Evidence map›Paper›PMID 26511239›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Retinoic Acid Receptor β Controls Development of Striatonigral Projection Neurons through FGF-Dependent and Meis1-Dependent Mechanisms.

Monika Rataj-Baniowska, Anna Niewiadomska-Cimicka, Marie Paschaki, Monika Szyszka-Niagolov, Laura Carramolino, Miguel Torres, Pascal Dollé, Wojciech Krężel

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 3 countries.

Monika Rataj-BaniowskaDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and.
Anna Niewiadomska-CimickaDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and.
Marie PaschakiDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and.ORCID http://orcid.org/0000-0002-9490-8997
Monika Szyszka-NiagolovDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and.
Laura CarramolinoCentro Nacional de Investigaciones Cardiovasculares, CNIC, Madrid 28029, Spain.ORCID http://orcid.org/0000-0002-1661-618X
Miguel TorresCentro Nacional de Investigaciones Cardiovasculares, CNIC, Madrid 28029, Spain.
Pascal DolléDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and.
Wojciech KrężelDevelopmental Biology and Stem Cells Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut de la Santé et de la Recherche Médicale, U964, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7104, Fédération de Médecine Translationnelle de Strasbourg, and Université de Strasbourg, 67404 Illkirch, France, and krezel@igbmc.fr.ORCID http://orcid.org/0000-0003-1605-3185
Institut de génétique et de biologie moléculaire et cellulaire · FRSpanish National Centre for Cardiovascular Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian striatum controls sensorimotor and psychoaffective functions through coordinated activities of its two striatonigral and striatopallidal output pathways. Here we show that retinoic acid receptor β (RARβ) controls development of a subpopulation of GABAergic, Gad65-positive striatonigral projection neurons. In Rarb(-/-) knock-out mice, concomitant reduction of Gad65, dopamine receptor D1 (Drd1), and substance P expression at different phases of prenatal development was associated with reduced number of Drd1-positive cells at birth, in contrast to normal numbers of striatopallidal projection neurons expressing dopamine receptor D2. Fate mapping using BrdU pulse-chase experiments revealed that such deficits may originate from compromised proliferation of late-born striosomal neurons and lead to decreased number of Drd1-positive cells retaining BrdU in postnatal day (P) 0 Rarb(-/-) striatum. Reduced expression of Fgf3 in the subventricular zone of the lateral ganglionic eminence (LGE) at embryonic day 13.5 may underlie such deficits by inducing premature differentiation of neuronal progenitors, as illustrated by reduced expression of the proneural gene Ascl1 (Mash1) and increased expression of Meis1, a marker of postmitotic LGE neurons. In agreement with a critical role of FGF3 in this control, reduced number of Ascl1-expressing neural progenitors, and a concomitant increase of Meis1-expressing cells, were observed in primary cell cultures of Rarb(-/-) LGE. This defect was normalized by addition of fibroblast growth factor (FGF). Such data point to role of Meis1 in striatal development, also supported by reduced neuronal differentiation in the LGE of Meis1(-/-) embryos. Our data unveil a novel mechanism of development of striatonigral projection neurons involving retinoic acid and FGF, two signals required for positioning the boundaries of Meis1-expressing cells.

Indexed as

AnimalsAntimetabolitesBromodeoxyuridineCorpus StriatumFemaleFibroblast Growth Factor 3Fibroblast Growth FactorsGlutamate DecarboxylaseHomeodomain ProteinsMiceMice, Inbred C57BLMice, KnockoutMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsNeurogenesisNeuronsAntimetabolitesBromodeoxyuridineFibroblast Growth Factor 3Fibroblast Growth FactorsGlutamate Decarboxylaseglutamate decarboxylase 2Homeodomain ProteinsMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsReceptors, Dopamine D1Receptors, Retinoic Acidretinoic acid receptor betadopamine receptorsFGFMEIS1neurogenesisretinoic acid receptorsstriatum

Identifiers

PMID26511239
PMCPMC6605468
OpenAlexW2413152458

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.