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Your search keyword '"Landry, Josette-Renee"' showing total 22 results
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22 results on '"Landry, Josette-Renee"'

1. Human models of NUP98-KDM5A megakaryocytic leukemia in mice contribute to uncovering new biomarkers and therapeutic vulnerabilities

Author

Cardin, Sophie, Bilodeau, Mélanie, Roussy, Mathieu, Aubert, Léo, Milan, Thomas, Jouan, Loubna, Rouette, Alexandre, Laramée, Louise, Gendron, Patrick, Duchaine, Jean, Decaluwe, Hélène, Spinella, Jean-François, Mourad, Stéphanie, Couture, Françoise, Sinnett, Daniel, Haddad, Élie, Landry, Josette-Renée, Ma, Jing, Humphries, R. Keith, Roux, Philippe P., Hébert, Josée, Gruber, Tanja A., Wilhelm, Brian T., and Cellot, Sonia

Published
2019
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2. Bélanger S, Tu MM, Rahim MM, et al. Impaired natural killer cell self-education and “missing-self” responses in Ly49-deficient mice. Blood. 2012;120(3):592-602.

Author

Belanger, Simon, Tu, Megan M, Rahim, Mir Munir Ahmed, Mahmoud, Ahmad B, Patel, Rajen, Tai, Lee-Hwa, Troke, Angela D, Wilhelm, Brian T, Landry, Josette-Renee, Zhu, Qinzhang, Tung, Kenneth S, Raulet, David H, and Makrigiannis, Andrew P

Subjects
Biomedical and Clinical Sciences, Immunology, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine, Biochemistry and cell biology, Cardiovascular medicine and haematology, Paediatrics
Published
2013

7. Expression of the leukemia oncogene Lmo2 is controlled by an array of tissue-specific elements dispersed over 100 kb and bound by Tal1/Lmo2, Ets, and Gata factors

Author

Landry, Josette-Renée, Bonadies, Nicolas, Kinston, Sarah, Knezevic, Kathy, Wilson, Nicola K., Oram, S. Helen, Janes, Mary, Piltz, Sandie, Hammett, Michelle, Carter, Jacinta, Hamilton, Tina, Donaldson, Ian J., Lacaud, Georges, Frampton, Jonathan, Follows, George, Kouskoff, Valerie, and Göttgens, Berthold

Published
2009
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11. Transcriptional regulation of human genes by endogenous retroviral elements

Author

Landry, Josette-Renee

Subjects
viruses, embryonic structures
Abstract

Human endogenous retroviruses (HERVs) and other long terminal repeat (LTR)- containing elements comprise a significant portion (8%) of the human genome and are likely vestiges of retroviral infections during primate evolution. Although the vast majority of HERVs are now unable to code for retroviral proteins, an unknown number have retained functional transcriptional elements within their LTRs and some of these regulatory sequences have been shown to participate in the transcription of nearby genes. The overall objective of my thesis was to further understand the role of HERVs in human gene regulation by investigating LTRs that provide alternative promoters to cellular genes. When I began my study, three putative endogenous retroviral promoters were identified by screening sequence databases for chimeric (viral-cellular) transcripts. These searches revealed fusion transcripts containing the LTRs of three HERV-E elements linked to the endothelin B receptor (EDNRB), the apolipoprotein C-l (APOC1) and the Opitz syndrome gene, midline 1. To confirm the authenticity of the chimeric transcript and to establish that the mRNAs were transcribed from the retroviral LTRs, we performed 5'RACE and determined the genomic organization for each gene. Our results indicated that the chimeric transcripts were alternatively promoted by the retroviral elements, as they initiated within HERV-E LTRs but spliced into the downstream coding sequence of the cellular genes. To determine the expression pattern and the relative contribution of the retroviral promoter, we quantified the percentage of transcripts which were chimeric in various tissues using real-time PCR. While chimeric APOC1 transcripts could be detected in several tissues tested, the retroviral promoter of EDNRB and MIDI appeared to be placenta-specific. Transient transfection studies supported a role for the EDNRB and MIDI LTRs as strong promoters in placenta and suggested a function for the LTRs as enhancers. Further deletion and hybrid constructs delineated regions within both LTRs necessary for strong promoter activity. Finally, to further characterize the APOC1, EDNRB and MIDI genes, the non-retro viral (native) promoters of these three genes were also analysed. These findings provide further evidence that some endogenous retroviruses have evolved a biological function as transcriptional regulatory elements by contributing alternative promoters to human genes.

Published
2003
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14. Gfi1 Expression Is Controlled by Five Distinct Regulatory Regions Spread over 100 Kilobases, with Scl/Tal1, Gata2, PU.1, Erg, Meis1, and Runx1 Acting as Upstream Regulators in Early Hematopoietic Cells

Author

Wilson, Nicola K., primary, Timms, Richard T., additional, Kinston, Sarah J., additional, Cheng, Yi-Han, additional, Oram, S. Helen, additional, Landry, Josette-Renee, additional, Mullender, Joanne, additional, Ottersbach, Katrin, additional, and Gottgens, Berthold, additional

Published
2010
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15. Genome-Wide Computational Screen for Blood Stem Cell Enhancers Integrates RUNX1 and the BMP Signaling Pathway into the SCL Transcriptional Network.

