7648.Full.Pdf
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
RBP-J Signaling − Cells Through Notch Novel IRF8-Controlled
Sca-1+Lin−CD117− Mesenchymal Stem/Stromal Cells Induce the Generation of Novel IRF8-Controlled Regulatory Dendritic Cells through Notch −RBP-J Signaling This information is current as of September 25, 2021. Xingxia Liu, Shaoda Ren, Chaozhuo Ge, Kai Cheng, Martin Zenke, Armand Keating and Robert C. H. Zhao J Immunol 2015; 194:4298-4308; Prepublished online 30 March 2015; doi: 10.4049/jimmunol.1402641 Downloaded from http://www.jimmunol.org/content/194/9/4298 Supplementary http://www.jimmunol.org/content/suppl/2015/03/28/jimmunol.140264 http://www.jimmunol.org/ Material 1.DCSupplemental References This article cites 59 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/194/9/4298.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 25, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Sca-1+Lin2CD1172 Mesenchymal Stem/Stromal Cells Induce the Generation of Novel IRF8-Controlled Regulatory Dendritic Cells through Notch–RBP-J Signaling Xingxia Liu,*,1 Shaoda Ren,*,1 Chaozhuo Ge,* Kai Cheng,* Martin Zenke,† Armand Keating,‡,x and Robert C. -
Cell Cycle Regulation of Proliferation Versus Differentiation in the Central Nervous System
Cell Tissue Res DOI 10.1007/s00441-014-1895-8 REVIEW Cell cycle regulation of proliferation versus differentiation in the central nervous system Laura J. A. Hardwick & Fahad R. Ali & Roberta Azzarelli & Anna Philpott Received: 4 February 2014 /Accepted: 10 April 2014 # The Author(s) 2014. This article is published with open access at Springerlink.com Abstract Formation of the central nervous system requires a precise coordination and the ultimate division versus differenti- period of extensive progenitor cell proliferation, accompanied ation decision. or closely followed by differentiation; the balance between these two processes in various regions of the central nervous system Keywords Cell cycle . Differentiation . Neurogenesis . gives rise to differential growth and cellular diversity. The Proneural . Central nervous system correlation between cell cycle lengthening and differentiation has been reported across several types of cell lineage and from diverse model organisms, both in vivo and in vitro. Introduction Furthermore, different cell fates might be determined during different phases of the preceding cell cycle, indicating direct cell During development of the central nervous system (CNS), a cycle influences on both early lineage commitment and terminal period of extensive proliferation is needed to generate the re- cell fate decisions. Significant advances have been made in the quired number of progenitor cells for correct tissue and organ last decade and have revealed multi-directional interactions formation. This must be accompanied or closely followed by cell between the molecular machinery regulating the processes of differentiation, in order to generate the range of functional neu- cell proliferation and neuronal differentiation. Here, we first rons and glial cells at the correct time and place. -
Neurod1 Regulates Survival and Migration of Neuroendocrine Lung Carcinomas Via Signaling Molecules Trkb and NCAM
NeuroD1 regulates survival and migration of neuroendocrine lung carcinomas via signaling molecules TrkB and NCAM Jihan K. Osbornea, Jill E. Larsenb, Misty D. Shieldsb, Joshua X. Gonzalesa, David S. Shamesb,1, Mitsuo Satob,2, Ashwinikumar Kulkarnia,3, Ignacio I. Wistubac, Luc Girarda,b, John D. Minnaa,b, and Melanie H. Cobba,4 aDepartment of Pharmacology and bHamon Cancer Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-9041; and cDepartment of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 Contributed by Melanie H. Cobb, March 4, 2013 (sent for review February 8, 2013) Small-cell lung cancer and other aggressive neuroendocrine can- and prostate cancers, and pituitary adenomas (10–16). To charac- cers are often associated with early dissemination and frequent terize the mechanisms of NeuroD1 action in lung tumor patho- metastases. We demonstrate that neurogenic differentiation genesis, we analyzed a panel of lung cell lines. HBEC cell lines, 1 (NeuroD1) is a regulatory hub securing cross talk among survival assigned a number to distinguish lines from different individuals, and migratory-inducing signaling pathways in neuroendocrine are immortalized by overexpression of cyclin-dependent kinase 4, lung carcinomas. We find that NeuroD1 promotes tumor cell and human telomerase reverse transcriptase (e.g., HBEC3KT) (17). survival and metastasis in aggressive neuroendocrine lung tumors The immortalized HBEC3KT cell line was sequentially trans- through regulation of the receptor tyrosine kinase tropomyosin- formed by knockdown of the tumor suppressor p53 and expression related kinase B (TrkB). Like TrkB, the prometastatic signaling of K-RasV12 (HBEC3KTRL53) (Table S1) (18, 19). -
