0631-y

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Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Pattern formation during animal development is often induced by extracellular signaling molecules, known as morphogens, which are secreted from localized sources. During wing development in Drosophila, Wingless (Wg) is activated by Notch signaling along the dorsal-ventral boundary of the wing imaginal disc and acts as a morphogen to organize gene expression and cell growth. Expression of wg is restricted to a narrow stripe by Wg itself, repressing its own expression in adjacent cells. This refinement of wg expression is essential for specification of the wing margin. Here, we show that a homeodomain protein, Defective proventriculus (Dve), mediates the refinement of wg expression in both the wing disc and embryonic proventriculus, where dve expression requires Wg signaling. Our results provide evidence for a feedback mechanism that establishes the wg-expressing domain through the action of a Wg-induced gene product. (C) 2002 Elsevier Science (USA).

DOI： 10.1006/dbio.2002.0746

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-LISS  

DOI： 10.1002/gene.10137

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：COLD SPRING HARBOR LAB PRESS  

Morphogen gradients of secreted molecules play critical roles in the establishment of the spatial pattern of gene expression. During midgut development in Drosophila, secreted molecules of Decapentaplegic (Dpp) and Wingless (Wg) establish unique transcriptional regulation within target cells to specify the resultant cell types. Here we report the identification of a novel homeobox gene, defective proventriculus (dve), which is required for the midgut specification under the control of Dpp and Wg. In dye mutants, two distinct parts of the midgut, the proventriculus and middle midgut, are abnormally organized. The Wg signal regulates dve? expression during proventriculus development. On the other hand, dye is a downstream target of Dpp in the middle midgut and defines the functional specificity of copper cells along with another Dpp target gene, labial. Thus, the dye gene acts under the two distinct extracellular signals at distant parts of the midgut primordia.

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：STOCKTON PRESS  

Primary murine fetal hemopoietic cells were transformed with a fusion protein consisting of the ligand-binding domain of the estrogen receptor and a carboxyl-terminally truncated c-Myb protein (ERMYB), The ERMYB-transformed hemopoietic cells exhibit an immature myeloid phenotype when grown in the presence of beta-estradiol. Upon removal of beta-estradiol, the ERMYB cells display increased adherence, decreased clonogenicity and differentiate to cells exhibiting granulocyte or macrophage morphology, The expression of the c-myc, c-kit, cdc2 and bcl-2 genes, which are putatively regulated by Myb, was investigated in ERMYB cells grown in the presence or absence of beta-estradiol. Neither c-myc nor cdc2 expression was down-regulated after removal of beta-estradiol demonstrating that differentiation is not a consequence of decreased transactivation of these genes by ERMYB. While bcl-2 expression was reduced by 50% in ERMYB cells grown in the absence of beta-estradiol, there was no increase in DNA laddering, suggesting that Myb was not protecting ERMYB cells from apoptosis, In contrast, a substantial (200-fold) decrease in c-kit mRNA level was observed following differentiation of ERMYB cells, and c-kit mRNA could be partially re-induced by the re-addition of beta-estradiol. Furthermore, a reporter construct containing the c-kit promoter was activated when cotransfected with a Myb expression vector, providing further evidence of a role for Myb in the regulation of c-kit.

DOI： 10.1038/sj.onc.1201472

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER ASSOC ADVANCEMENT SCIENCE  

The morphology of axon terminals changes with differentiation into mature synapses. A molecule that might regulate this process was identified by a screen of Drosophila mutants for abnormal motor activities. The still life (sif) gene encodes a protein homologous to guanine nucleotide exchange factors, which convert Rho-like guanosine triphosphatases (GTPases) from a guanosine diphosphate-bound inactive state to a guanosine triphosphate-bound active state. The SIF proteins are found adjacent to the plasma membrane of synaptic terminals. Expression of a truncated SIF protein resulted in defects in neuronal morphology and induced membrane ruffling with altered actin localization in human KB cells. Thus, SIF proteins may regulate synaptic differentiation through the organization of the actin cytoskeleton by activating Rho-like GTPases.

DOI： 10.1126/science.275.5299.543

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：MACMILLAN MAGAZINES LTD  

ASYMMETRIC divisions that produce two distinct cells play fundamental roles in generating different cell types during development(1,2). In the Drosophila central nervous system, neural stem cells called neuroblasts divide unequally into another neuroblast and a ganglion mother cell which is Subsequently cleaved into neurons. Correct gene expression of ganglion mother tells requires the transcription factor Prospero(3-5). Here we demonstrate the asymmetric segregation of Prospero on neuroblast division, Prospero synthesized in neuroblasts is retained in the cytoplasm and at mitosis is exclusively partitioned to ganglion mother cells, in which it is translocated to the nucleus, Differential segregation of Prospero was also found in the endoderm. We have identified a region in Prospero that is responsible for this event, The region shares a common motif with Numb(6), which also shows unequal segregation(7). We propose that asymmetric segregation of transcription factors is an intrinsic mechanism for establishing asymmetry in gene expression between sibling cells.

