Genesis and Migration 3
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Role of Notch Signaling in Establishing the Hemilineages of Secondary Neurons in Drosophila Melanogaster James W
RESEARCH ARTICLE 53 Development 137, 53-61 (2010) doi:10.1242/dev.041749 Role of Notch signaling in establishing the hemilineages of secondary neurons in Drosophila melanogaster James W. Truman*,§, Wanda Moats, Janet Altman*, Elizabeth C. Marin† and Darren W. Williams‡ SUMMARY The secondary neurons generated in the thoracic central nervous system of Drosophila arise from a hemisegmental set of 25 neuronal stem cells, the neuroblasts (NBs). Each NB undergoes repeated asymmetric divisions to produce a series of smaller ganglion mother cells (GMCs), which typically divide once to form two daughter neurons. We find that the two daughters of the GMC consistently have distinct fates. Using both loss-of-function and gain-of-function approaches, we examined the role of Notch signaling in establishing neuronal fates within all of the thoracic secondary lineages. In all cases, the ‘A’ (NotchON) sibling assumes one fate and the ‘B’ (NotchOFF) sibling assumes another, and this relationship holds throughout the neurogenic period, resulting in two major neuronal classes: the A and B hemilineages. Apparent monotypic lineages typically result from the death of one sibling throughout the lineage, resulting in a single, surviving hemilineage. Projection neurons are predominantly from the B hemilineages, whereas local interneurons are typically from A hemilineages. Although sibling fate is dependent on Notch signaling, it is not necessarily dependent on numb, a gene classically involved in biasing Notch activation. When Numb was removed at the start of larval neurogenesis, both A and B hemilineages were still generated, but by the start of the third larval instar, the removal of Numb resulted in all neurons assuming the A fate. -
Drosophila Mef2 Is Essential for Normal Mushroom Body and Wing Development
bioRxiv preprint doi: https://doi.org/10.1101/311845; this version posted April 30, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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. Drosophila mef2 is essential for normal mushroom body and wing development Jill R. Crittenden1, Efthimios M. C. Skoulakis2, Elliott. S. Goldstein3, and Ronald L. Davis4 1McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA 2Division of Neuroscience, Biomedical Sciences Research Centre "Alexander Fleming", Vari, 16672, Greece 3 School of Life Science, Arizona State University, Tempe, AZ, 85287, USA 4Department of Neuroscience, The Scripps Research Institute Florida, Jupiter, FL 33458, USA Key words: MEF2, mushroom bodies, brain, muscle, wing, vein, Drosophila 1 bioRxiv preprint doi: https://doi.org/10.1101/311845; this version posted April 30, 2018. 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. ABSTRACT MEF2 (myocyte enhancer factor 2) transcription factors are found in the brain and muscle of insects and vertebrates and are essential for the differentiation of multiple cell types. We show that in the fruitfly Drosophila, MEF2 is essential for normal development of wing veins, and for mushroom body formation in the brain. In embryos mutant for D-mef2, there was a striking reduction in the number of mushroom body neurons and their axon bundles were not detectable. -
Neuronal Diversification in the Postembryonic Drosophila Brain: A
University of Massachusetts Medical School eScholarship@UMMS GSBS Dissertations and Theses Graduate School of Biomedical Sciences 2011-08-31 Neuronal Diversification in the ostembrP yonic Drosophila Brain: A Dissertation Suewei Lin University of Massachusetts Medical School Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/gsbs_diss Part of the Animal Experimentation and Research Commons, Cells Commons, Nervous System Commons, and the Neuroscience and Neurobiology Commons Repository Citation Lin S. (2011). Neuronal Diversification in the ostembrP yonic Drosophila Brain: A Dissertation. GSBS Dissertations and Theses. https://doi.org/10.13028/eh7z-7w05. