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Journal articles on the topic 'Gene overlaps'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Decrulle, Antoine L., Antoine Frénoy, Thomas A. Meiller-Legrand, Aude Bernheim, Chantal Lotton, Arnaud Gutierrez, and Ariel B. Lindner. "Engineering gene overlaps to sustain genetic constructs in vivo." PLOS Computational Biology 17, no. 10 (October 8, 2021): e1009475. http://dx.doi.org/10.1371/journal.pcbi.1009475.

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Evolution is often an obstacle to the engineering of stable biological systems due to the selection of mutations inactivating costly gene circuits. Gene overlaps induce important constraints on sequences and their evolution. We show that these constraints can be harnessed to increase the stability of costly genes by purging loss-of-function mutations. We combine computational and synthetic biology approaches to rationally design an overlapping reading frame expressing an essential gene within an existing gene to protect. Our algorithm succeeded in creating overlapping reading frames in 80% of E. coli genes. Experimentally, scoring mutations in both genes of such overlapping construct, we found that a significant fraction of mutations impacting the gene to protect have a deleterious effect on the essential gene. Such an overlap thus protects a costly gene from removal by natural selection by associating the benefit of this removal with a larger or even lethal cost. In our synthetic constructs, the overlap converts many of the possible mutants into evolutionary dead-ends, reducing the evolutionary potential of the system and thus increasing its stability over time.
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2

Muñoz-Baena, Laura, and Art F. Y. Poon. "Using networks to analyze and visualize the distribution of overlapping genes in virus genomes." PLOS Pathogens 18, no. 2 (February 24, 2022): e1010331. http://dx.doi.org/10.1371/journal.ppat.1010331.

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Gene overlap occurs when two or more genes are encoded by the same nucleotides. This phenomenon is found in all taxonomic domains, but is particularly common in viruses, where it may increase the information content of compact genomes or influence the creation of new genes. Here we report a global comparative study of overlapping open reading frames (OvRFs) of 12,609 virus reference genomes in the NCBI database. We retrieved metadata associated with all annotated open reading frames (ORFs) in each genome record to calculate the number, length, and frameshift of OvRFs. Our results show that while the number of OvRFs increases with genome length, they tend to be shorter in longer genomes. The majority of overlaps involve +2 frameshifts, predominantly found in dsDNA viruses. Antisense overlaps in which one of the ORFs was encoded in the same frame on the opposite strand (−0) tend to be longer. Next, we develop a new graph-based representation of the distribution of overlaps among the ORFs of genomes in a given virus family. In the absence of an unambiguous partition of ORFs by homology at this taxonomic level, we used an alignment-free k-mer based approach to cluster protein coding sequences by similarity. We connect these clusters with two types of directed edges to indicate (1) that constituent ORFs are adjacent in one or more genomes, and (2) that these ORFs overlap. These adjacency graphs not only provide a natural visualization scheme, but also a novel statistical framework for analyzing the effects of gene- and genome-level attributes on the frequencies of overlaps.
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3

Lartey, R. T., T. C. Voss, and U. Melcher. "Tobamovirus evolution: gene overlaps, recombination, and taxonomic implications." Molecular Biology and Evolution 13, no. 10 (December 1, 1996): 1327–38. http://dx.doi.org/10.1093/oxfordjournals.molbev.a025579.

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4

Makałowska, Izabela, Chiao-Feng Lin, and Krisitina Hernandez. "Birth and death of gene overlaps in vertebrates." BMC Evolutionary Biology 7, no. 1 (2007): 193. http://dx.doi.org/10.1186/1471-2148-7-193.

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5

Jain, Kanika, Tyler H. Stanage, Elizabeth A. Wood, and Michael M. Cox. "The Escherichia coli serS gene promoter region overlaps with the rarA gene." PLOS ONE 17, no. 4 (April 15, 2022): e0260282. http://dx.doi.org/10.1371/journal.pone.0260282.

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Deletion of the entire gene encoding the RarA protein of Escherichia coli results in a growth defect and additional deficiencies that were initially ascribed to a lack of RarA function. Further work revealed that most of the effects reflected the presence of sequences in the rarA gene that affect expression of the downstream gene, serS. The serS gene encodes the seryl aminoacyl-tRNA synthetase. Decreases in the expression of serS can trigger the stringent response. The sequences that affect serS expression are located in the last 15 nucleotides of the rarA gene.
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6

Pribyl, T., C. Campagnoni, S. Amur-Umarjee, K. Kampf, B. Garbay, V. Handley, and A. Campagnoni. "Identification and characterization of Golli, a gene which overlaps the MBP gene." Neurochemistry International 21 (January 1992): C1. http://dx.doi.org/10.1016/0197-0186(92)92037-5.

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7

Brauburger, Kristina, Yannik Boehmann, Verena Krähling, and Elke Mühlberger. "Transcriptional Regulation in Ebola Virus: Effects of Gene Border Structure and Regulatory Elements on Gene Expression and Polymerase Scanning Behavior." Journal of Virology 90, no. 4 (December 9, 2015): 1898–909. http://dx.doi.org/10.1128/jvi.02341-15.

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ABSTRACTThe highly pathogenic Ebola virus (EBOV) has a nonsegmented negative-strand (NNS) RNA genome containing seven genes. The viral genes either are separated by intergenic regions (IRs) of variable length or overlap. The structure of the EBOV gene overlaps is conserved throughout all filovirus genomes and is distinct from that of the overlaps found in other NNS RNA viruses. Here, we analyzed how diverse gene borders and noncoding regions surrounding the gene borders influence transcript levels and govern polymerase behavior during viral transcription. Transcription of overlapping genes in EBOV bicistronic minigenomes followed the stop-start mechanism, similar to that followed by IR-containing gene borders. When the gene overlaps were extended, the EBOV polymerase was able to scan the template in an upstream direction. This polymerase feature seems to be generally conserved among NNS RNA virus polymerases. Analysis of IR-containing gene borders showed that the IR sequence plays only a minor role in transcription regulation. Changes in IR length were generally well tolerated, but specific IR lengths led to a strong decrease in downstream gene expression. Correlation analysis revealed that these effects were largely independent of the surrounding gene borders. Each EBOV gene contains exceptionally long untranslated regions (UTRs) flanking the open reading frame. Our data suggest that the UTRs adjacent to the gene borders are the main regulators of transcript levels. A highly complex interplay between the differentcis-acting elements to modulate transcription was revealed for specific combinations of IRs and UTRs, emphasizing the importance of the noncoding regions in EBOV gene expression control.IMPORTANCEOur data extend those from previous analyses investigating the implication of noncoding regions at the EBOV gene borders for gene expression control. We show that EBOV transcription is regulated in a highly complex yet not easily predictable manner by a set of interactingcis-active elements. These findings are important not only for the design of recombinant filoviruses but also for the design of other replicon systems widely used as surrogate systems to study the filovirus replication cycle under low biosafety levels. Insights into the complex regulation of EBOV transcription conveyed by noncoding sequences will also help to interpret the importance of mutations that have been detected within these regions, including in isolates of the current outbreak.
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8

Kepler, T. B., M. Borrero, B. Rugerio, S. K. McCray, and S. H. Clarke. "Interdependence of N nucleotide addition and recombination site choice in V(D)J rearrangement." Journal of Immunology 157, no. 10 (November 15, 1996): 4451–57. http://dx.doi.org/10.4049/jimmunol.157.10.4451.