DOI： 10.1038/377627a0

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

The myb gene family has three members, c-myb, A-myb, and B-myb. A-myb mRNA is mainly expressed in testis and peripheral blood leukocytes. A-Myb can activate transcription from the promoter containing Myb-binding sites in all cells examined. In addition to the two domains (a DNA-binding domain and a transcriptional activation domain), two negative regulatory domains have been identified in A-Myb. These results indicate that A-Myb functions as a transcriptional activator mainly in testis and peripheral blood cells, and the regulatory mechanism of A-Myb activity is similar to that of c-Myb.

DOI： 10.1016/0014-5793(94)01402-M

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHAPMAN HALL LTD  

In order to reveal cellular processes sensitive to abnormal c-myb expression in vivo, transgenic mice were produced by introducing the c-myb nuclear proto-oncogene under the ubiquitous transcriptional regulatory unit of the cytoplasmic beta-actin gene. Expression of c-myb in thymus did not cause apparent abnormality, but the mice unexpectedly developed degenerative abnormalities in skeletal and cardiac muscles; this occurred predominantly in males. Expression of c-myb in skeletal muscle was correlated with an inflammation of muscle and was accompanied by vacuolar degeneration of muscle fibres, their regeneration, and lymphocyte infiltration. The identical pathological progression in cardiac muscle was associated with cardiomegaly.

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

Three members of the human myb gene family (c-myb, A-myb, and B-myb) encode transcriptional regulators that can bind to specific DNA sequences. High levels of c-myb expression are usually found in immature hemopoietic cells, but the B-myb is more commonly expressed in many types of cells. To understand the regulation of the activity of B-myb gene product (B-Myb), its functional domains were analyzed. Like c-Myb, B-Myb also has a transcriptional activation domain containing a cluster of acidic amino acids in the region downstream of the DNA-binding domain, which consists of three tandem repeats of 51-52 amino acids. In contrast to c-Myb, B-Myb does not contain a negative regulatory domain. Furthermore, the multiple nuclear localization signals are in at least two regions in the COOH-terminal half of B-Myb, and one of them is adjacent to a potential cdc2 kinase site. These results indicate that B-Myb contains DNA-binding and transcriptional activation domains similar to those of c-Myb, but a regulatory mechanism of B-Myb activity is quite different from that for c-Myb.

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：STOCKTON PRESS  

To identify the target genes modulated by the myb gene product (Myb), a co-transfection assay with a Myb expression plasmid was performed. Both c-Myb and B-Myb, another member of the myb gene family, trans-activated the human c-myc promoter. DNAase I footprint analysis using the bacterially expressed c-Myb, identified multiple c-Myb binding sites in the c-myc promoter region. Deletion analysis of the c-myc promoter suggested that some number of Myb binding sites, not a specific Myb binding site, is important for the c-Myb-induced trans-activation of the c-myc promoter. Using the c-myc-chloramphenicol acetyltransferase (CAT) construct as a reporter in a co-transfection assay, the domains of c-Myb required for trans-activation were examined. The functional domains of c-Myb identified using the c-myc promoter were almost the same as those identified previously with the artificial target gene containing Myb binding sites, but unlike the case with the artificial target gene the N-terminal half of the previously identified negative regulatory domains and the C-terminal 136 amino acids were required for the maximal trans-activation of the c-myc promoter. These results indicate that there are some differences in the regulation of Myb-dependent trans-activation in different target genes.

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATL ACAD PRESS  

The wild-type p53 protein suppresses transformation, but certain missense mutants of p53 can transform cells. Although the wild-type p53 protein contains a transcriptional activation domain, no p53-responsive element has been identified. Here, we identified the p53-responsive element within the Tax-responsive element [21-base-pair (bp) enhancer] of human T-cell leukemia virus type I. Mutation analysis of the 21-bp enhancer indicated that the 16-bp sequence containing the cAMP-responsive element and its surrounding sequence was responsible for p53-induced transactivation. This 16-bp sequence was demonstrated to bind specifically to wild-type human p53 protein in vitro. Using a series of deletion mutants of p53, we showed that almost the entire region of p53 is needed for the transactivating capacity. Furthermore, the transforming mutants of p53 were unable to act as transcriptional activators. The p53-responsive element identified here should be useful to analyze the mechanism by which p53 regulates expression of a set of genes with a negative effect on cellular growth.

DOI： 10.1073/pnas.89.12.5403

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN BIOCHEMICAL SOC  

Three prokaryotic termination signals, the Escherichia coli trp attenuator, lambda-4S RNA terminator, and lambda-tR1 terminator, were examined as to their effects on transcription in vivo in HeLa cells. The trp attenuator inhibited the expression of downstream genes in an orientation-dependent manner, but both the lambda-4S RNA and lambda-tR1 terminators did not. Furthermore, a point mutation of the attenuator that disrupted the secondary structure of mRNA abolished this inhibitory effect. These results suggest that an attenuator-like secondary structure is effective in inhibiting transcriptional elongation by RNA polymerase II.

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS UNITED KINGDOM  

DOI： 10.1093/nar/17.18.7315

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATL ACAD SCIENCES  

DOI： 10.1073/pnas.86.15.5758

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS UNITED KINGDOM  

DOI： 10.1093/nar/17.1.107

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE BIOCHEMICAL SOC  

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Event date： 2020.12.2 - 2020.12.4

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Event date： 2020.12.2 - 2020.12.4

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