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/565 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in GSBS Dissertations and Theses by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. NEURONAL DIVERSIFICATION IN THE POSTEMBRYONIC DROSOPHILA BRAIN A Dissertation Presented By Suewei Lin Submitted to the Faculty of the University of Massachusetts Graduate School of Biomedical Sciences, Worcester in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY August 31, 2011 iii Dedications To my parents for their patience and support & To my wife, for her selfless love that carries me through all the ups and downs in the five years of my PhD life. iv Acknowledgements I would like to thank Tzumin Lee for his guidance and support, and all my TRAC committee members for valuable suggestions. Thanks to Sen-Lin Lai and Hung- Hsiang Yu for their contributions on the study of “Lineage-specific effects of Notch/Numb signaling in postembryonic development of the antennal lobe lineages (Chapter IV)”. -
Control of Neuronal Cell Fate and Number by Integration of Distinct Daughter Cell Proliferation Modes with Temporal Progression
Control of neuronal cell fate and number by integration of distinct daughter cell proliferation modes with temporal progression Carina Ulvklo, Ryan MacDonald, Caroline Bivik, Magnus Baumgardt, Daniel Karlsson and Stefan Thor Linköping University Post Print N.B.: When citing this work, cite the original article. Original Publication: Carina Ulvklo, Ryan MacDonald, Caroline Bivik, Magnus Baumgardt, Daniel Karlsson and Stefan Thor, Control of neuronal cell fate and number by integration of distinct daughter cell proliferation modes with temporal progression, 2012, Development, (139), 4, 678-689. http://dx.doi.org/10.1242/dev.074500 Copyright: Company of Biologists http://www.biologists.com/ Postprint available at: Linköping University Electronic Press http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-74790 678 RESEARCH ARTICLE DEVELOPMENT AND STEM CELLS Development 139, 678-689 (2012) doi:10.1242/dev.074500 © 2012. Published by The Company of Biologists Ltd Control of neuronal cell fate and number by integration of distinct daughter cell proliferation modes with temporal progression Carina Ulvklo, Ryan MacDonald, Caroline Bivik, Magnus Baumgardt, Daniel Karlsson and Stefan Thor* SUMMARY During neural lineage progression, differences in daughter cell proliferation can generate different lineage topologies. This is apparent in the Drosophila neuroblast 5-6 lineage (NB5-6T), which undergoes a daughter cell proliferation switch from generating daughter cells that divide once to generating neurons directly. Simultaneously, neural lineages, e.g. NB5-6T, undergo temporal changes in competence, as evidenced by the generation of different neural subtypes at distinct time points. When daughter proliferation is altered against a backdrop of temporal competence changes, it may create an integrative mechanism for simultaneously controlling cell fate and number. -
Neural Stem Cells: Balancing Self-Renewal with Differentiation Chris Q
Development ePress online publication date 20 March 2008 REVIEW 1575 Development 135, 1575-1587 (2008) doi:10.1242/dev.014977 Neural stem cells: balancing self-renewal with differentiation Chris Q. Doe Stem cells are captivating because they have the potential to of proneural gene expression. High levels of the proneural genes make multiple cell types yet maintain their undifferentiated achaete, scute or lethal of scute repress Notch activity and state. Recent studies of Drosophila and mammalian neural stem promote NB formation; low levels of proneural gene expression cells have shed light on how stem cells regulate self-renewal allow high Notch activity, which maintains neuroectodermal fate versus differentiation and have revealed the proteins, processes and ultimately leads to epidermal differentiation (Artavanis- and pathways that all converge to regulate neural progenitor Tsakonas et al., 1991). Thus, proneural genes promote self-renewal. If we can better understand how stem cells neurogenesis (i.e. NB formation), whereas Notch signaling balance self-renewal versus differentiation, we will significantly inhibits neurogenesis. In this review, I briefly discuss embryonic advance our knowledge of embryogenesis, cancer biology and NBs and focus instead on the central brain NBs, where most is brain evolution, as well as the use of stem cells for therapeutic known about the mechanisms that regulate self-renewal. purposes. Larval NBs, which have many attributes of self-renewing stem cells, lie in a specialized cellular niche; they are undifferentiated, do Introduction not express any known neuron- or glial-specific markers; are highly A defining feature of stem cells is their ability to continuously proliferative yet never form tumors; can undergo mitotic quiescence maintain a stem cell population (self-renew) while generating without differentiating; and, most importantly, can generate differentiated progeny. -
