Topic
Transcription (biology)
About: Transcription (biology) is a research topic. Over the lifetime, 56532 publications have been published within this topic receiving 2952782 citations. The topic is also known as: genetic transcription & transcription, genetic.
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TL;DR: In this paper, the human transcription factor Jun/AP-1 was found to be responsible for increased transcription of different cellular genes in response to tumor promoters, such as TPA, and serum factors.
1,095 citations
TL;DR: A novel differential approach selective for the 5′ end of primary transcripts is presented, establishing a paradigm for mapping and annotating the primary transcriptomes of many living species and discovering hundreds of transcriptional start sites within operons, and opposite to annotated genes.
Abstract: Genome sequencing of Helicobacter pylori has revealed the potential proteins and genetic diversity of this prevalent human pathogen, yet little is known about its transcriptional organization and noncoding RNA output. Massively parallel cDNA sequencing (RNA-seq) has been revolutionizing global transcriptomic analysis. Here, using a novel differential approach (dRNA-seq) selective for the 5' end of primary transcripts, we present a genome-wide map of H. pylori transcriptional start sites and operons. We discovered hundreds of transcriptional start sites within operons, and opposite to annotated genes, indicating that complexity of gene expression from the small H. pylori genome is increased by uncoupling of polycistrons and by genome-wide antisense transcription. We also discovered an unexpected number of approximately 60 small RNAs including the epsilon-subdivision counterpart of the regulatory 6S RNA and associated RNA products, and potential regulators of cis- and trans-encoded target messenger RNAs. Our approach establishes a paradigm for mapping and annotating the primary transcriptomes of many living species.
1,094 citations
1,093 citations
TL;DR: Delineation of these two cooperative regions explains at the level of transcription how IFN-gamma and LPS act in concert to induce maximally the mac-NOS gene and, furthermore, howIFN-Gamma augments the inflammatory response to LPS.
Abstract: The promoter region of the mouse gene for macrophage-inducible nitric oxide synthase (mac-NOS; EC 1.14.13.39) has been characterized. A putative TATA box is 30 base pairs upstream of the transcription start site. Computer analysis reveals numerous potential binding sites for transcription factors, many of them associated with stimuli that induce mac-NOS expression. To localize functionally important portions of the regulatory region, we constructed deletion mutants of the mac-NOS 5' flanking region and placed them upstream of a luciferase reporter gene. The macrophage cell line RAW 264.7, when transfected with a minimal promoter construct, expresses little luciferase activity when stimulated by lipopolysaccharide (LPS), interferon gamma (IFN-gamma), or both. Maximal expression depends on two discrete regulatory regions upstream of the putative TATA box. Region I (position -48 to -209) increases luciferase activity approximately 75-fold over the minimal promoter construct. Region I contains LPS-related responsive elements, including a binding site for nuclear factor interleukin 6 (NF-IL6) and the kappa B binding site for NF-kappa B, suggesting that this region regulates LPS-induced expression of the mac-NOS gene. Region II (position -913 to -1029) alone does not increase luciferase expression, but together with region I it causes an additional 10-fold increase in expression. Together the two regions increase expression 750-fold over activity obtained from a minimal promoter construct. Region II contains motifs for binding IFN-related transcription factors and thus probably is responsible for IFN-mediated regulation of LPS-induced mac-NOS. Delineation of these two cooperative regions explains at the level of transcription how IFN-gamma and LPS act in concert to induce maximally the mac-NOS gene and, furthermore, how IFN-gamma augments the inflammatory response to LPS.
1,083 citations
TL;DR: DNA footprinting studies suggest that in the absence of coinducer many LTTRs bind to regulated promoters via a 15-bp dyadic sequence with a common structure and position (near -65).
Abstract: The LysR family is composed of > 50 similar-sized, autoregulatory transcriptional regulators (LTTRs) that apparently evolved from a distant ancestor into subfamilies found in diverse prokaryotic genera. In response to different coinducers, LTTRs activate divergent transcription of linked target genes or unlinked regulons encoding extremely diverse functions. Mutational studies and amino acid sequence similarities of LTTRs identify: (a) a DNA-binding domain employing a helix-turn-helix motif (residues 1-65), (b) domains involved in coinducer recognition and/or response (residues 100-173 and 196-206), (c) a domain required for both DNA binding and coinducer response (residues 227-253). DNA footprinting studies suggest that in the absence of coinducer many LTTRs bind to regulated promoters via a 15-bp dyadic sequence with a common structure and position (near -65). Coinducer causes additional interactions of LTTRs with sequences near the -35 RNA polymerase binding site and/or DNA bending that results in transcription activation.
1,079 citations