Single Cell Transcriptomics Reveal Temporal Dynamics of Critical Regulators of Germ Cell Fate During Mouse Sex Determination
bioRxiv preprint doi: https://doi.org/10.1101/747279; this version posted November 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Single cell transcriptomics reveal temporal dynamics of critical regulators of germ 2 cell fate during mouse sex determination 3 Authors: Chloé Mayère1,2, Yasmine Neirijnck1,3, Pauline Sararols1, Chris M Rands1, 4 Isabelle Stévant1,2, Françoise Kühne1, Anne-Amandine Chassot3, Marie-Christine 5 Chaboissier3, Emmanouil T. Dermitzakis1,2, Serge Nef1,2,*. 6 Affiliations: 7 1Department of Genetic Medicine and Development, University of Geneva, 1211 Geneva, 8 Switzerland; 9 2iGE3, Institute of Genetics and Genomics of Geneva, University of Geneva, 1211 10 Geneva, Switzerland; 11 3Université Côte d'Azur, CNRS, Inserm, iBV, France; 12 Lead Contact: 13 *Corresponding Author: Serge Nef, 1 rue Michel-Servet CH-1211 Genève 4, 14 [email protected]. + 41 (0)22 379 51 93 15 Running Title: Single cell transcriptomics of germ cells 1 bioRxiv preprint doi: https://doi.org/10.1101/747279; this version posted November 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 16 Abbreviations; 17 AGC: Adrenal Germ Cell 18 GC: Germ cell 19 OGC: Ovarian Germ Cell 20 TGC: Testicular Germ Cell 21 scRNA-seq: Single-cell RNA-Sequencing 22 DEG: Differentially Expressed Gene 23 24 25 Keywords: 26 Single-cell RNA-Sequencing (scRNA-seq), sex determination, ovary, testis, gonocytes, 27 oocytes, prospermatogonia, meiosis, gene regulatory network, germ cells, development, 28 RNA splicing 29 2 bioRxiv preprint doi: https://doi.org/10.1101/747279; this version posted November 2, 2020. -
Olig2 and Ngn2 Function in Opposition to Modulate Gene Expression in Motor Neuron Progenitor Cells
Downloaded from genesdev.cshlp.org on September 29, 2021 - Published by Cold Spring Harbor Laboratory Press Olig2 and Ngn2 function in opposition to modulate gene expression in motor neuron progenitor cells Soo-Kyung Lee,1 Bora Lee,1 Esmeralda C. Ruiz, and Samuel L. Pfaff2 Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA Spinal motor neurons and oligodendrocytes are generated sequentially from a common pool of progenitors termed pMN cells. Olig2 is a bHLH-class transcription factor in pMN cells, but it has remained unclear how its transcriptional activity is modulated to first produce motor neurons and then oligodendrocytes. Previous studies have shown that Olig2 primes pMN cells to become motor neurons by triggering the expression of Ngn2 and Lhx3. Here we show that Olig2 also antagonizes the premature expression of post-mitotic motor neuron genes in pMN cells. This blockade is counteracted by Ngn2, which accumulates heterogeneously in pMN cells, thereby releasing a subset of the progenitors to differentiate and activate expression of post-mitotic motor neuron genes. The antagonistic relationship between Ngn2 and Olig2 is mediated by protein interactions that squelch activity as well as competition for shared DNA-binding sites. Our data support a model in which the Olig2/Ngn2 ratio in progenitor cells serves as a gate for timing proper gene expression during the development of pMN cells: Olig2high maintains the pMN state, thereby holding cells in reserve for oligodendrocyte generation, whereas Ngn2high favors the conversion of pMN cells into post-mitotic motor neurons. [Keywords: Motor neuron; oligodendrocyte; development; basic helix–loop–helix (bHLH); neurogenin (Ngn); Olig] Supplemental material is available at http://www.genesdev.org. -
Role of Bmp4 in Female Reproductive Tract