Linking Neuronal Lineage and Wiring Specificity Hongjie Li1†, S
Li et al. Neural Development (2018) 13:5 https://doi.org/10.1186/s13064-018-0102-0 REVIEW Open Access Linking neuronal lineage and wiring specificity Hongjie Li1†, S. Andrew Shuster1,2†, Jiefu Li1† and Liqun Luo1* Abstract Brain function requires precise neural circuit assembly during development. Establishing a functional circuit involves multiple coordinated steps ranging from neural cell fate specification to proper matching between pre- and post- synaptic partners. How neuronal lineage and birth timing influence wiring specificity remains an open question. Recent findings suggest that the relationships between lineage, birth timing, and wiring specificity vary in different neuronal circuits. In this review, we summarize our current understanding of the cellular, molecular, and developmental mechanisms linking neuronal lineage and birth timing to wiring specificity in a few specific systems in Drosophila and mice, and review different methods employed to explore these mechanisms. Introduction immature neurons, is tightly controlled. In some neur- Multiple developmental processes, including cellular onal systems, different neuronal subtypes are sequen- specification, axon and dendrite targeting, and synaptic tially generated from one progenitor or a pool of partner matching, must be tightly coordinated to ensure common progenitors, and birth order or birth timing precise neural circuit assembly. Accordingly, many can predict their cell fates and wiring patterns; we studies have focused on exploring the developmental classify such lineage-related processes, which specify mechanisms underlying wiring specificity, revealing, over neuronal cell fate and wiring, as intrinsic mechanisms. the past several decades, numerous molecular and cellu- In other neuronal systems, cell fate and consequent lar mechanisms that regulate neural cell fate specifica- wiring patterns have been demonstrated to independent tion, axon guidance, and dendrite morphogenesis [1–3]. -
Pdm and Castor Specify Late-Born Motor Neuron Identity in the NB7-1 Lineage
Downloaded from genesdev.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Pdm and Castor specify late-born motor neuron identity in the NB7-1 lineage Ruth Grosskortenhaus, Kristin J. Robinson, and Chris Q. Doe1 Institute of Neuroscience, Institute of Molecular Biology, Howard Hughes Medical Institute, University of Oregon, Eugene, Oregon 97403, USA Embryonic development requires generating cell types at the right place (spatial patterning) and the right time (temporal patterning). Drosophila neuroblasts undergo stem cell-like divisions to generate an ordered sequence of neuronal progeny, making them an attractive system to study temporal patterning. Embryonic neuroblasts sequentially express Hunchback, Krüppel, Pdm1/Pdm2 (Pdm), and Castor (Cas) transcription factors. Hunchback and Krüppel specify early-born temporal identity, but the role of Pdm and Cas in specifying temporal identity has never been addressed. Here we show that Pdm and Cas regulate late-born motor neuron identity within the NB7-1 lineage: Pdm specifies fourth-born U4 motor neuron identity, while Pdm/Cas together specify fifth-born U5 motor neuron identity. We conclude that Pdm and Cas specify late-born neuronal identity; that Pdm and Cas act combinatorially to specify a temporal identity distinct from either protein alone, and that Cas repression of pdm expression regulates the generation of neuronal diversity. [Keywords: Drosophila; birth order; neuroblast; temporal; timing] Supplemental material is available at http://www.genesdev.org. Received April 28, 2006; revised version accepted July 31, 2006. In the mammalian CNS, individual neural progenitors essary and sufficient to repress early-born layer 1 neuro- give rise to an ordered series of cell types in the cerebral nal identity (Hanashima et al. -
Neural Diversity in the Drosophila Olfactory Circuitry: a Dissertation