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Abstract Diversity in the Ag binding receptors of B and T cells is achieved through a process of genomic rearrangement involving selection of recombination sites and, in adult mice, addition of nontemplated (N) nucleotides. We have analyzed 543 Ig heavy chain nonproductive rearrangements, involving a single variable region gene segment, from adult and perinatal mice. We infer several fundamental and novel features of the recombination mechanism. N regions are formed predominantly from the DNA plus strand or from the DNA minus strand polymerizations, rather than as a concatenation of the two. Homologous overlaps of as few as one nucleotide between gene segments cause significant skewing of recombination sites. The V(H) recombination site spectrum differs in perinatal and adult mice, with sites representing overlap between V(H) and D over-represented in the perinatal mice, and sites representing overlaps between V(H) and the N strand polymerized onto the D segment over-represented in the adult mice. Thus, in V(D)J joining, N nucleotide addition and recombination site choice are highly interdependent events.
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9

Chen, Quan, Xianghong J. Zhou, and Fengzhu Sun. "Finding Genetic Overlaps Among Diseases Based on Ranked Gene Lists." Journal of Computational Biology 22, no. 2 (February 2015): 111–23. http://dx.doi.org/10.1089/cmb.2014.0149.

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10

Ray, Bryan L., Charles I. White, and James E. Haber. "The TSM1 gene of Saccharomyces cerevisiae overlaps the MAT locus." Current Genetics 20, no. 1-2 (July 1991): 25–31. http://dx.doi.org/10.1007/bf00312761.

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11

Stonestrom, Aaron J., Sarah C. Hsu, Kristen S. Jahn, Peng Huang, Cheryl A. Keller, Belinda M. Giardine, Stephan Kadauke, et al. "Functions of BET proteins in erythroid gene expression." Blood 125, no. 18 (April 30, 2015): 2825–34. http://dx.doi.org/10.1182/blood-2014-10-607309.

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Key Points BETs promote GATA1 chromatin occupancy and subsequently activate transcription; they are generally not required for repression. BRD2 and BRD4 are essential for full GATA1 activity whereas BRD3 function overlaps with BRD2.
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12

Cock, P. J. A., and D. E. Whitworth. "Evolution of Relative Reading Frame Bias in Unidirectional Prokaryotic Gene Overlaps." Molecular Biology and Evolution 27, no. 4 (December 14, 2009): 753–56. http://dx.doi.org/10.1093/molbev/msp302.

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13

Bishop, Cameron R., Troy Dumenil, Daniel J. Rawle, Thuy T. Le, Kexin Yan, Bing Tang, Gunter Hartel, and Andreas Suhrbier. "Mouse models of COVID-19 recapitulate inflammatory pathways rather than gene expression." PLOS Pathogens 18, no. 9 (September 26, 2022): e1010867. http://dx.doi.org/10.1371/journal.ppat.1010867.

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How well mouse models recapitulate the transcriptional profiles seen in humans remains debatable, with both conservation and diversity identified in various settings. Herein we use RNA-Seq data and bioinformatics approaches to analyze the transcriptional responses in SARS-CoV-2 infected lungs, comparing 4 human studies with the widely used K18-hACE2 mouse model, a model where hACE2 is expressed from the mouse ACE2 promoter, and a model that uses a mouse adapted virus and wild-type mice. Overlap of single copy orthologue differentially expressed genes (scoDEGs) between human and mouse studies was generally poor (≈15–35%). Rather than being associated with batch, sample treatment, viral load, lung damage or mouse model, the poor overlaps were primarily due to scoDEG expression differences between species. Importantly, analyses of immune signatures and inflammatory pathways illustrated highly significant concordances between species. As immunity and immunopathology are the focus of most studies, these mouse models can thus be viewed as representative and relevant models of COVID-19.
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14

Pallejà, Albert, Eoghan D. Harrington, and Peer Bork. "Large gene overlaps in prokaryotic genomes: result of functional constraints or mispredictions?" BMC Genomics 9, no. 1 (2008): 335. http://dx.doi.org/10.1186/1471-2164-9-335.

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15

Dar, Mubasher E., and Ashok S. Bhagwat. "Mechanism of expression of DNA repair gene vsr, an Escherichia coli gene that overlaps the DNA cytosine methylase gene, dcm." Molecular Microbiology 9, no. 4 (August 1993): 823–33. http://dx.doi.org/10.1111/j.1365-2958.1993.tb01741.x.

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16

Luca, Bogdan-Alexandru, Vincent Moulton, Christopher Ellis, Shea P. Connell, Daniel S. Brewer, and Colin S. Cooper. "Convergence of Prognostic Gene Signatures Suggests Underlying Mechanisms of Human Prostate Cancer Progression." Genes 11, no. 7 (July 16, 2020): 802. http://dx.doi.org/10.3390/genes11070802.

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The highly heterogeneous clinical course of human prostate cancer has prompted the development of multiple RNA biomarkers and diagnostic tools to predict outcome for individual patients. Biomarker discovery is often unstable with, for example, small changes in discovery dataset configuration resulting in large alterations in biomarker composition. Our hypothesis, which forms the basis of this current study, is that highly significant overlaps occurring between gene signatures obtained using entirely different approaches indicate genes fundamental for controlling cancer progression. For prostate cancer, we found two sets of signatures that had significant overlaps suggesting important genes (p < 10−34 for paired overlaps, hypergeometrical test). These overlapping signatures defined a core set of genes linking hormone signalling (HES6-AR), cell cycle progression (Prolaris) and a molecular subgroup of patients (PCS1) derived by Non Negative Matrix Factorization (NNMF) of control pathways, together designated as SIG-HES6. The second set (designated SIG-DESNT) consisted of the DESNT diagnostic signature and a second NNMF signature PCS3. Stratifications using SIG-HES6 (HES6, PCS1, Prolaris) and SIG-DESNT (DESNT) classifiers frequently detected the same individual high-risk cancers, indicating that the underlying mechanisms associated with SIG-HES6 and SIG-DESNT may act together to promote aggressive cancer development. We show that the use of combinations of a SIG-HES6 signature together with DESNT substantially increases the ability to predict poor outcome, and we propose a model for prostate cancer development involving co-operation between the SIG-HES6 and SIG-DESNT pathways that has implication for therapeutic design.
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17

Asatryan, Babken, and Argelia Medeiros-Domingo. "Molecular and genetic insights into progressive cardiac conduction disease." EP Europace 21, no. 8 (April 26, 2019): 1145–58. http://dx.doi.org/10.1093/europace/euz109.

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Abstract Progressive cardiac conduction disease (PCCD) is often a primarily genetic disorder, with clinical and genetic overlaps with other inherited cardiac and metabolic diseases. A number of genes have been implicated in PCCD pathogenesis with or without structural heart disease or systemic manifestations. Precise genetic diagnosis contributes to risk stratification, better selection of specific therapy and allows familiar cascade screening. Cardiologists should be aware of the different phenotypes emerging from different gene-mutations and the potential risk of sudden cardiac death. Genetic forms of PCCD often overlap or coexist with other inherited heart diseases or manifest in the context of multisystem syndromes. Despite the significant advances in the knowledge of the genetic architecture of PCCD and overlapping diseases, in a measurable fraction of PCCD cases, including in familial clustering of disease, investigations of known cardiac disease-associated genes fail to reveal the underlying substrate, suggesting that new causal genes are yet to be discovered. Here, we provide insight into genetics and molecular mechanisms of PCCD and related diseases. We also highlight the phenotypic overlaps of PCCD with other inherited cardiac and metabolic diseases, present unmet challenges in clinical practice, and summarize the available therapeutic options for affected patients.
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18

Huang, Kai, Monica L. Bailey, and Dwayne L. Barber. "Stress Erythropoiesis Elicits a Program of Gene Regulation That Overlaps with Interferon-γ." Blood 104, no. 11 (November 16, 2004): 2161. http://dx.doi.org/10.1182/blood.v104.11.2161.2161.

