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      An Obligatory Role of Mind Bomb-1 in Notch Signaling of Mammalian Development

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          Abstract

          Background

          The Notch signaling pathway is an evolutionarily conserved intercellular signaling module essential for cell fate specification that requires endocytosis of Notch ligands. Structurally distinct E3 ubiquitin ligases, Neuralized (Neur) and Mind bomb (Mib), cooperatively regulate the endocytosis of Notch ligands in Drosophila. However, the respective roles of the mammalian E3 ubiquitin ligases, Neur1, Neur2, Mib1, and Mib2, in mammalian development are poorly understood.

          Methodology/Principal Findings

          Through extensive use of mammalian genetics, here we show that Neur1 and Neur2 double mutants and Mib2 −/− mice were viable and grossly normal. In contrast, conditional inactivation of Mib1 in various tissues revealed the representative Notch phenotypes: defects of arterial specification as deltalike4 mutants, abnormal cerebellum and skin development as jagged1 conditional mutants, and syndactylism as jagged2 mutants.

          Conclusions/Significance

          Our data provide the first evidence that Mib1 is essential for Jagged as well as Deltalike ligand-mediated Notch signaling in mammalian development, while Neur1, Neur2, and Mib2 are dispensable.

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          Notch signaling: control of cell communication and cell fate.

          Eric Lai (2004)
          Notch is a transmembrane receptor that mediates local cell-cell communication and coordinates a signaling cascade present in all animal species studied to date. Notch signaling is used widely to determine cell fates and to regulate pattern formation; its dysfunction results in a tremendous variety of developmental defects and adult pathologies. This primer describes the mechanism of Notch signal transduction and how it is used to control the formation of biological patterns.
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            hGFAP-cre transgenic mice for manipulation of glial and neuronal function in vivo.

            L. Zhuo, M Theis, I Alvarez-Maya … (2001)
            With the goal of performing astrocyte-specific modification of genes in the mouse, we have generated a transgenic line expressing Cre recombinase under the control of the human glial fibrillary acidic protein (hGFAP) promoter. Activity was monitored by crossing the hGFAP-cre transgenics with either of two reporter lines carrying a lacZ gene whose expression requires excision of loxP-flanked stop sequences. We found that lacZ expression was primarily limited to the central nervous system, but therein was widespread in neurons and ependyma. Cell types within the brain that notably failed to activate lacZ expression included Purkinje neurons of the cerebellum and choroid plexus epithelium. Onset of Cre expression began in the forebrain by e13.5, suggesting that the hGFAP promoter is active in a multi-potential neural stem cell. Copyright 2001 Wiley-Liss, Inc.
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              Mind bomb is a ubiquitin ligase that is essential for efficient activation of Notch signaling by Delta.

              Kevin Lorick, Cheol Kim, Gregory Palardy … (2002)
              Lateral inhibition, mediated by Notch signaling, leads to the selection of cells that are permitted to become neurons within domains defined by proneural gene expression. Reduced lateral inhibition in zebrafish mib mutant embryos permits too many neural progenitors to differentiate as neurons. Positional cloning of mib revealed that it is a gene in the Notch pathway that encodes a RING ubiquitin ligase. Mib interacts with the intracellular domain of Delta to promote its ubiquitylation and internalization. Cell transplantation studies suggest that mib function is essential in the signaling cell for efficient activation of Notch in neighboring cells. These observations support a model for Notch activation where the Delta-Notch interaction is followed by endocytosis of Delta and transendocytosis of the Notch extracellular domain by the signaling cell. This facilitates intramembranous cleavage of the remaining Notch receptor, release of the Notch intracellular fragment, and activation of target genes in neighboring cells.
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                Author and article information

                Contributors
                : Role: Academic Editor
                Journal
                Journal ID (nlm-ta): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2007
                Publication date (Electronic): 28 November 2007
                Volume: 2
                Issue: 11
                Electronic Location Identifier: e1221
                Affiliations
                [1 ]Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, Kyungbuk, South Korea
                [2 ]Department of Biology, Chungnam National University, Daejeon, South Korea
                [3 ]Howard Hughes Medical Institute, Department of Physiology, University of California at San Francisco, San Francisco, California, United States of America
                [4 ]Howard Hughes Medical Institute, Department of Biochemistry, University of California at San Francisco, San Francisco, California, United States of America
                Ecole Normale Superieure, France
                Author notes
                * To whom correspondence should be addressed. E-mail: ykong@ 123456postech.ac.kr

                Conceived and designed the experiments: YJ YK BK MY KY CK PS. Performed the experiments: BK MY KY SI YK. Analyzed the data: YK BK MY KY SI YK. Contributed reagents/materials/analysis tools: YJ. Wrote the paper: YK BK MY KY SI YK.

                Article
                Publisher ID: 07-PONE-RA-02030R1
                DOI: 10.1371/journal.pone.0001221
                PMC ID: 2082076
                PubMed ID: 18043734
                SO-VID: 2ec479bb-9a85-4940-8b56-28627927d713
                Copyright © Koo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Date received : 20 August 2007
                Date accepted : 31 October 2007
                Page count
                Pages: 12
                Categories
                Subject: Research Article
                Subject: Developmental Biology/Developmental Molecular Mechanisms
                Subject: Developmental Biology/Molecular Development
                Subject: Evolutionary Biology/Developmental Molecular Mechanisms
                Subject: Genetics and Genomics/Animal Genetics
                Subject: Genetics and Genomics/Gene Function

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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