MECHANISMS OF STRUCTURAL PLASTICITY IN MATURE SENSORY AXONS: ROLE OF BMP4 IN FEMALE REPRODUCTIVE TRACT By Aritra Bhattacherjee Submitted to the graduate degree program in Molecular and Integrative Physiology and the Graduate Faculty of the University of Kansas in partial fulfillment of requirements for the degree of Doctor of Philosophy. ________________________________ Peter G. Smith, Ph.D., Chairman ________________________________ Nancy Berman, Ph.D. ________________________________ Kenneth E. McCarson, Ph.D. ________________________________ Hiroshi Nishimune, Ph.D. ________________________________ Douglas Wright, Ph.D. Date Defended: 03/01/13 The Dissertation Committee for Aritra Bhattacherjee certifies that this is the approved version of the following dissertation: MECHANISMS OF STRUCTURAL PLASTICITY IN MATURE SENSORY AXONS: ROLE OF BMP4 IN FEMALE REPRODUCTIVE TRACT ________________________________ Peter G. Smith, PhD., Chairperson. Date approved: 03/01/13 ii ABSTRACT Structural changes in sensory axons are associated with many peripheral nerve disorders. Degenerative loss or excessive sprouting of axons are hallmarks of sensory neuropathies or hyperinnervating pain syndromes respectively. While much is known about mechanisms of developmental axon growth or regenerative outgrowth following nerve injury, there is little information about mechanisms that can induce plasticity in intact adult axons. Lack of model systems, where extensive plasticity can be predictably induced under physiological conditions, has been a fundamental impediment in studying sensory neuroplasticity mechanisms in adult. The female reproductive tract presents a highly tractable model where sensory axons cyclically undergo extensive plasticity under the influence of estrogen. In rat, high estrogen levels induce reduction in vaginal sensory nerve density, and low estrogen conditions promote sprouting leading to hyperinnervation. We used this model to explore potential factors that can initiate spontaneous plasticity in intact sensory axons. -
Landscape of Transcriptional Deregulation in Lung Cancer Shu Zhang1,2,3,4, Mingfa Li1, Hongbin Ji2,3,4,5* and Zhaoyuan Fang2,3,4,6*
Zhang et al. BMC Genomics (2018) 19:435 https://doi.org/10.1186/s12864-018-4828-1 RESEARCHARTICLE Open Access Landscape of transcriptional deregulation in lung cancer Shu Zhang1,2,3,4, Mingfa Li1, Hongbin Ji2,3,4,5* and Zhaoyuan Fang2,3,4,6* Abstract Background: Lung cancer is a very heterogeneous disease that can be pathologically classified into different subtypes including small-cell lung carcinoma (SCLC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large-cell carcinoma (LCC). Although much progress has been made towards the oncogenic mechanism of each subtype, transcriptional circuits mediating the upstream signaling pathways and downstream functional consequences remain to be systematically studied. Results: Here we trained a one-class support vector machine (OC-SVM) model to establish a general transcription factor (TF) regulatory network containing 325 TFs and 18724 target genes. We then applied this network to lung cancer subtypes and identified those deregulated TFs and downstream targets. We found that the TP63/SOX2/ DMRT3 module was specific to LUSC, corresponding to squamous epithelial differentiation and/or survival. Moreover, the LEF1/MSC module was specifically activated in LUAD and likely to confer epithelial-to-mesenchymal transition, known important for cancer malignant progression and metastasis. The proneural factor, ASCL1, was specifically up-regulated in SCLC which is known to have a neuroendocrine phenotype. Also, ID2 was differentially regulated between SCLC and LUSC, with its up-regulation in SCLC linking to energy supply for fast mitosis and its down-regulation in LUSC linking to the attenuation of immune response. We further described the landscape of TF regulation among the three major subtypes of lung cancer, highlighting their functional commonalities and specificities. -
The E–Id Protein Axis Modulates the Activities of the PI3K–AKT–Mtorc1
