Show simple item record

Changes in Notch signaling coordinates maintenance and differentiation of the Drosophila larval optic lobe neuroepithelia

dc.contributor.authorWeng, Moen_US
dc.contributor.authorHaenfler, Jill M.en_US
dc.contributor.authorLee, Cheng‐yuen_US
dc.date.accessioned2012-11-07T17:04:38Z
dc.date.available2014-01-07T14:51:08Zen_US
dc.date.issued2012-11en_US
dc.identifier.citationWeng, Mo; Haenfler, Jill M.; Lee, Cheng‐yu (2012). "Changes in Notch signaling coordinates maintenance and differentiation of the Drosophila larval optic lobe neuroepithelia." Developmental Neurobiology 72(11): 1376-1390. <http://hdl.handle.net/2027.42/94272>en_US
dc.identifier.issn1932-8451en_US
dc.identifier.issn1932-846Xen_US
dc.identifier.urihttps://hdl.handle.net/2027.42/94272
dc.description.abstractA dynamic balance between stem cell maintenance and differentiation paces generation of post‐mitotic progeny during normal development and maintenance of homeostasis. Recent studies show that Notch plays a key role in regulating the identity of neuroepithelial stem cells, which generate terminally differentiated neurons that populate the adult optic lobe via the intermediate progenitor cell type called neuroblast. Thus, understanding how Notch controls neuroepithelial cell maintenance and neuroblast formation will provide critical insight into the intricate regulation of stem cell function during tissue morphogenesis. Here, we showed that a low level of Notch signaling functions to maintain the neuroepithelial cell identity by suppressing the expression of pointedP1 gene through the transcriptional repressor Anterior open. Increased Notch signaling, which coincides with transient cell cycle arrest but precedes the expression of PointedP1 in cells near the medial edge of neuroepithelia, defines transitioning neuroepithelial cells that are in the process of acquiring the neuroblast identity. Transient up‐regulation of Notch signaling in transitioning neuroepithelial cells decreases their sensitivity to PointedP1 and prevents them from becoming converted into neuroblasts prematurely. Down‐regulation of Notch signaling combined with a high level of PointedP1 trigger a synchronous conversion from transitioning neuroepithelial cells to immature neuroblasts at the medial edge of neuroepithelia. Thus, changes in Notch signaling orchestrate a dynamic balance between maintenance and conversion of neuroepithelial cells during optic lobe neurogenesis. © 2011 Wiley Periodicals, Inc. Develop Neurobiol, 2012en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherPointedP1en_US
dc.subject.otherNeuroepitheliaen_US
dc.subject.otherNeuroblasten_US
dc.subject.otherOptic Lobeen_US
dc.subject.otherNotchen_US
dc.titleChanges in Notch signaling coordinates maintenance and differentiation of the Drosophila larval optic lobe neuroepitheliaen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumProgram in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumDivision of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumCenter for Stem Cell Biology, Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationotherDepartment of Molecular Biology, Howard Hughes Medical Institute, Princeton University, NJ 08544en_US
dc.identifier.pmid22038743en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/94272/1/20995_ftp.pdf
dc.identifier.doi10.1002/dneu.20995en_US
dc.identifier.sourceDevelopmental Neurobiologyen_US
dc.identifier.citedreferenceReddy BVVG, Rauskolb C, Irvine KD. 2010. Influence of Fat‐Hippo and Notch signaling on the proliferation and differentiation of Drosophila optic neuroepithelia. Development 137: 2397 – 2408.en_US
dc.identifier.citedreferenceDaul AL, Komori H, Lee C‐Y. EdU (5‐ethynyl‐2′‐deoxyuridine) labeling of Drosophila mitotic neuroblasts. Cold Spring Harb Protoc 2010:pdb prot5461.en_US
dc.identifier.citedreferencedel Álamo D, Rouault H, Schweisguth F. 2011. Mechanism and significance of cis‐inhibition in Notch signalling. Curr Biol 21: R40 – R47.en_US
dc.identifier.citedreferenceDoroquez DB, Rebay I. 2006. Signal integration during development: mechanisms of EGFR and Notch pathway function and cross‐talk. Crit Rev Biochem Mol Biol 41: 339 – 385.en_US
dc.identifier.citedreferenceEgger B, Boone JQ, Stevens N, Brand AH, Doe C. 2007. Regulation of spindle orientation and neural stem cell fate in the Drosophila optic lobe. Neural Dev 2: 1.en_US
dc.identifier.citedreferenceEgger B, Gold KS, Brand AH. 2010. Notch regulates the switch from symmetric to asymmetric neural stem cell division in the Drosophila optic lobe. Development 137: 2981 – 2987.en_US
dc.identifier.citedreferenceFrancis R, McGrath G, Zhang J, Ruddy DA, Sym M, Apfeld J, Nicoll M, et al. 2002. aph‐1 and pen‐2 are required for Notch pathway signaling, gamma‐secretase cleavage of betaAPP, and presenilin protein accumulation. Dev Cell 3: 85 – 97.en_US