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Abstract Erythropoietin (EPO), the primary cytokine regulator of red blood cell production, acts through binding to its cognate receptor (EPO-R), which is primarily expressed on erythroid precursors. Knockout studies have illustrated a critical role for EPO, EPO-R and the downstream tyrosine kinase JAK2 in embryogenesis as mice lacking any of these components die from a fatal anemia at E13.5. These data suggest that EPO-R and/or JAK2 are required to promote erythropoiesis in vivo. EPO provides mitogenic, differentiative and cell survival signals to erythroid progenitors. We have performed microarray studies to identify target genes regulated by EPO in cell lines and primary cells. We utilized an erythroid cell line (HCD-57), a myeloid cell line stably expressing the EPO-R (Ba/F3-EPO-R), fetal liver cells isolated from E13.5 mice as well as splenocytes isolated from Phenylhydrazine (PHZ)-primed adult mice. Fetal liver cells permit the study of normal erythropoiesis in a fetal setting whereas the PHZ-primed erythroblasts permit analysis of stress erythropoiesis in adult mice. We harvested cells at 1, 8, 12 and 24 hr after EPO stimulation which correspond to immediate early gene induction (1 hr), S phase entry (8 hr) and G2/M (24 hr) time points. RNA was prepared and hybridized to the Affymetrix U74A mouse chip. Data was analyzed and only those genes with statistical significance (p < 0.05) were considered for further characterization. Analysis of the 1 hr time points has revealed that six genes are co-regulated by EPO in all four cellular environments. Included within this co-hort are the Suppressor of Cytokine Signaling genes (Cis, SOCS-1 and SOCS-3) and Myc, as well as two novel genes. We compared our datasets with other published analyses. The Williams laboratory has identified an Interferon-Stimulated Gene “ISG” data set corresponding to genes induced by Type I or Type II Interferon’s. We queried our PHZ-primed erythroblast data set against the Williams ISG database. Of the 305 human genes in the ISG database, 218 are expressed on the Affymetrix chip. We searched our dataset for genes that are induced 1.5-fold or greater at 2 of 4, 3 of 4 or 4 of 4 time points. Thirty-four genes are also stimulated by EPO in PHZ-primed erythroblasts including classical IFN-regulated genes such as Interferon-regulator factor-1 (IRF-1), Interferon-stimulated gene-15 (ISG-15), Interferon-induced transmembrane protein 3-like (IFITM-3l), Protein Kinase R (PKR) and Signal Transducer and Activator of Transcription-1 (STAT1). We have previously demonstrated that STAT1 is a negative regulator of murine erythropoiesis utilizing STAT1-deficient mice. We also analyzed immediate early gene regulation in fetal liver cells and PHZ-primed erythroblasts isolated from STAT1-deficient mice stimulated with EPO for 1 hr. These data were compared with the relevant wild type data sets. EPO stimulates the induction of the ubiquitin-like protein, ISG-15 in both wild type and STAT1−/− erythroblasts. Several signaling proteins have been shown to be covalently modified by ISG-15 including STAT1. ISG-15 is removed from ISGylated products by the deubiquitinating enzyme, Ubp43. EPO stimulates a rapid accumulation of Ubp43 in wild type cells, however, EPO fails to induce Ubp43 mRNA in STAT1-deficient fetal liver and PHZ-primed erythroblasts. Experiments are underway to confirm that the mechanism by which STAT1 exerts negative regulation of erythropoiesis is via upregulation of the deubiquitinating enzyme, Ubp43.
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19

Metzner, Christoph, and Marianne Zaruba. "On the Relationship of Viral Particles and Extracellular Vesicles: Implications for Viral Vector Technology." Viruses 13, no. 7 (June 26, 2021): 1238. http://dx.doi.org/10.3390/v13071238.

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Gene therapy vectors derived from different viral species have become a fixture in biomedicine, both for direct therapeutic intervention and as tools to facilitate cell-based therapies, such as chimeric antigen receptor-based immunotherapies. On the contrary, extracellular vesicles have only recently gained a massive increase in interest and, concomitantly, knowledge in the field has drastically risen. Viral infections and extracellular vesicle biology overlap in many ways, both with pro- and antiviral outcomes. In this review, we take a closer look at these interactions for the most prominent groups of viral vectors (Adenoviral, Adeno-associated and Retro/Lentiviral vectors) and the possible implications of these overlaps for viral vector technology and its biomedical applications.
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20

Parida, Bibhu Prasad, Biswapriya Biswavas Misra, and Amarendra Narayan Misra. "Visual gene network analysis of aging-specific gene co-expression in human indicates overlaps with immuno-pathological regulations." 4open 1 (2018): 4. http://dx.doi.org/10.1051/fopen/2018004.

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Introduction: Aging is a complex biological process that brings about a gradual decline of physiological and metabolic machineries as a result of maturity. Also, aging is irreversible and leads ultimately to death in biological organisms. Methods: We intend to characterize aging at the gene expression level using publicly available human gene expression arrays obtained from gene expression omnibus (GEO) and ArrayExpress. Candidate genes were identified by rigorous screening using filtered data sets, i.e., GSE11882, GSE47881, and GSE32719. Using Aroma and Limma packages, we selected the top 200 genes showing up and down regulation (p < 0.05 and fold change >2.5) out of which 185 were chosen for further comparative analysis. Results: This investigation enabled identification of candidate genes involved in aging that are associated with several signaling cascades demonstrating strong correlation with ATP binding and protease functions. Conclusion: A majority of these gene encoded proteins function extracellularly, and also provide insights into the immunopathological basis of aging.
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21

Strey, Jan, Klaus D. Wittchen, and Friedhelm Meinhardt. "Regulation of β-Galactosidase Expression in Bacillus megaterium DSM319 by a XylS/AraC-Type Transcriptional Activator." Journal of Bacteriology 181, no. 10 (May 15, 1999): 3288–92. http://dx.doi.org/10.1128/jb.181.10.3288-3292.1999.

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ABSTRACT The β-galactosidase-encoding bgaM gene ofBacillus megaterium DSM319 and the divergently orientatedbgaR operon were isolated and sequenced. Both traits are subject to catabolite repression. A set of single-gene replacement mutants was generated and used to analyze gene function. BgaR was found to be a XylS/AraC-type positive transcriptional regulator ofbgaM; a potential regulator binding site overlaps thebgaM promoter. A mechanism for regulation of β-galactosidase expression in B. megaterium is proposed.
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22

Morgan, Kevin, Darrell Conklin, Adam J. Pawson, Robin Sellar, Thomas R. Ott, and Robert P. Millar. "A Transcriptionally Active Human Type II Gonadotropin-Releasing Hormone Receptor Gene Homolog Overlaps Two Genes in the Antisense Orientation on Chromosome 1q.12." Endocrinology 144, no. 2 (February 1, 2003): 423–36. http://dx.doi.org/10.1210/en.2002-220622.

