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Article: Tlx3 Exerts Direct Control in Specifying Excitatory Over Inhibitory Neurons in the Dorsal Spinal Cord.

Monteiro, Filipe A / Miranda, Rafael M / Samina, Marta C / Dias, Ana F / Raposo, Alexandre A S F / Oliveira, Patrícia / Reguenga, Carlos / Castro, Diogo S / Lima, Deolinda

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 642697

Abstract: The spinal cord dorsal horn is a major station for integration and relay of somatosensory information and comprises both excitatory and inhibitory neuronal populations. The homeobox gene Tlx3 acts as a selector gene to control the development of late- ... ...

Abstract	The spinal cord dorsal horn is a major station for integration and relay of somatosensory information and comprises both excitatory and inhibitory neuronal populations. The homeobox gene Tlx3 acts as a selector gene to control the development of late-born excitatory (dILB) neurons by specifying glutamatergic transmitter fate in dorsal spinal cord. However, since Tlx3 direct transcriptional targets remain largely unknown, it remains to be uncovered how Tlx3 functions to promote excitatory cell fate. Here we combined a genomics approach based on chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) and expression profiling, with validation experiments in
Language	English
Publishing date	2021-04-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.642697
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Article ; Online: PAD2-Mediated Citrullination Contributes to Efficient Oligodendrocyte Differentiation and Myelination.

Falcão, Ana Mendanha / Meijer, Mandy / Scaglione, Antonella / Rinwa, Puneet / Agirre, Eneritz / Liang, Jialiang / Larsen, Sara C / Heskol, Abeer / Frawley, Rebecca / Klingener, Michael / Varas-Godoy, Manuel / Raposo, Alexandre A S F / Ernfors, Patrik / Castro, Diogo S / Nielsen, Michael L / Casaccia, Patrizia / Castelo-Branco, Gonçalo

Cell reports

2019 Volume 27, Issue 4, Page(s) 1090–1102.e10

Abstract: Citrullination, the deimination of peptidylarginine residues into peptidylcitrulline, has been implicated in the etiology of several diseases. In multiple sclerosis, citrullination is thought to be a major driver of pathology through hypercitrullination ... ...

Abstract	Citrullination, the deimination of peptidylarginine residues into peptidylcitrulline, has been implicated in the etiology of several diseases. In multiple sclerosis, citrullination is thought to be a major driver of pathology through hypercitrullination and destabilization of myelin. As such, inhibition of citrullination has been suggested as a therapeutic strategy for MS. Here, in contrast, we show that citrullination by peptidylarginine deiminase 2 (PAD2) contributes to normal oligodendrocyte differentiation, myelination, and motor function. We identify several targets for PAD2, including myelin and chromatin-related proteins, implicating PAD2 in epigenomic regulation. Accordingly, we observe that PAD2 inhibition and its knockdown affect chromatin accessibility and prevent the upregulation of oligodendrocyte differentiation genes. Moreover, mice lacking PAD2 display motor dysfunction and a decreased number of myelinated axons in the corpus callosum. We conclude that citrullination contributes to proper oligodendrocyte lineage progression and myelination.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Lineage ; Cell Nucleus/metabolism ; Citrullination ; Cytoplasm/metabolism ; Gene Expression Profiling ; Mice ; Myelin Sheath/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/metabolism ; Protein Interaction Maps ; Protein-Arginine Deiminase Type 2/analysis ; Protein-Arginine Deiminase Type 2/metabolism ; Protein-Arginine Deiminase Type 2/physiology
Chemical Substances	Padi2 protein, mouse (EC 3.5.3.15) ; Protein-Arginine Deiminase Type 2 (EC 3.5.3.15)
Language	English
Publishing date	2019-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.03.108
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Article ; Online: Monozygotic Twins Concordant for Common Variable Immunodeficiency: Strikingly Similar Clinical and Immune Profile Associated With a Polygenic Burden.

Silva, Susana L / Fonseca, Mariana / Pereira, Marcelo L M / Silva, Sara P / Barbosa, Rita R / Serra-Caetano, Ana / Blanco, Elena / Rosmaninho, Pedro / Pérez-Andrés, Martin / Sousa, Ana Berta / Raposo, Alexandre A S F / Gama-Carvalho, Margarida / Victorino, Rui M M / Hammarstrom, Lennart / Sousa, Ana E

Frontiers in immunology

2019 Volume 10, Page(s) 2503

Abstract: Monozygotic twins provide a unique opportunity to better understand complex genetic diseases and the relative contribution of heritable factors in shaping the immune system throughout life. Common Variable Immunodeficiency Disorders (CVID) are primary ... ...