dc.identifier.citedreferenceHsiung F, Moses K. 2002. Retinal development in Drosophila: Specifying the first neuron. Hum Mol Genet 2002; 11: 1207 – 1214.en_US
dc.identifier.citedreferenceIzergina N, Balmer J, Bello B, Reichert H. 2009. Postembryonic development of transit amplifying neuroblast lineages in the Drosophila brain. Neural Dev 11: 44.en_US
dc.identifier.citedreferenceKolch W. 2005. Coordinating ERK/MAPK signalling through scaffolds and inhibitors. Nat Rev Mol Cell Biol 6: 827 – 837.en_US
dc.identifier.citedreferenceKrejcí A, Bernard F, Housden BE, Collins S, Bray SJ. 2009. Direct response to Notch activation: Signaling crosstalk and incoherent logic. Sci Signal 2: ra1.en_US
dc.identifier.citedreferenceKriegstein A, Alvarez‐Buylla A. 2009. The glial nature of embryonic and adult neural stem cells. Annu Rev Neurosci 32: 149 – 184.en_US
dc.identifier.citedreferenceMiller AC, Lyons EL, Herman TG. 2009. cis‐Inhibition of Notch by endogenous Delta biases the outcome of lateral inhibition. Curr Biol 19: 1378 – 1378.en_US
dc.identifier.citedreferenceNgo KT, Wang J, Junker M, Kriz S, Vo G, Asem B, Olson JM, Banerjee U, Hartenstein V. 2010. Concomitant requirement for Notch and Jak/Stat signaling during neuro‐epithelial differentiation in the Drosophila optic lobe. Dev Biol 346: 284 – 295.en_US
dc.identifier.citedreferenceOkajima T, Irvine KD. 2002. Regulation of notch signaling by o‐linked fucose. Cell 111: 893 – 904.en_US
dc.identifier.citedreferenceOrihara‐Ono M, Toriya M, Nakao K, Okano H. 2011. Downregulation of Notch mediates the seamless transition of individual Drosophila neuroepithelial progenitors into optic medullar neuroblasts during prolonged G1. Dev Biol 351: 163 – 175.en_US
dc.identifier.citedreferencePerkins LA, Larsen I, Perrimon N. 1992. corkscrew encodes a putative protein tyrosine phosphatase that functions to transduce the terminal signal from the receptor tyrosine kinase torso. Cell 70: 225 – 236.en_US
dc.identifier.citedreferenceRohrbaugh M, Ramos E, Nguyen D, Price M, Wen Y, Lai Z‐C. 2002. Notch Activation of yan Expression Is Antagonized by RTK/Pointed Signaling in the Drosophila Eye. Curr Biol 12: 576 – 581.en_US
dc.identifier.citedreferenceSasamura T, Ishikawa HO, Sasaki N, Higashi S, Kanai M, Nakao S, Ayukawa T, et al. 2007. The O‐fucosyltransferase O‐fut1 is an extracellular component that is essential for the constitutive endocytic trafficking of Notch in Drosophila. Development 134: 1347 – 1356.en_US
dc.identifier.citedreferenceSprinzak D, Lakhanpal A, LeBon L, Santat LA, Fontes ME, Anderson GA, Garcia‐Ojalvo J, et al. 2010. Cis‐interactions between Notch and Delta generate mutually exclusive signalling states. Nature 465: 86 – 90.en_US
dc.identifier.citedreferenceTherrien M, Wong AM, Rubin GM. 1998. CNK, a RAF‐binding multidomain protein required for RAS signaling. Cell 95: 343 – 353.en_US
dc.identifier.citedreferenceVan Vactor D, O'Reilly AM, Neel BG. 1996. Genetic analysis of protein tyrosine phosphatases. Curr Opin Genet Dev 8: 112 – 126.en_US
dc.identifier.citedreferenceWang W, Liu W, Wang Y, Zhou L, Tang X, Luo H. 2011. Notch signaling regulates neuroepithelial stem cell maintenance and neuroblast formation in Drosophila optic lobe development. Dev Biol 350: 414 – 428.en_US
dc.identifier.citedreferenceWech I, Bray S, Delidakis C, Preiss A. 1999. Distinct expression patterns of different enhancer of split bHLH genes during embryogenesis of Drosophila melanogaster. Dev Genes Evol 209: 370 – 375.en_US
dc.identifier.citedreferenceYasugi T, Sugie A, Umetsu D, Tabata T. 2010. Coordinated sequential action of EGFR and Notch signaling pathways regulates proneural wave progression in the Drosophila optic lobe. Development 137: 3193 – 3203.en_US
dc.identifier.citedreferenceYogev S, Schejter ED, Shilo BZ. 2010. Polarized secretion of Drosophila EGFR ligand from photoreceptor neurons is controlled by ER localization of the ligand‐processing machinery. PLoS Biol 8.en_US
dc.identifier.citedreferenceZhao B, Li L, Guan K‐L. 2010. Hippo signaling at a glance. J Cell Sci 123: 4001 – 4006.en_US
dc.identifier.citedreferenceBayraktar OA, Boone JQ, Drummond ML, Doe CQ. 2010. Drosophila type II neuroblast lineages keep Prospero levels low to generate large clones that contribute to the adult brain central complex. Neural Dev 5: 26.en_US
dc.identifier.citedreferenceBray SJ. 2006. Notch signalling: A simple pathway becomes complex. Nat Rev Mol Cell Biol 7: 678 – 689.en_US
dc.identifier.citedreferenceChung HM, Struhl G. 2001. Nicastrin is required for Presenilin‐mediated transmembrane cleavage in Drosophila. Nat Cell Biol 3: 1129 – 1132.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.