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GnRH-II peptide hormone exhibits complete sequence conservation across vertebrate species, including man. Type-II GnRH receptor genes have been characterized recently in nonhuman primates, but the human receptor gene homolog contains a frameshift, a premature stop codon (UGA), and a 3′ overlap of the RBM8A gene on chromosome 1q.12. A retrotransposed pseudogene, RBM8B, retains partial receptor sequence. In this study, bioinformatics show that the human receptor gene promoter overlaps the peroxisomal protein11-β gene promoter and the premature UGA is positionally conserved in chimpanzee. A CGA [arginine (Arg)] occurs in porcine DNA, but UGA is shifted one codon to the 5′ direction in bovine DNA, suggesting independent evolution of premature stop codons. In contrast to marmoset tissue RNA, exon- and strand-specific probes are required to distinguish differently spliced human receptor gene transcripts in cell lines (HP75, IMR-32). RBM8B is not transcribed. Sequencing of cDNAs for spliced receptor mRNAs showed no evidence for alteration of the premature UGA by RNA editing, but alternative splicing circumvents the frameshift to encode a two-membrane-domain protein before this UGA. A stem-loop motif resembling a selenocysteine insertion sequence and a potential alternative translation initiation site might enable expression of further proteins involved in interactions within the GnRH system.
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23

Tanaka, Makoto, Naohito Yamasaki, and Seigo Izumo. "Phenotypic Characterization of the Murine Nkx2.6 Homeobox Gene by Gene Targeting." Molecular and Cellular Biology 20, no. 8 (April 15, 2000): 2874–79. http://dx.doi.org/10.1128/mcb.20.8.2874-2879.2000.

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ABSTRACT The NK-2 homeobox genes have been shown to play critical roles in the development of specific organs and tissues. Nkx2.6 is a member of the NK-2 homeobox gene family and is most closely related to theDrosophila tinman gene. Nkx2.6 is expressed in the caudal pharyngeal pouches, the caudal heart progenitors, the sinus venosus, and the outflow tract of the heart and in a short segment of the gut at early stages of embryogenesis. To investigate the function of Nkx2.6 in vivo, we generated mice with null mutations of Nkx2.6 by the gene targeting technique. Homozygous Nkx2.6 mutant mice were viable and fertile. There were no obvious abnormalities in the caudal pharyngeal pouch derivatives (the thymus, parathyroid glands, and thyroid gland), heart, and gut. Expression of Nkx2.6 overlaps that of Nkx2.5 in the pharynx and heart and that of Nkx2.3 in the pharynx. Interestingly, in mutant embryos homozygous for Nkx2.6, Nkx2.5 expression extended to the lateral side of the pharynx, suggesting a compensatory function of Nkx2.5 in the mutant pharyngeal pouches.
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24

Pavesi, Angelo. "Different patterns of codon usage in the overlapping polymerase and surface genes of hepatitis B virus suggest a de novo origin by modular evolution." Journal of General Virology 96, no. 12 (December 1, 2015): 3577–86. http://dx.doi.org/10.1099/jgv.0.000307.

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The polymerase (P) and surface (S) genes of hepatitis B virus (HBV) show the longest gene overlap in animal viruses. Gene overlaps originate by the overprinting of a novel frame onto an ancestral pre-existing frame. Identifying which frame is ancestral and which frame is de novo (the genealogy of the overlap) is an appealing topic. However, the P/S overlap of HBV is an intriguing paradox, because both genes are indispensable for virus survival. Thus, the hypothesis of a primordial virus without the surface protein or without the polymerase makes no biological sense. With the aim to determine the genealogy of the overlap, the codon usage of the overlapping frames P and S was compared to that of the non-overlapping region. It was found that the overlap of human HBV had two patterns of codon usage. One was localized in the 5′ one-third of the overlap and the other in the 3′ two-thirds. By extending the analysis to non-human HBVs, it was found that this feature occurred in all hepadnaviruses. Under the assumption that the ancestral frame has a codon usage significantly closer to that of the non-overlapping region than the de novo frame, the ancestral frames in the 5′ and 3′ region of the overlap could be predicted. They were, respectively, frame S and frame P. These results suggest that the spacer domain of the polymerase and the S domain of the surface protein originated de novo by overprinting. They support a modular evolution hypothesis for the origin of the overlap.
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Peterson, D. O., K. K. Beifuss, and K. L. Morley. "Context-dependent gene expression: cis-acting negative effects of specific procaryotic plasmid sequences on eucaryotic genes." Molecular and Cellular Biology 7, no. 4 (April 1987): 1563–67. http://dx.doi.org/10.1128/mcb.7.4.1563-1567.1987.

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A sequence element within pBR322 DNA mediates a cis-acting negative effect on expression from eucaryotic genes in transient expression assays. The negative element overlaps with sequences that inhibit DNA replication, but its effect is observed in the absence of detectable replication of transfected DNA.
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Peterson, D. O., K. K. Beifuss, and K. L. Morley. "Context-dependent gene expression: cis-acting negative effects of specific procaryotic plasmid sequences on eucaryotic genes." Molecular and Cellular Biology 7, no. 4 (April 1987): 1563–67. http://dx.doi.org/10.1128/mcb.7.4.1563.

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A sequence element within pBR322 DNA mediates a cis-acting negative effect on expression from eucaryotic genes in transient expression assays. The negative element overlaps with sequences that inhibit DNA replication, but its effect is observed in the absence of detectable replication of transfected DNA.
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27

Dhiman, Anjali, and Robert Schleif. "Recognition of Overlapping Nucleotides by AraC and the Sigma Subunit of RNA Polymerase." Journal of Bacteriology 182, no. 18 (September 15, 2000): 5076–81. http://dx.doi.org/10.1128/jb.182.18.5076-5081.2000.

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ABSTRACT The Escherichia coli promoterpBAD , under the control of the AraC protein, drives the expression of mRNA encoding the AraB, AraA, and AraD gene products of the arabinose operon. The binding site of AraC atpBAD overlaps the RNA polymerase −35 recognition region by 4 bases, leaving 2 bases of the region not contacted by AraC. This overlap raises the question of whether AraC substitutes for the sigma subunit of RNA polymerase in recognition of the −35 region or whether both AraC and sigma make important contacts with the DNA in the −35 region. If sigma does not contact DNA near the −35 region, pBAD activity should be independent of the identity of the bases in the hexamer region that are not contacted by AraC. We have examined this issue in thepBAD promoter and in a second promoter where the AraC binding site overlaps the −35 region by only 2 bases. In both cases promoter activity is sensitive to changes in bases not contacted by AraC, showing that despite the overlap, sigma does read DNA in the −35 region. Since sigma and AraC are thus closely positioned atpBAD , it is possible that AraC and sigma contact one another during transcription initiation. DNA migration retardation assays, however, showed that there exists only a slight degree of DNA binding cooperativity between AraC and sigma, thus suggesting either that the normal interactions between AraC and sigma are weak or that the presence of the entire RNA polymerase is necessary for significant interaction.
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Shimmoto, Michie, Yutaka Nakahori, Ikumi Matsushita, Toshikatsu Shinka, Yoko Kuroki, Kohji Itoh, and Hitoshi Sakuraba. "A Human Protective Protein Gene Partially Overlaps the Gene Encoding Phospholipid Transfer Protein on the Complementary Strand of DNA." Biochemical and Biophysical Research Communications 220, no. 3 (March 1996): 802–6. http://dx.doi.org/10.1006/bbrc.1996.0484.