Downloaded from genesdev.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press The E–Id protein axis modulates the activities of the PI3K–AKT–mTORC1– Hif1a and c-myc/p19Arf pathways to suppress innate variant TFH cell development, thymocyte expansion, and lymphomagenesis Masaki Miyazaki,1,8 Kazuko Miyazaki,1,8 Shuwen Chen,1 Vivek Chandra,1 Keisuke Wagatsuma,2 Yasutoshi Agata,2 Hans-Reimer Rodewald,3 Rintaro Saito,4 Aaron N. Chang,5 Nissi Varki,6 Hiroshi Kawamoto,7 and Cornelis Murre1 1Department of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA; 2Department of Biochemistry and Molecular Biology, Shiga University of Medical School, Shiga 520-2192, Japan; 3Division of Cellular Immunology, German Cancer Research Center, D-69120 Heidelberg, Germany; 4Department of Medicine, University of California at San Diego, La Jolla, California 92093, USA; 5Center for Computational Biology, Institute for Genomic Medicine, University of California at San Diego, La Jolla, California 92093, USA; 6Department of Pathology, University of California at San Diego, La Jolla, California 92093, USA; 7Department of Immunology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan It is now well established that the E and Id protein axis regulates multiple steps in lymphocyte development. However, it remains unknown how E and Id proteins mechanistically enforce and maintain the naı¨ve T-cell fate. Here we show that Id2 and Id3 suppressed the development and expansion of innate variant follicular helper T (TFH) cells. Innate variant TFH cells required major histocompatibility complex (MHC) class I-like signaling and were associated with germinal center B cells. -
Molecular Mechanisms Regulating Mammalian Forebrain Development
Molecular Mechanisms Regulating Mammalian Forebrain Development By David Chun Cheong Tsui A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy Institute of Medical Science University of Toronto © Copyright by David Chun Cheong Tsui (2013) Title: Molecular Mechanisms Regulating Mammalian Forebrain Development Name: David Chun Cheong Tsui Degree: Doctor of Philosophy, 2013 Department: Institute of Medical Sciences, University of Toronto ABSTRACT While the extrinsic factors regulating neurogenesis in the developing forebrain have been widely studied, the mechanisms downstream of the various signaling pathways are relatively ill-defined. In particular, we focused on proteins that have been implicated in cognitive dysfunction. Here, we ask what role two cell intrinsic factors play in the development of two different neurogenic compartments in the forebrain. In the first part of the thesis, the transcription factor FoxP2, which is mutated in individuals who have specific language deficits, was identified to regulate neurogenesis in the developing cortex, in part by regulating the transition from the radial precursors to the transit amplifying intermediate progenitors. Moreover, we found that ectopic expression of the human homologue of the protein promotes neurogenesis in the murine cortex, thereby acting as a gain-of-function isoform. In the second part of the thesis, the histone acetyltransferase CREB-binding protein (CBP) was identified as regulating the generation of neurons from medial ganglionic eminence precursors, similar to its role in the developing cortex. But CBP also plays a more substantial role in the expression of late interneuron markers, suggesting that it is continuously required for the various stages of neurogenesis at least in the ventral neurogenic niche. -
Investigating the Co-Regulatory Role of Midline and Extramacrochaetae in Regulating Eye Development and Vision in Drosophila Melanogaster
The University of Southern Mississippi The Aquila Digital Community Honors Theses Honors College Spring 5-2014 Investigating the Co-Regulatory Role of Midline and Extramacrochaetae In Regulating Eye Development and Vision in Drosophila melanogaster Lillian M. Forstall University of Southern Mississippi Follow this and additional works at: https://aquila.usm.edu/honors_theses Part of the Developmental Biology Commons Recommended Citation Forstall, Lillian M., "Investigating the Co-Regulatory Role of Midline and Extramacrochaetae In Regulating Eye Development and Vision in Drosophila melanogaster" (2014). Honors Theses. 236. https://aquila.usm.edu/honors_theses/236 This Honors College Thesis is brought to you for free and open access by the Honors College at The Aquila Digital Community. It has been accepted for inclusion in Honors Theses by an authorized administrator of The Aquila Digital Community. For more information, please contact [email protected]. The University of Southern Mississippi Investigating the Co-Regulatory Role of midline and extramacrochaetae In Regulating Eye Development and Vision in Drosophila melanogaster by Lillian Forstall A Thesis Submitted to the Honors College of The University of Southern Mississippi in Partial Fulfillment of the Requirements for the Degree of Bachelor of Science in the Department of Biological Sciences May 2014 ii Approved by _________________________________ Dr. Sandra Leal, Ph.D., Thesis Adviser Assistant Professor of Biology _________________________________ Dr. Shiao Wang, Ph.D., Interim Chair Department of Biological Sciences _________________________________ Dr. David R. Davies, Ph.D., Dean Honors College iii Abstract The Honors thesis research focused on the roles of extramacrochaetae and midline in regulating eye development and the vision of Drosophila melanogaster. -