Abstract	Monozygotic twins provide a unique opportunity to better understand complex genetic diseases and the relative contribution of heritable factors in shaping the immune system throughout life. Common Variable Immunodeficiency Disorders (CVID) are primary antibody defects displaying wide phenotypic and genetic heterogeneity, with monogenic transmission accounting for only a minority of the cases. Here, we report a pair of monozygotic twins concordant for CVID without a family history of primary immunodeficiency. They featured a remarkably similar profile of clinical manifestations and immunological alterations at diagnosis (established at age 37) and along the subsequent 15 years of follow-up. Interestingly, whole-exome sequencing failed to identify a monogenic cause for CVID, but unraveled a combination of heterozygous variants, with a predicted deleterious impact. These variants were found in genes involved in relevant immunological pathways, such as
MeSH term(s)	Adult ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Biomarkers ; Common Variable Immunodeficiency/diagnosis ; Common Variable Immunodeficiency/etiology ; Disease Susceptibility/immunology ; Genetic Predisposition to Disease ; Humans ; Immunophenotyping ; Male ; Multifactorial Inheritance ; Pedigree ; Phenotype ; Polymorphism, Single Nucleotide ; Symptom Assessment ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Twins, Monozygotic ; Whole Exome Sequencing
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-11-22
Publishing country	Switzerland
Document type	Case Reports ; Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.02503
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Article: A multi-resource data integration approach: identification of candidate genes regulating cell proliferation during neocortical development.

Vied, Cynthia M / Freudenberg, Florian / Wang, Yuting / Raposo, Alexandre A S F / Feng, David / Nowakowski, Richard S

Frontiers in neuroscience

2014 Volume 8, Page(s) 257

Abstract: Neurons of the mammalian neocortex are produced by proliferating cells located in the ventricular zone (VZ) lining the lateral ventricles. This is a complex and sequential process, requiring precise control of cell cycle progression, fate commitment and ... ...

Abstract	Neurons of the mammalian neocortex are produced by proliferating cells located in the ventricular zone (VZ) lining the lateral ventricles. This is a complex and sequential process, requiring precise control of cell cycle progression, fate commitment and differentiation. We have analyzed publicly available databases from mouse and human to identify candidate genes that are potentially involved in regulating early neocortical development and neurogenesis. We used a mouse in situ hybridization dataset (The Allen Institute for Brain Science) to identify 13 genes (Cdon, Celsr1, Dbi, E2f5, Eomes, Hmgn2, Neurog2, Notch1, Pcnt, Sox3, Ssrp1, Tead2, Tgif2) with high correlation of expression in the proliferating cells of the VZ of the neocortex at early stages of development (E15.5). We generated a similar human brain network using microarray and RNA-seq data (BrainSpan Atlas) and identified 407 genes with high expression in the developing human VZ and subventricular zone (SVZ) at 8-9 post-conception weeks. Seven of the human genes were also present in the mouse VZ network. The human and mouse networks were extended using available genetic and proteomic datasets through GeneMANIA. A gene ontology search of the mouse and human networks indicated that many of the genes are involved in the cell cycle, DNA replication, mitosis and transcriptional regulation. The reported involvement of Cdon, Celsr1, Dbi, Eomes, Neurog2, Notch1, Pcnt, Sox3, Tead2, and Tgif2 in neural development or diseases resulting from the disruption of neurogenesis validates these candidate genes. Taken together, our knowledge-based discovery method has validated the involvement of many genes already known to be involved in neocortical development and extended the potential number of genes by 100's, many of which are involved in functions related to cell proliferation but others of which are potential candidates for involvement in the regulation of neocortical development.
Language	English
Publishing date	2014-08-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2014.00257
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Article ; Online: MyT1 Counteracts the Neural Progenitor Program to Promote Vertebrate Neurogenesis.

Vasconcelos, Francisca F / Sessa, Alessandro / Laranjeira, Cátia / Raposo, Alexandre A S F / Teixeira, Vera / Hagey, Daniel W / Tomaz, Diogo M / Muhr, Jonas / Broccoli, Vania / Castro, Diogo S

Cell reports

2016 Volume 17, Issue 2, Page(s) 469–483

Abstract: The generation of neurons from neural stem cells requires large-scale changes in gene expression that are controlled to a large extent by proneural transcription factors, such as Ascl1. While recent studies have characterized the differentiation genes ... ...