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29

Lin, Guangyun, Jeffrey M. Slack, and Gary W. Blissard. "Expression and localization of LEF-11 in Autographa californica nucleopolyhedrovirus-infected Sf9 cells." Journal of General Virology 82, no. 9 (September 1, 2001): 2289–94. http://dx.doi.org/10.1099/0022-1317-82-9-2289.

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The Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) lef-11 gene was found previously to be necessary to support optimal levels of transient expression from an AcMNPV late promoter. The lef-11 gene is unusual in that it overlaps both upstream (orf38) and downstream (pp31) genes. In this study, the expression and cellular localization of LEF-11 were examined. The lef-11 transcripts were detected from 4 to 36 h post-infection (p.i.). The 1·5 kb lef-11 mRNA initiates 196 nt upstream of the lef-11 translation initiation codon, within the upstream orf38 gene. This relatively long 5′ upstream region encodes a potential small upstream open reading frame (ORF) of 58 amino acids that overlaps the lef-11 ORF. The 3′ end of the lef-11 mRNA was mapped as co-terminal with mRNAs from the downstream pp31 gene. Using affinity purified anti-LEF-11 antibodies, levels of LEF-11 expression were found to be maximal between approximately 8 and 24 h p.i., although LEF-11 could be detected as late as 72 h p.i. Using immunofluorescence microscopy, it was determined that LEF-11 localized to dense regions of infected cell nuclei, consistent with its role as a possible late transcription factor.
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Ochsner, Urs A., Adriana I. Vasil, Zaiga Johnson, and Michael L. Vasil. "Pseudomonas aeruginosa fur Overlaps with a Gene Encoding a Novel Outer Membrane Lipoprotein, OmlA." Journal of Bacteriology 181, no. 4 (February 15, 1999): 1099–109. http://dx.doi.org/10.1128/jb.181.4.1099-1109.1999.

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ABSTRACT A novel outer membrane lipoprotein in Pseudomonas aeruginosa is encoded by the omlA gene, which was identified immediately upstream of the fur (ferric uptake regulator) gene. The omlA and fur genes were divergently transcribed and had overlapping promoter regions. The proximal fur P2 promoter and the omlA promoter shared a 5-bp DNA motif for their −10 promoter elements. The distalfur P1 promoter was located within the omlAcoding sequence, and the omlA and fur T1 mRNAs overlapped by 154 nucleotides. Optimal expression of bothfur and omlA required roughly 200 bp of DNA upstream of the promoter regions, suggesting the presence ofcis-acting transcriptional activation elements located within the omlA and fur genes, respectively. The levels of Fur and OmlA proteins had no influence onomlA or fur expression, excluding anytrans-acting cross-regulation between fur andomlA. Expression of omlA was constitutive regardless of growth phase, oxygen tension, iron concentration, pH, and temperature. OmlA contained a signal sequence typical of bacterial lipoproteins, with a cysteine as a putative cleavage and lipid attachment site. Inhibition of signal peptidase II by globomycin resulted in failure to process OmlA, thus giving strong evidence that OmlA is a lipoprotein. Cell fractionation followed by Western blot analysis indicated that all OmlA protein is localized in the outer membrane. Mature OmlA was an acidic (pI = 4.5) protein of 17.3 kDa and had close to 40% amino acid sequence identity to SmpA (small protein A) of Escherichia coli, Vibrio cholerae, and Haemophilus influenzae, a protein of unknown function. All P. aeruginosa strains tested as well as Pseudomonas fluorescens were found to produce OmlA. A mutant strain with impaired production of OmlA but no change in the expression of the overlapping fur gene was constructed. TheomlA mutant was hypersusceptible to anionic detergents such as sodium dodecyl sulfate and deoxycholate, and it showed increased susceptibility to various antibiotics, including nalidixic acid, rifampin, novobiocin, and chloramphenicol. A structural role of OmlA in maintaining the cell envelope integrity is proposed.
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Cock, Peter J. A., and David E. Whitworth. "Evolution of Gene Overlaps: Relative Reading Frame Bias in Prokaryotic Two-Component System Genes." Journal of Molecular Evolution 64, no. 4 (March 19, 2007): 457–62. http://dx.doi.org/10.1007/s00239-006-0180-1.

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32

Liu, Bo, Chang-Lin Dou, Leena Prabhu, and Eseng Lai. "FAST-2 Is a Mammalian Winged-Helix Protein Which Mediates Transforming Growth Factor β Signals." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 424–30. http://dx.doi.org/10.1128/mcb.19.1.424.

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ABSTRACT The mechanisms by which transforming growth factor β (TGF-β) and related ligands regulate transcription remain poorly understood. The winged-helix (WH) transcription factor fork head activin signal transducer 1 (FAST-1) was identified as a mediator of activin signaling in Xenopus embryos (X. Chen, M. J. Rubock, and M. Whitman, Nature 383:691–696, 1996). We have cloned a novel WH gene from the mouse which shares many properties with FAST-1. We find that this gene, which we call FAST-2, is able to mediate transcriptional activation by TGF-β. FAST-2 also interacts directly with Smad2, a cytoplasmic protein which is translocated to the nucleus in response to TGF-β, and forms a multimeric complex with Smad2 and Smad4 on the activin response element, a high-affinity binding site for FAST-1. Analysis of the sequences of FAST-1 and FAST-2 reveals substantial protein sequence divergence compared to known vertebrate orthologs in the WH family. This suggests that FAST-2 represents a new WH gene related to FAST-1, which functions to mediate TGF-β signals in mammals. We have also examined the structure of the FAST-2 gene and find that it overlaps with a kinesin motor protein gene. The genes are transcribed in opposite orientations, and their transcripts overlap in the 3′ untranslated region.
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TSUKAGUCHI, HIROYASU, HENRY YAGER, JOHN DAWBORN, LUIS JOST, JERRY COHLMIA, PATRICIA F. ABREU, APARECIDO B. PEREIRA, and MARTIN R. POLLAK. "A Locus for Adolescent and Adult Onset Familial Focal Segmental Glomerulosclerosis on Chromosome 1q25-31." Journal of the American Society of Nephrology 11, no. 9 (September 2000): 1674–80. http://dx.doi.org/10.1681/asn.v1191674.

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Abstract. Focal segmental glomerulosclerosis is a nonspecific renal lesion observed both as a primary (idiopathic) entity and in a secondary form, typically in association with reduced functional renal mass. Familial forms have been observed and two loci for autosomal dominant FSGS have been mapped. This study shows that an adolescent/adult form of recessive FSGS maps to a locus on chromosome 1q25-31, which overlaps with a region previously identified as harboring a locus for an early childhood onset recessive form of nephrotic syndrome (SRN1). Evaluation of a large family demonstrated linkage with a maximum two-point lod score of 3.98 at D1S254 and D1S222. Lod score calculations support the conclusion of linkage in four of five additional families. Haplotype analysis suggests that this FSGS gene is located in a 19-cM region flanked by D1S416 and D1S413, of which 6 cM overlaps with SRN1, suggesting that these distinct clinical subsets of kidney disease may be allelic. These regions may also overlap with the syntenic region of the glomerulosclerosis susceptibility locus in the BUF/Mna rat. Because the presentation of FSGS may be subtle, inherited FSGS may be much more common than generally realized and grossly underestimated because of the absence of clear familial patterns. This result increases the suspicion that polymorphisms at this locus may contribute to sporadic FSGS.
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KIM, Richard H., Jack J. LI, Yorimasa OGATA, Masato YAMAUCHI, Leonard P. FREEDMAN, and Jaro SODEK. "Identification of a vitamin D3-response element that overlaps a unique inverted TATA box in the rat bone sialoprotein gene." Biochemical Journal 318, no. 1 (August 15, 1996): 219–26. http://dx.doi.org/10.1042/bj3180219.