Author

Pimanda, John E., primary, Donaldson, Ian J., primary, Bruijn, Marella F., primary, Kinston, Sarah J., primary, Knezevic, Kathy, primary, Huckle, Liz, primary, Piltz, Sandie, primary, Landry, Josette-Renee, primary, Green, Anthony R., primary, Tannahill, David, primary, and Gottgens, Berthold, primary

Published
2006
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16. The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl–/– phenotype

Author

Chan, Wan Y. I., primary, Follows, George A., additional, Lacaud, Georges, additional, Pimanda, John E., additional, Landry, Josette-Renee, additional, Kinston, Sarah, additional, Knezevic, Kathy, additional, Piltz, Sandie, additional, Donaldson, Ian J., additional, Gambardella, Laure, additional, Sablitzky, Fred, additional, Green, Anthony R., additional, Kouskoff, Valerie, additional, and Göttgens, Berthold, additional

Published
2006
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18. The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl–/– phenotype

Author

Chan, Wan Y. I., Follows, George A., Lacaud, Georges, Pimanda, John E., Landry, Josette-Renee, Kinston, Sarah, Knezevic, Kathy, Piltz, Sandie, Donaldson, Ian J., Gambardella, Laure, Sablitzky, Fred, Green, Anthony R., Kouskoff, Valerie, and Göttgens, Berthold

Abstract

Transcription factors are key regulators of hematopoietic stem cells (HSCs), yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of Scl/Tal1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterize the molecular mechanisms controlling expression of Lyl1, a paralog of Scl also required for HSC function. Two closely spaced promoters directed expression to hematopoietic progenitor, megakaryocytic, and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg, and PU.1. However, despite coregulation of Scl and Lyl1 by the same Ets and GATA factors, Scl expression was initiated prior to Lyl1 in embryonic stem (ES) cell differentiation assays. Moreover, ectopic expression of Scl but not Lyl1 rescued hematopoietic differentiation in Scl−/− ES cells, thus providing a molecular explanation for the vastly different phenotypes of Scl−/− and Lyl1−/− mouse embryos. Furthermore, coregulation of Scl and Lyl1 later during development may explain the mild phenotype of Scl−/− adult HSCs.

Published
2007
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19. The paralogous hematopoietic regulators Lyl1and Sclare coregulated by Ets and GATA factors, but Lyl1cannot rescue the early Scl–/–phenotype

Author

Chan, Wan Y.I., Follows, George A., Lacaud, Georges, Pimanda, John E., Landry, Josette-Renee, Kinston, Sarah, Knezevic, Kathy, Piltz, Sandie, Donaldson, Ian J., Gambardella, Laure, Sablitzky, Fred, Green, Anthony R., Kouskoff, Valerie, and Göttgens, Berthold

Abstract

Transcription factors are key regulators of hematopoietic stem cells (HSCs), yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of Scl/Tal1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterize the molecular mechanisms controlling expression of Lyl1, a paralog of Sclalso required for HSC function. Two closely spaced promoters directed expression to hematopoietic progenitor, megakaryocytic, and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg, and PU.1. However, despite coregulation of Scland Lyl1by the same Ets and GATA factors, Sclexpression was initiated prior to Lyl1in embryonic stem (ES) cell differentiation assays. Moreover, ectopic expression of Sclbut not Lyl1rescued hematopoietic differentiation in Scl−/−ES cells, thus providing a molecular explanation for the vastly different phenotypes of Scl−/−and Lyl1−/−mouse embryos. Furthermore, coregulation of Scland Lyl1later during development may explain the mild phenotype of Scl−/−adult HSCs.

Published
2007
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22. Integration of Elf-4 into Stem/Progenitor and Erythroid Regulatory Networks through Locus-Wide Chromatin Studies Coupled with InVivo Functional Validation.

Author

Smith, Aileen M., Calero-Nieto, Fernando J., Schütte, Judith, Kinston, Sarah, Timms, Richard T., Wilson, Nicola K., Hannah, Rebecca L., Landry, Josette-Renee, and Göttgens, Berthold

Subjects
T cells, HOMEOSTASIS, CHROMATIN, STEM cells, TRANSCRIPTION factors
Abstract

The ETS transcription factor Elf-4 is an important regulator of hematopoietic stem cell (HSC) and T cell homeostasis. T o gain insights into the transcriptional circuitry within which Elf-4 operates, we used comparative sequence analysis coupled with chromatin immunoprecipitation (ChIP) with microarray technology (ChIP-chip) assays for specific chromatin marks to identify three promoters and two enhancers active in hematopoietic and endothelial cell lines. Comprehensive functional validation of each of these regulatory regions in transgenic mouse embryos identified a tissue-specific enhancer (-10E) that displayed activity in fetal liver, dorsal aorta, vitelline vessels, yolk sac, and heart. Integration of a ChIP-sequencing (ChIP-Seq) data set for 10 key stem cell transcription factors showed Pu.1, Fli-1, and Erg were bound to the -10E element, and mutation of three highly conserved ETS sites within the enhancer abolished its activity. Finally, the transcriptional repressor Gfi1b was found to bind to and repress one of the Elf-4 promoters (-30P), and we show that this repression of Elf-4 is important for the maturation of primary fetal liver erythroid cells. T aken together, our results provide a comprehensive overview of the transcriptional control of Elf-4 within the hematopoietic system and, thus, integrate Elf-4 into the wider transcriptional regulatory networks that govern hematopoietic development. [ABSTRACT FROM AUTHOR]

Published
2012
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