University of Massachusetts Medical School eScholarship@UMMS GSBS Dissertations and Theses Graduate School of Biomedical Sciences 2007-07-31 Neural Diversity in the Drosophila Olfactory Circuitry: A Dissertation Sen-Lin Lai University of Massachusetts Medical School Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/gsbs_diss Part of the Animal Experimentation and Research Commons, Cells Commons, and the Nervous System Commons Repository Citation Lai S. (2007). Neural Diversity in the Drosophila Olfactory Circuitry: A Dissertation. GSBS Dissertations and Theses. https://doi.org/10.13028/0tc8-tg27. Retrieved from https://escholarship.umassmed.edu/ gsbs_diss/340 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in GSBS Dissertations and Theses by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. A Dissertation Presented By Sen-Lin Lai Submitted to the Faculty of the University of Massachusetts Graduate School of Biomedical Sciences, Worcester in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY July 31st, 2007 ii NEURAL DIVERSITY IN THE DROSOPHILA OLFACTORY CIRCUITRY A Dissertation Presented By Sen-Lin Lai Approval as to style and content by: Tzumin Lee, M.D., Ph.D., Thesis Advisor Marc. R. Freeman Ph.D., Chair of Committee Vivian Budnik, Ph.D., Member of Committee Paul Garrity, Ph.D., Member of Committee Gregory Pazour, Ph.D., Member of Committee Scott Waddell, Ph.D., Member of Committee Anthony Carruthers, Ph.D., Dean of the Graduate School of Biomedical Sciences Program in Neuroscience July 31st, 2007 iii Dedications To my mom and sisters for their support along the way. -
Comparative Single-Cell Transcriptomics of Complete Insect Nervous Systems
bioRxiv preprint doi: https://doi.org/10.1101/785931; this version posted September 30, 2019. 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. Comparative single-cell transcriptomics of complete insect nervous systems B.T. Cocanougher1,2†, J.D. Wittenbach1†, X. Long1†, A.B. Kohn3, T.P. Norekian3,4,5, J. Yan1, J. Colonell1, J.-B. Masson7, J.W. Truman1, A. Cardona1,6, S. Turaga1, R.H. Singer1,8‡, L.L. Moroz3,4‡*, M. Zlatic1,2‡* Affiliations: 1Howard Hughes Medical Institute Janelia Research Campus, Ashburn, Virginia, USA. 2Department of Zoology, Cambridge University, Cambridge, UK. 3Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, Florida, USA. 4Friday Harbor Laboratories, University of Washington, Friday Harbor, Washington, USA 5Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia 6Department of Physiology, Development, and Neuroscience, Cambridge University, Cambridge, UK. 7Decision and Bayesian Computation, CNRS UMR 3571, Neuroscience and Computational Biology Department, Institut Pasteur, Paris, France 8Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, USA †These authors contributed equally to this work. ‡These authors contributed equally to this work. *Corresponding author. Email: [email protected] (L.L.M.); [email protected] (M.Z.) 1 bioRxiv preprint doi: https://doi.org/10.1101/785931; this version posted September 30, 2019. 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. -
Gliogenesis Depends on Glide/Gcm Through Asymmetric Division Of
Developmental Biology 216, 265–275 (1999) Article ID dbio.1999.9511, available online at http://www.idealibrary.com on View metadata, citation and similar papers at core.ac.uk brought to you by CORE Gliogenesis Depends on glide/gcm through provided by Elsevier - Publisher Connector Asymmetric Division of Neuroglioblasts Roberto Bernardoni, Martial Kammerer, Jean-Luc Vonesch, and Angela Giangrande1 Institut de Ge´ne´tique et Biologie Mole´culaire et Cellulaire, IGBMC/CNRS/INSERM/ULP, BP 163, 67404 Illkirch, c.u. de Strasbourg, France Some neurons and glial cells originate from neuroblasts and glioblasts, stem cells that delaminate from the ectoderm of developing fly embryos. A second class of glial cells and neurons differentiates from multipotent precursors, the neuroglioblasts. The differentiation of both glial cell types depends on glial cell deficient/glial cell missing (glide/gcm). Although it has been shown that this transcription factor promotes gliogenesis at the expense of neurogenesis, the cellular mechanisms underlying this fate choice are poorly understood. Using loss and gain of function glide/gcm mutations here we show that the cell fate choice takes place in the neuroglioblast, which divides and produces a glioblast and a neuroblast. Such choice requires the asymmetric distribution of glide/gcm RNA, which accumulates preferentially on one side of the neuroglioblast and is inherited by one cell, the presumptive glioblast. Interestingly, glial cells can differentiate from cells that delaminate as neuroglioblasts or they can arise from cells that start expressing glide/gcm several hours after delamination of a neuroblast. Altogether, these findings identify a novel type of asymmetric cell division and disclose the lineage relationships between glia and neurons. -