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Bone sialoprotein (BSP), an early marker of osteoblast differentiation, has been implicated in the nucleation of hydroxyapatite during bone formation de novo. Our studies, using the osteoblastic cell line ROS 17/2.8, have revealed that rat BSP gene expression is suppressed by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], which is a powerful regulator of bone formation and resorption. To determine the molecular basis of the transcriptional suppression of BSP gene transcription by 1,25(OH)2D3, we have conducted transient transfection analyses with chimaeric constructs of the rat BSP gene promoter linked to a luciferase reporter gene. 1,25(OH)2D3 suppressed expression in all constructs, including a short construct (pLUC 3; nt -116 to +60) that contained a putative vitamin D3-response element (VDRE; AGGGTTTATAGGTCA; nt -28 to -14) that overlaps a unique inverted TATA (TTTATA) box. Mobility shift assays demonstrated strong binding of recombinant human vitamin D3 receptor protein (hVDR) to the VDRE. Point mutations introduced into each half-site and analysed for 1,25(OH)2D3-mediated suppression of transcription and for hVDR binding either decreased or increased both transcriptional suppression and binding. In comparison with activating VDREs, the rat BSP VDRE bound VDR–VDR homodimers more avidly than VDR–RXRα heterodimers (where RXR is retinoid X receptor). These studies have therefore identified a novel 1,25(OH)2D3 suppressor element that overlaps the inverted TATA box in the rat BSP gene and indicate that transcriptional suppression of the rat BSP gene by 1,25(OH)2D3 might involve competition between the VDR and the TATA binding protein (TBP).
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35

Oehler, Stefan. "Feedback Regulation of Lac Repressor Expression in Escherichia coli." Journal of Bacteriology 191, no. 16 (June 5, 2009): 5301–3. http://dx.doi.org/10.1128/jb.00427-09.

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ABSTRACT Negative feedback regulation, mediated through repressor binding site O3, which overlaps the lacI gene, could explain the robustness of the weak expression of Lac repressor. Significant autorepression of Lac repressor has never been ruled out. In the work presented here, the degree of autoregulation of Lac repressor was determined. It is negligible.
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36

Guertin, M., H. LaRue, D. Bernier, O. Wrange, M. Chevrette, M. C. Gingras, and L. Bélanger. "Enhancer and promoter elements directing activation and glucocorticoid repression of the alpha 1-fetoprotein gene in hepatocytes." Molecular and Cellular Biology 8, no. 4 (April 1988): 1398–407. http://dx.doi.org/10.1128/mcb.8.4.1398-1407.1988.

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Mutations were introduced in 7 kilobases of 5'-flanking rat alpha 1-fetoprotein (AFP) genomic DNA, linked to the chloramphenicol acetyltransferase gene. AFP promoter activity and its repression by a glucocorticoid hormone were assessed by stable and transient expression assays. Stable transfection assays were more sensitive and accurate than transient expression assays in a Morris 7777 rat hepatoma recipient (Hepa7.6), selected for its strong AFP repression by dexamethasone. The segment of DNA encompassing a hepatocyte-constitutive chromatin DNase I-hypersensitive site at -3.7 kilobases and a liver developmental stage-specific site at -2.5 kilobases contains interacting enhancer elements sufficient for high AFP promoter activity in Hepa7.6 or HepG2 cells. Deletions and point mutations define an upstream promoter domain of AFP gene activation, operating with at least three distinct promoter-activating elements, PEI at -65 base pairs, PEII at -120 base pairs, and DE at -160 base pairs. PEI and PEII share homologies with albumin promoter sequences, PEII is a near-consensus nuclear factor I recognition sequence, and DE overlaps a glucocorticoid receptor recognition sequence. An element conferring glucocorticoid repression of AFP gene activity is located in the upstream AFP promoter domain. Receptor-binding assays indicate that this element is the glucocorticoid receptor recognition sequence which overlaps with promoter-activating element DE.
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37

Guertin, M., H. LaRue, D. Bernier, O. Wrange, M. Chevrette, M. C. Gingras, and L. Bélanger. "Enhancer and promoter elements directing activation and glucocorticoid repression of the alpha 1-fetoprotein gene in hepatocytes." Molecular and Cellular Biology 8, no. 4 (April 1988): 1398–407. http://dx.doi.org/10.1128/mcb.8.4.1398.

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Mutations were introduced in 7 kilobases of 5'-flanking rat alpha 1-fetoprotein (AFP) genomic DNA, linked to the chloramphenicol acetyltransferase gene. AFP promoter activity and its repression by a glucocorticoid hormone were assessed by stable and transient expression assays. Stable transfection assays were more sensitive and accurate than transient expression assays in a Morris 7777 rat hepatoma recipient (Hepa7.6), selected for its strong AFP repression by dexamethasone. The segment of DNA encompassing a hepatocyte-constitutive chromatin DNase I-hypersensitive site at -3.7 kilobases and a liver developmental stage-specific site at -2.5 kilobases contains interacting enhancer elements sufficient for high AFP promoter activity in Hepa7.6 or HepG2 cells. Deletions and point mutations define an upstream promoter domain of AFP gene activation, operating with at least three distinct promoter-activating elements, PEI at -65 base pairs, PEII at -120 base pairs, and DE at -160 base pairs. PEI and PEII share homologies with albumin promoter sequences, PEII is a near-consensus nuclear factor I recognition sequence, and DE overlaps a glucocorticoid receptor recognition sequence. An element conferring glucocorticoid repression of AFP gene activity is located in the upstream AFP promoter domain. Receptor-binding assays indicate that this element is the glucocorticoid receptor recognition sequence which overlaps with promoter-activating element DE.
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38

Davies, Andrew G., Caroline A. Spike, Jocelyn E. Shaw, and Robert K. Herman. "Functional Overlap Between the mec-8 Gene and Five sym Genes in Caenorhabditis elegans." Genetics 153, no. 1 (September 1, 1999): 117–34. http://dx.doi.org/10.1093/genetics/153.1.117.

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Abstract Earlier work showed that the Caenorhabditis elegans gene mec-8 encodes a regulator of alternative RNA splicing and that mec-8 null mutants have defects in sensory neurons and body muscle attachment but are generally viable and fertile. We have used a genetic screen to identify five mutations in four genes, sym-1–sym-4, that are synthetically lethal with mec-8 loss-of-function mutations. The phenotypes of sym single mutants are essentially wild type. mec-8; sym-1 embryos arrest during embryonic elongation and exhibit defects in the attachment of body muscle to extracellular cuticle. sym-1 can encode a protein containing a signal sequence and 15 contiguous leucine-rich repeats. A fusion of sym-1 and the gene for green fluorescent protein rescued the synthetic lethality of mec-8; sym-1 mutants; the fusion protein was secreted from the apical hypodermal surface of the embryo. We propose that SYM-1 helps to attach body muscle to the extracellular cuticle and that another gene that is dependent upon mec-8 for pre-mRNA processing overlaps functionally with sym-1. RNA-mediated interference experiments indicated that a close relative of sym-1 functionally overlaps both sym-1 and mec-8 in affecting muscle attachment. sym-2, sym-3, and sym-4 appear to provide additional functions that are essential in the absence of mec-8(+).
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39

Sturm, R. A., H. J. Eyre, E. Baker, and G. R. Sutherland. "The human OTF1 locus which overlaps the CD3Z gene is located at 1q22→q23." Cytogenetic and Genome Research 68, no. 3-4 (1995): 231–32. http://dx.doi.org/10.1159/000133919.