Abstract	The generation of neurons from neural stem cells requires large-scale changes in gene expression that are controlled to a large extent by proneural transcription factors, such as Ascl1. While recent studies have characterized the differentiation genes activated by proneural factors, less is known on the mechanisms that suppress progenitor cell identity. Here, we show that Ascl1 induces the transcription factor MyT1 while promoting neuronal differentiation. We combined functional studies of MyT1 during neurogenesis with the characterization of its transcriptional program. MyT1 binding is associated with repression of gene transcription in neural progenitor cells. It promotes neuronal differentiation by counteracting the inhibitory activity of Notch signaling at multiple levels, targeting the Notch1 receptor and many of its downstream targets. These include regulators of the neural progenitor program, such as Hes1, Sox2, Id3, and Olig1. Thus, Ascl1 suppresses Notch signaling cell-autonomously via MyT1, coupling neuronal differentiation with repression of the progenitor fate.
Language	English
Publishing date	2016-10-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2016.09.024
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Article ; Online: What are the roles of microRNAs at the mammalian synapse?

Konecna, Anetta / Heraud, Jacki E / Schoderboeck, Lucia / Raposo, Alexandre A S F / Kiebler, Michael A

Neuroscience letters

2009 Volume 466, Issue 2, Page(s) 63–68

Abstract: The modification of neuronal connections in response to stimuli is believed to be the basis of long-term memory formation. It is currently accepted that local protein synthesis critically contributes to site-restricted modulation of individual synapses. ... ...

Abstract	The modification of neuronal connections in response to stimuli is believed to be the basis of long-term memory formation. It is currently accepted that local protein synthesis critically contributes to site-restricted modulation of individual synapses. Here, we summarize recent evidence implicating miRNAs in this process, leading to altered dendrite morphogenesis and synaptic plasticity. Second, we discuss findings in non-neuronal systems about how RNA-binding proteins can modulate miRNA-mRNA interactions, and how these mechanisms might apply to neurons. Finally, we review recent findings that P-bodies may be important sites for miRNA action at the synapse.
MeSH term(s)	Animals ; Dendrites/metabolism ; Humans ; Mammals/anatomy & histology ; Mammals/physiology ; MicroRNAs/physiology ; Models, Biological ; Neurons/cytology ; Neurons/physiology ; Synapses/physiology ; Synaptic Transmission/physiology
Chemical Substances	MicroRNAs
Language	English
Publishing date	2009-12-04
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2009.06.050
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Zs.A 1166: Show issues

Location:
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Jg. 1995 - 2021: Lesesall (1.OG)
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Article: From stem cell to embryo without centrioles.

Stevens, Naomi R / Raposo, Alexandre A S F / Basto, Renata / St Johnston, Daniel / Raff, Jordan W

Current biology : CB

2007 Volume 17, Issue 17, Page(s) 1498–1503

Abstract: Centrosome asymmetry plays a key role in ensuring the asymmetric division of Drosophila neural stem cells (neuroblasts [NBs]) and male germline stem cells (GSCs) [1-3]. In both cases, one centrosome is anchored close to a specific cortical region during ... ...

Abstract	Centrosome asymmetry plays a key role in ensuring the asymmetric division of Drosophila neural stem cells (neuroblasts [NBs]) and male germline stem cells (GSCs) [1-3]. In both cases, one centrosome is anchored close to a specific cortical region during interphase, thus defining the orientation of the spindle during the ensuing mitosis. To test whether asymmetric centrosome behavior is a general feature of stem cells, we have studied female GSCs, which divide asymmetrically, producing another GSC and a cystoblast. The cystoblast then divides and matures into an oocyte, a process in which centrosomes exhibit a series of complex behaviors proposed to play a crucial role in oogenesis [4-6]. We show that the interphase centrosome does not define spindle orientation in female GSCs and that DSas-4 mutant GSCs [7], lacking centrioles and centrosomes, invariably divide asymmetrically to produce cystoblasts that proceed normally through oogenesis-remarkably, oocyte specification, microtubule organization, and mRNA localization are all unperturbed. Mature oocytes can be fertilized, but embryos that cannot support centriole replication arrest very early in development. Thus, centrosomes are dispensable for oogenesis but essential for early embryogenesis. These results reveal that asymmetric centrosome behavior is not an essential feature of stem cell divisions.
MeSH term(s)	Animals ; Centrioles/physiology ; Drosophila/physiology ; Drosophila Proteins/physiology ; Embryonic Development/physiology ; Female ; Microtubule-Associated Proteins ; Microtubules/physiology ; Oocytes/physiology ; Oogenesis/physiology ; RNA, Messenger/metabolism ; Totipotent Stem Cells/physiology
Chemical Substances	Drosophila Proteins ; Microtubule-Associated Proteins ; RNA, Messenger ; Sas-4 protein, Drosophila
Language	English
Publishing date	2007-08-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2007.07.060
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Zs.A 3208: Show issues

Location:
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Jg. 1995 - 2021: Lesesall (2.OG)
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Article: Capu and Spire assemble a cytoplasmic actin mesh that maintains microtubule organization in the Drosophila oocyte.