Suppression of Adult Neurogenesis Impairs Olfactory Learning and Memory in an Adult Insect
The Journal of Neuroscience, October 15, 2003 • 23(28):9289–9296 • 9289 Behavioral/Systems/Cognitive Suppression of Adult Neurogenesis Impairs Olfactory Learning and Memory in an Adult Insect Sophie Scotto-Lomassese, Colette Strambi, Alain Strambi, Aı¨cha Aouane, Roger Augier, Genevie`ve Rougon, and Myriam Cayre Laboratoire NMDA, Institut de Biologie du Développement de Marseille, Centre National de la Recherche Scientifique, Unite´ Mixte de Recherche 6156, Campus de Luminy, 13288 Marseille Cedex 9, France Although adult neurogenesis has now been demonstrated in many different species, the functional role of newborn neurons still remains unclear. In the house cricket, a cluster of neuroblasts, located in the main associative center of the insect brain, keeps producing new interneurons throughout the animal’s life. Here we address the functional significance of adult neurogenesis by specific suppression of neuroblast proliferation using ␥ irradiation of the insect’s head and by examining the impact on the insect’s learning ability. Forty gray irradiation performed on the first day of adult life massively suppressed neuroblasts and their progeny without inducing any noticeable side effect. We developed a new operant conditioning paradigm especially designed for crickets: the “escape paradigm.” Using olfactory cues, visual cues, or both, crickets had to choose between two holes, one allowing them to escape and the other leading to a trap. Crickets lacking adult neurogenesis exhibited delayed learning when olfactory cues alone were used. Furthermore, retention 24 hr after condi- tioning was strongly impaired in irradiated crickets. By contrast, when visual cues instead of olfactory ones were provided, performance ofirradiatedinsectswasonlyslightlyaffected;whenbotholfactoryandvisualcueswerepresent,theirperformancewasnotdifferentfrom that of controls. -
The P21-Activated Kinase Mbt Is a Component of the Apical Protein Complex in Central Brain Neuroblasts and Controls Cell Proliferation Juliane Melzer1,*, Karoline F
DEVELOPMENT AND STEM CELLS RESEARCH ARTICLE 1871 Development 140, 1871-1881 (2013) doi:10.1242/dev.088435 © 2013. Published by The Company of Biologists Ltd The p21-activated kinase Mbt is a component of the apical protein complex in central brain neuroblasts and controls cell proliferation Juliane Melzer1,*, Karoline F. Kraft2,*, Rolf Urbach2,‡ and Thomas Raabe1,‡ SUMMARY The final size of the central nervous system is determined by precisely controlled generation, proliferation and death of neural stem cells. We show here that the Drosophila PAK protein Mushroom bodies tiny (Mbt) is expressed in central brain progenitor cells (neuroblasts) and becomes enriched to the apical cortex of neuroblasts in a cell cycle- and Cdc42-dependent manner. Using mushroom body neuroblasts as a model system, we demonstrate that in the absence of Mbt function, neuroblasts and their progeny are correctly specified and are able to generate different neuron subclasses as in the wild type, but are impaired in their proliferation activity throughout development. In general, loss of Mbt function does not interfere with establishment or maintenance of cell polarity, orientation of the mitotic spindle and organization of the actin or tubulin cytoskeleton in central brain neuroblasts. However, we show that mbt mutant neuroblasts are significantly reduced in cell size during different stages of development, which is most pronounced for mushroom body neuroblasts. This phenotype correlates with reduced mitotic activity throughout development. Additionally, postembryonic neuroblasts are lost prematurely owing to apoptosis. Yet, preventing apoptosis did not rescue the loss of neurons seen in the adult mushroom body of mbt mutants. From these results, we conclude that Mbt is part of a regulatory network that is required for neuroblast growth and thereby allows proper proliferation of neuroblasts throughout development.