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40

Matsui, Masayuki, Thazha P. Prakash, and David R. Corey. "Transcriptional Silencing by Single-Stranded RNAs Targeting a Noncoding RNA That Overlaps a Gene Promoter." ACS Chemical Biology 8, no. 1 (October 24, 2012): 122–26. http://dx.doi.org/10.1021/cb300490j.

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41

Soerensen, Mette, Jonas Mengel-From, Kaare Christensen, Lene Christiansen, and Qihua Tan. "A Genome-Wide Integrative Study of DNA Methylation, Gene Expression, and Later Life Hand Grip Strength." Innovation in Aging 4, Supplement_1 (December 1, 2020): 128–29. http://dx.doi.org/10.1093/geroni/igaa057.422.

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Abstract Hand grip strength (HS) measures muscular strength and associates with multiple health outcomes and mortality. Studies of epigenetic and transcriptomic markers could help elucidate the biology behind HS; markers for which monozygotic (MZ) twins are excellent study populations. We performed integrated enrichment analyses (IEA) of an epigenome-wide association analysis (EWAS) and a transcriptome-wide association analysis (TWAS) of HS in blood samples of 452 MZ twins (56-80 years of age). Unsupervised IEA were conducted by the KeyPathwayMiner algorithm, while supervised IEA were performed by the KEGG and Reactome databases. No individual CpG site or probe passed correction for multiple testing. Investigating the overlap in genes with p-values&lt;0.01, 0.005 or 0.001 in the EWAS and TWAS, revealed 67, 21 and 2 unique genes, respectively. The latter 2 were TESK2 and VWA1. By the supervised approach, the 67-gene overlap identified three pathways related to “antigen processing and presentation”, driven by HLA-A, HLA-B, TAP2 and PSME2. With the unsupervised approach the 21-gene and 67-gene overlaps revealed networks containing 7 and 19 genes, respectively. Exception nodes (added by the algorithm for structure) were CREBBP and CSNK2A2 for the former, and APP and HSP90AB1 for the latter. The remaining IEA revealed no gene sets or networks. Several of these genes have previously been linked to HS relevant traits, e.g. arthritis (HLA-A, HLA-B and TAP2), smooth muscle and cardiovascular function (TESK2, HLA-B and APP) and sarcopenia (HSP90AB1). Hence, this study reports genes and pathways previously reported for physical functioning, yet also novel candidates for further verification.
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42

Bristow, J., MK Tee, SE Gitelman, SH Mellon, and WL Miller. "Tenascin-X: a novel extracellular matrix protein encoded by the human XB gene overlapping P450c21B." Journal of Cell Biology 122, no. 1 (July 1, 1993): 265–78. http://dx.doi.org/10.1083/jcb.122.1.265.

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A human gene termed XB overlaps the P450c21B gene encoding steroid 21-hydroxylase and encodes a protein that closely resembles extracellular matrix proteins. Sequencing of phage and cosmid clones and of cDNA fragments shows that the XB gene spans 65 kb of DNA, consisting of 39 exons that encode a 12-kb mRNA. The predicted protein of over 400 kD consists of five distinct domains: a signal peptide, a hydrophobic domain containing three heptad repeats, a series of 18.5 EGF-like repeats, 29 fibronectin type III repeats, and a carboxy-terminal fibrinogen-like domain. Because the structure of the protein encoded by the XB gene closely resembles tenascin, we term this protein tenascin-X (TN-X), and propose a simplified nomenclature system for the family of tenascins. RNase protection experiments show that the TN-X transcript is expressed ubiquitously in human fetal tissues, with the greatest expression in the fetal testis and in fetal skeletal, cardiac, and smooth muscle. Two adrenal-specific transcripts, P450c21B (steroid 21-hydroxylase) and Y (an untranslated transcript) overlap the XB gene on the complementary strand of DNA, yielding a unique array of overlapping transcripts: a "polygene." In situ hybridization histochemistry experiments show that the TN-X transcript and the P450c21 and Y transcripts encoded on the complementary DNA strand are all expressed in the same cells of the human adrenal cortex. Genetic data suggest that TN-X may be essential for life.
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43

Henry, Stephen P., Masamine Takanosu, Tanya C. Boyd, Pauline M. Mayne, Heidi Eberspaecher, Wei Zhou, Benoit de Crombrugghe, Magnus Höök, and Richard Mayne. "Expression Pattern and Gene Characterization ofAsporin." Journal of Biological Chemistry 276, no. 15 (January 10, 2001): 12212–21. http://dx.doi.org/10.1074/jbc.m011290200.

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We have discovered a new member of the class I small leucine-rich repeat proteoglycan (SLRP) family which is distinct from the other class I SLRPs since it possesses a unique stretch of aspartate residues at its N terminus. For this reason, we called the moleculeasporin. The deduced amino acid sequence is about 50% identical (and 70% similar) to decorin and biglycan. However, asporin does not contain a serine/glycine dipeptide sequence required for the assembly ofO-linked glycosaminoglycans and is probably not a proteoglycan. The tissue expression ofasporinpartially overlaps with the expression ofdecorinandbiglycan. During mouse embryonic development,asporinmRNA expression was detected primarily in the skeleton and other specialized connective tissues; very littleasporinmessage was detected in the major parenchymal organs. The mouseasporingene structure is similar to that ofbiglycananddecorinwith 8 exons. Theasporingene is localized to human chromosome 9q22–9q21.3 whereasporinis part of a SLRP gene cluster that includesextracellular matrix protein 2,osteoadherin, andosteoglycin. Further analysis shows that, with the exception ofbiglycan, all known SLRP genes reside in three gene clusters.
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44

Górecka, Ewa, Romain Gastineau, Nikolai A. Davidovich, Olga I. Davidovich, Matt P. Ashworth, Jamal S. M. Sabir, Claude Lemieux, Monique Turmel, and Andrzej Witkowski. "Mitochondrial and Plastid Genomes of the Monoraphid Diatom Schizostauron trachyderma." International Journal of Molecular Sciences 22, no. 20 (October 15, 2021): 11139. http://dx.doi.org/10.3390/ijms222011139.

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We provide for the first time the complete plastid and mitochondrial genomes of a monoraphid diatom: Schizostauron trachyderma. The mitogenome is 41,957 bp in size and displays two group II introns in the cox1 gene. The 187,029 bp plastid genome features the typical quadripartite architecture of diatom genomes. It contains a group II intron in the petB gene that overlaps the large single-copy and the inverted repeat region. There is also a group IB4 intron encoding a putative LAGLIDADG homing endonuclease in the rnl gene. The multigene phylogenies conducted provide more evidence of the proximity between S. trachyderma and fistula-bearing species of biraphid diatoms.
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45

McNair, Katelyn, Carol Zhou, Elizabeth A. Dinsdale, Brian Souza, and Robert A. Edwards. "PHANOTATE: a novel approach to gene identification in phage genomes." Bioinformatics 35, no. 22 (April 25, 2019): 4537–42. http://dx.doi.org/10.1093/bioinformatics/btz265.