Regulation of the Drosophila ID Protein Extra Macrochaetae by Proneural Dimerization Partners Ke Li1†, Nicholas E Baker1,2,3*
RESEARCH ARTICLE Regulation of the Drosophila ID protein Extra macrochaetae by proneural dimerization partners Ke Li1†, Nicholas E Baker1,2,3* 1Department of Genetics, Albert Einstein College of Medicine, Bronx, United States; 2Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, United States; 3Department of Ophthalmology and Visual Sciences, Albert Einstein College of Medicine, Bronx, United States Abstract Proneural bHLH proteins are transcriptional regulators of neural fate specification. Extra macrochaetae (Emc) forms inactive heterodimers with both proneural bHLH proteins and their bHLH partners (represented in Drosophila by Daughterless). It is generally thought that varying levels of Emc define a prepattern that determines where proneural bHLH genes can be effective. We report that instead it is the bHLH proteins that determine the pattern of Emc levels. Daughterless level sets Emc protein levels in most cells, apparently by stabilizing Emc in heterodimers. Emc is destabilized in proneural regions by local competition for heterodimer formation by proneural bHLH proteins including Atonal or AS-C proteins. Reflecting this post- translational control through protein stability, uniform emc transcription is sufficient for almost normal patterns of neurogenesis. Protein stability regulated by exchanges between bHLH protein *For correspondence: dimers could be a feature of bHLH-mediated developmental events. [email protected] DOI: https://doi.org/10.7554/eLife.33967.001 Present address: †Howard Hughes Medical Institute, Department of Physiology, University of California, San Introduction Francisco, San Francisco, United Proneural bHLH genes play a fundamental role in neurogenesis. Genes from Drosophila such as States atonal (ato) and genes of the Achaete-Scute gene complex (AS-C) define the proneural regions that Competing interests: The have the potential for neural fate (Baker and Brown, 2018; Bertrand et al., 2002; Go´mez- authors declare that no Skarmeta et al., 2003). -
Cell Proliferation Control by Notch Signalling During Imaginal Discs
Published online: 2021-05-10 Manuscript submitted to: Volume 2, Issue 1, 70-96. AIMS Genetics DOI: 10.3934/genet.2015.1.70 Received date 13 November 2014, Accepted date 25 January 2015, Published date 5 February 2015 Review Cell proliferation control by Notch signalling during imaginal discs development in Drosophila Carlos Estella 1 and Antonio Baonza 2, * 1 Departamento de Biología Molecular and Centro de Biología Molecular SeveroOchoa, Universidad Autónoma de Madrid (UAM), Madrid, Spain 2 Centro de Biología Molecular Severo Ochoa (CSIC/UAM) c/Nicolás Cabrera 1, 28049, Madrid, Spain * Correspondence: Email: [email protected]; Tel: 0034 914974129; Fax: 0034 914978632. Abstract: The Notch signalling pathway is evolutionary conserved and participates in numerous developmental processes, including the control of cell proliferation. However, Notch signalling can promote or restrain cell division depending on the developmental context, as has been observed in human cancer where Notch can function as a tumor suppressor or an oncogene. Thus, the outcome of Notch signalling can be influenced by the cross-talk between Notch and other signalling pathways. The use of model organisms such as Drosophila has been proven to be very valuable to understand the developmental role of the Notch pathway in different tissues and its relationship with other signalling pathways during cell proliferation control. Here we review recent studies in Drosophila that shed light in the developmental control of cell proliferation by the Notch pathway in different contexts such as the eye, wing and leg imaginal discs. We also discuss the autonomous and non-autonomous effects of the Notch pathway on cell proliferation and its interactions with different signalling pathways.