Dahlgaard, Katja / Raposo, Alexandre A S F / Niccoli, Teresa / St Johnston, Daniel

Developmental cell

2007 Volume 13, Issue 4, Page(s) 539–553

Abstract: Mutants in the actin nucleators Cappuccino and Spire disrupt the polarized microtubule network in the Drosophila oocyte that defines the anterior-posterior axis, suggesting that microtubule organization depends on actin. Here, we show that Cappuccino and ...

Abstract	Mutants in the actin nucleators Cappuccino and Spire disrupt the polarized microtubule network in the Drosophila oocyte that defines the anterior-posterior axis, suggesting that microtubule organization depends on actin. Here, we show that Cappuccino and Spire organize an isotropic mesh of actin filaments in the oocyte cytoplasm. capu and spire mutants lack this mesh, whereas overexpressed truncated Cappuccino stabilizes the mesh in the presence of Latrunculin A and partially rescues spire mutants. Spire overexpression cannot rescue capu mutants, but prevents actin mesh disassembly at stage 10B and blocks late cytoplasmic streaming. We also show that the actin mesh regulates microtubules indirectly, by inhibiting kinesin-dependent cytoplasmic flows. Thus, the Capu pathway controls alternative states of the oocyte cytoplasm: when active, it assembles an actin mesh that suppresses kinesin motility to maintain a polarized microtubule cytoskeleton. When inactive, unrestrained kinesin movement generates flows that wash microtubules to the cortex.
MeSH term(s)	Actins/physiology ; Animals ; Cytoplasm/physiology ; Cytoplasm/ultrastructure ; Drosophila/metabolism ; Drosophila/ultrastructure ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Female ; Kinesins/metabolism ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Microtubules/physiology ; Mutation ; Oocytes/metabolism ; Oocytes/ultrastructure
Chemical Substances	Actins ; Drosophila Proteins ; Microfilament Proteins ; capu protein, Drosophila ; spir protein, Drosophila ; Kinesins (EC 3.6.4.4)
Language	English
Publishing date	2007-10-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2007.09.003
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Zs.A 5742: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 76: Show issues

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Article ; Online: Ascl1 Coordinately Regulates Gene Expression and the Chromatin Landscape during Neurogenesis.

Raposo, Alexandre A S F / Vasconcelos, Francisca F / Drechsel, Daniela / Marie, Corentine / Johnston, Caroline / Dolle, Dirk / Bithell, Angela / Gillotin, Sébastien / van den Berg, Debbie L C / Ettwiller, Laurence / Flicek, Paul / Crawford, Gregory E / Parras, Carlos M / Berninger, Benedikt / Buckley, Noel J / Guillemot, François / Castro, Diogo S

Cell reports

2015 Volume 10, Issue 9, Page(s) 1544–1556

Abstract: The proneural transcription factor Ascl1 coordinates gene expression in both proliferating and differentiating progenitors along the neuronal lineage. Here, we used a cellular model of neurogenesis to investigate how Ascl1 interacts with the chromatin ... ...

Abstract	The proneural transcription factor Ascl1 coordinates gene expression in both proliferating and differentiating progenitors along the neuronal lineage. Here, we used a cellular model of neurogenesis to investigate how Ascl1 interacts with the chromatin landscape to regulate gene expression when promoting neuronal differentiation. We find that Ascl1 binding occurs mostly at distal enhancers and is associated with activation of gene transcription. Surprisingly, the accessibility of Ascl1 to its binding sites in neural stem/progenitor cells remains largely unchanged throughout their differentiation, as Ascl1 targets regions of both readily accessible and closed chromatin in proliferating cells. Moreover, binding of Ascl1 often precedes an increase in chromatin accessibility and the appearance of new regions of open chromatin, associated with de novo gene expression during differentiation. Our results reveal a function of Ascl1 in promoting chromatin accessibility during neurogenesis, linking the chromatin landscape at Ascl1 target regions with the temporal progression of its transcriptional program.
Language	English
Publishing date	2015-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2015.02.025
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