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Abstract Motivation Currently there are no tools specifically designed for annotating genes in phages. Several tools are available that have been adapted to run on phage genomes, but due to their underlying design, they are unable to capture the full complexity of phage genomes. Phages have adapted their genomes to be extremely compact, having adjacent genes that overlap and genes completely inside of other longer genes. This non-delineated genome structure makes it difficult for gene prediction using the currently available gene annotators. Here we present PHANOTATE, a novel method for gene calling specifically designed for phage genomes. Although the compact nature of genes in phages is a problem for current gene annotators, we exploit this property by treating a phage genome as a network of paths: where open reading frames are favorable, and overlaps and gaps are less favorable, but still possible. We represent this network of connections as a weighted graph, and use dynamic programing to find the optimal path. Results We compare PHANOTATE to other gene callers by annotating a set of 2133 complete phage genomes from GenBank, using PHANOTATE and the three most popular gene callers. We found that the four programs agree on 82% of the total predicted genes, with PHANOTATE predicting more genes than the other three. We searched for these extra genes in both GenBank’s non-redundant protein database and all of the metagenomes in the sequence read archive, and found that they are present at levels that suggest that these are functional protein-coding genes. Availability and implementation https://github.com/deprekate/PHANOTATE Supplementary information Supplementary data are available at Bioinformatics online.
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46

Brassinga, Ann Karen C., Rania Siam, and Gregory T. Marczynski. "Conserved Gene Cluster at Replication Origins of the α-Proteobacteria Caulobacter crescentus andRickettsia prowazekii." Journal of Bacteriology 183, no. 5 (March 1, 2001): 1824–29. http://dx.doi.org/10.1128/jb.183.5.1824-1829.2001.

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ABSTRACT A 30-kb region surrounding the replication origin inCaulobacter crescentus was analyzed. Comparison to the genome sequence of another α-proteobacterium, Rickettsia prowazekii, revealed a conserved cluster of genes (RP001,hemE, hemH, and RP883) that overlaps the established origin of replication in C. crescentus and the putative origin of replication in R. prowazekii. The genes flanking this cluster differ between these two organisms. We therefore propose that this conserved gene cluster can be used to identify the origin of replication in other α-proteobacteria.
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47

Mukai, Takahito. "Bioinformatic Prediction of an tRNASec Gene Nested inside an Elongation Factor SelB Gene in Alphaproteobacteria." International Journal of Molecular Sciences 22, no. 9 (April 27, 2021): 4605. http://dx.doi.org/10.3390/ijms22094605.

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In bacteria, selenocysteine (Sec) is incorporated into proteins via the recoding of a particular codon, the UGA stop codon in most cases. Sec-tRNASec is delivered to the ribosome by the Sec-dedicated elongation factor SelB that also recognizes a Sec-insertion sequence element following the codon on the mRNA. Since the excess of SelB may lead to sequestration of Sec-tRNASec under selenium deficiency or oxidative stress, the expression levels of SelB and tRNASec should be regulated. In this bioinformatic study, I analyzed the Rhizobiales SelB species because they were annotated to have a non-canonical C-terminal extension. I found that the open reading frame (ORF) of diverse Alphaproteobacteria selB genes includes an entire tRNASec sequence (selC) and overlaps with the start codon of the downstream ORF. A remnant tRNASec sequence was found in the Sinorhizobium melilotiselB genes whose products have a shorter C-terminal extension. Similar overlapping traits were found in Gammaproteobacteria and Nitrospirae. I hypothesized that once the tRNASec moiety is folded and processed, the expression of the full-length SelB may be repressed. This is the first report on a nested tRNA gene inside a protein ORF in bacteria.
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Ozisik, Ozan, Friederike Ehrhart, Chris T. Evelo, Alberto Mantovani, and Anaı̈s Baudot. "Overlap of vitamin A and vitamin D target genes with CAKUT-related processes." F1000Research 10 (May 18, 2021): 395. http://dx.doi.org/10.12688/f1000research.51018.1.

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Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) are a group of abnormalities affecting the kidneys and their outflow tracts, which include the ureters, the bladder, and the urethra. CAKUT patients display a large clinical variability as well as a complex aetiology, as only 5% to 20% of the cases have a monogenic origin. It is thereby suspected that interactions of both genetic and environmental factors contribute to the disease. Vitamins are among the environmental factors that are considered for CAKUT aetiology. In this study, we collected vitamin A and vitamin D target genes and computed their overlap with CAKUT-related gene sets. We observed significant overlaps between vitamin A target genes and CAKUT causal genes, or with genes involved in renal system development, which indicates that an excess or deficiency of vitamin A might be relevant to a broad range of urogenital abnormalities.
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49

Karunanithi, Sivarajan, Vidya Oruganti, Simone Marker, Angela M. Rodriguez-Viana, Franziska Drews, Marcello Pirritano, Karl Nordström, Martin Simon, and Marcel H. Schulz. "Exogenous RNAi mechanisms contribute to transcriptome adaptation by phased siRNA clusters in Paramecium." Nucleic Acids Research 47, no. 15 (June 28, 2019): 8036–49. http://dx.doi.org/10.1093/nar/gkz553.

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Abstract Extensive research has characterized distinct exogenous RNAi pathways interfering in gene expression during vegetative growth of the unicellular model ciliate Paramecium. However, role of RNAi in endogenous transcriptome regulation, and environmental adaptation is unknown. Here, we describe the first genome-wide profiling of endogenous sRNAs in context of different transcriptomic states (serotypes). We developed a pipeline to identify, and characterize 2602 siRNA producing clusters (SRCs). Our data show no evidence that SRCs produce miRNAs, and in contrast to other species, no preference for strand specificity of siRNAs. Interestingly, most SRCs overlap coding genes and a separate group show siRNA phasing along the entire open reading frame, suggesting that the mRNA transcript serves as a source for siRNAs. Integrative analysis of siRNA abundance and gene expression levels revealed surprisingly that mRNA and siRNA show negative as well as positive associations. Two RNA-dependent RNA Polymerase mutants, RDR1 and RDR2, show a drastic loss of siRNAs especially in phased SRCs accompanied with increased mRNA levels. Importantly, most SRCs depend on both RDRs, reminiscent to primary siRNAs in the RNAi against exogenous RNA, indicating mechanistic overlaps between exogenous and endogenous RNAi contributing to flexible transcriptome adaptation.
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Loviny, T., P. M. Norton, and B. S. Hartley. "Ribitol dehydrogenase of Klebsiella aerogenes. Sequence of the structural gene." Biochemical Journal 230, no. 3 (September 15, 1985): 579–85. http://dx.doi.org/10.1042/bj2300579.

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The ribitol dehydrogenase gene was cloned from wild-type Klebsiella aerogenes and also from a transducing phage lambda prbt which expresses the rbt operon constitutively. The coding sequence for 249 amino acids is separated from the following D-ribulokinase gene by 31 base pairs containing three stop codons, one of which overlaps the ribosome binding site for D-ribulokinase. Three residues in the amino acid sequence differ from that predicted from the DNA sequence: Asp-212 for Asn-212 is probably a protein sequencing error, but -Ala-Val- for -Ser-Ser- at 146-147 appears to be a ‘neutral mutation’ that may have arisen during prolonged chemostat selection of a strain that superproduces the enzyme from which the protein sequence was determined.
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