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1. The molecular logic of Nanog-induced self-renewal in mouse embryonic stem cells

Author

Victor Heurtier, Nick Owens, Inma Gonzalez, Florian Mueller, Caroline Proux, Damien Mornico, Philippe Clerc, Agnes Dubois, and Pablo Navarro

Subjects
Science
Abstract

Transcription factor (TF) networks are essential for the molecular identity of each cell type. Here, the authors show that TF Nanog utilises multiple molecular strategies to enhance embryonic stem cell self-renewal, which include regulation of chromatin accessibility in the presence of LIF or maintenance of H3K27me3 at developmental regulators in its absence.

Published
2019
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2. IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice.

Author

Lyvianne Decourtye, Erik Mire, Maud Clemessy, Victor Heurtier, Tatiana Ledent, Iain C Robinson, Patrice Mollard, Jacques Epelbaum, Michael J Meaney, Sonia Garel, Yves Le Bouc, and Laurent Kappeler

Subjects
Medicine, Science
Abstract

Nutrition during the perinatal period programs body growth. Growth hormone (GH) secretion from the pituitary regulates body growth and is controlled by Growth Hormone Releasing Hormone (GHRH) neurons located in the arcuate nucleus of the hypothalamus. We observed that dietary restriction during the early postnatal period (i.e. lactation) in mice influences postnatal growth by permanently altering the development of the somatotropic axis in the pituitary gland. This alteration may be due to a lack of GHRH signaling during this critical developmental period. Indeed, underfed pups showed decreased insulin-like growth factor I (IGF-I) plasma levels, which are associated with lower innervation of the median eminence by GHRH axons at 10 days of age relative to normally fed pups. IGF-I preferentially stimulated axon elongation of GHRH neurons in in vitro arcuate explant cultures from 7 day-old normally fed pups. This IGF-I stimulating effect was selective since other arcuate neurons visualized concomitantly by neurofilament labeling, or AgRP immunochemistry, did not significantly respond to IGF-I stimulation. Moreover, GHRH neurons in explants from age-matched underfed pups lost the capacity to respond to IGF-I stimulation. Molecular analyses indicated that nutritional restriction was associated with impaired activation of AKT. These results highlight a role for IGF-I in axon elongation that appears to be cell selective and participates in the complex cellular mechanisms that link underfeeding during the early postnatal period with programming of the growth trajectory.

Published
2017
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4. OCT4 activates a Suv39h1-repressive antisense lncRNA to couple histone H3 Lysine 9 methylation to pluripotency

Author

Laure D Bernard, Agnès Dubois, Victor Heurtier, Véronique Fischer, Inma Gonzalez, Almira Chervova, Alexandra Tachtsidi, Noa Gil, Nick Owens, Lawrence E Bates, Sandrine Vandormael-Pournin, José C R Silva, Igor Ulitsky, Michel Cohen-Tannoudji, Pablo Navarro, Epigénomique, Prolifération et Identité Cellulaire - Epigenomics, Proliferation and the Identity of Cells (EPIC), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Collège Doctoral, Sorbonne Université (SU), Weizmann Institute of Science [Rehovot, Israël], University of Edinburgh, Guangzhou International Bio Island [Guangdong, China] (GIBI), L.B. acknowledges the Ecole Normale Supérieure and Sorbonne Université for funding, P.N. and M.C.-T. acknowledge the Labex Revive [Investissement d’Avenir, ANR-10-LABX-73], Institut Pasteur, CNRS. Funding for open access charge: Pasteur core funding., and ANR-10-LABX-0073,REVIVE,Stem Cells in Regenerative Biology and Medicine(2010)

Subjects
Histones/genetics, Repressor Proteins/genetics, Methyltransferases, Methylation, Chromatin, Histones, Repressor Proteins, Histone Code, Methyltransferases/genetics, Mice, Genetics, Animals, RNA, Long Noncoding, RNA, Long Noncoding/genetics, Octamer Transcription Factor-3, [SDV.BDD]Life Sciences [q-bio]/Development Biology, Octamer Transcription Factor-3/metabolism
Abstract

Histone H3 Lysine 9 (H3K9) methylation, a characteristic mark of heterochromatin, is progressively implemented during development to contribute to cell fate restriction as differentiation proceeds. Accordingly, in undifferentiated and pluripotent mouse Embryonic Stem (ES) cells the global levels of H3K9 methylation are rather low and increase only upon differentiation. How global H3K9 methylation levels are coupled with the loss of pluripotency remains largely unknown. Here, we identify SUV39H1, a major H3K9 di- and tri-methylase, as an indirect target of the pluripotency network of Transcription Factors (TFs). We find that pluripotency TFs, principally OCT4, activate the expression of Suv39h1as, an antisense long non-coding RNA to Suv39h1. In turn, Suv39h1as downregulates Suv39h1 transcription in cis via a mechanism involving the modulation of the chromatin status of the locus. The targeted deletion of the Suv39h1as promoter region triggers increased SUV39H1 expression and H3K9me2 and H3K9me3 levels, affecting all heterochromatic regions, particularly peri-centromeric major satellites and retrotransposons. This increase in heterochromatinization efficiency leads to accelerated and more efficient commitment into differentiation. We report, therefore, a simple genetic circuitry coupling the genetic control of pluripotency with the global efficiency of H3K9 methylation associated with a major cell fate restriction, the irreversible loss of pluripotency.

Published
2022

5. The activation of a Suv39h1 -repressive antisense lncRNA by OCT4 couples the control of H3K9 methylation to pluripotency

Author

Agnès Dubois, Sandrine Vandormael-Pournin, Pablo Navarro, Michel Cohen-Tannoudji, Victor Heurtier, Laure Bernard, Nick D.L. Owens, Igor Ulitsky, Noa Gil, Almira Chervova, Alexandra Tachtsidi, Institut Pasteur [Paris] (IP), Epigénomique, Prolifération et Identité Cellulaire - Epigenomics, Proliferation and the Identity of Cells (EPIC), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Collège Doctoral, Sorbonne Université (SU), Weizmann Institute of Science [Rehovot, Israël], Friedrich Miescher Institute for Biomedical Research (FMI), Novartis Research Foundation, University of Exeter, L.B. acknowledges the Ecole Normale Supérieure and Sorbonne Université for funding. P.N. and M.C-T. acknowledge the Labex Revive (Investissement d’Avenir, ANR-10-LABX-73), the Institut Pasteur and the CNRS for funding., ANR-10-LABX-0073,REVIVE,Stem Cells in Regenerative Biology and Medicine(2010), Institut Pasteur [Paris], Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and Collège doctoral [Sorbonne universités]

Subjects
0303 health sciences, Methylation, Biology, Embryonic stem cell, Chromatin, Cell biology, 03 medical and health sciences, Histone H3, 0302 clinical medicine, Transcription (biology), Epigenetics, Transcription factor, Reprogramming, [SDV.BDD]Life Sciences [q-bio]/Development Biology, 030217 neurology & neurosurgery, 030304 developmental biology
Abstract

Histone H3 Lysine 9 (H3K9) methylation, a characteristic mark of heterochromatin, is progressively implemented during development to contribute to cell fate restriction as differentiation proceeds. For instance, in pluripotent mouse Embryonic Stem (ES) cells the global levels of H3K9 methylation are rather low and increase only upon differentiation. Conversely, H3K9 methylation represents an epigenetic barrier for reprogramming somatic cells back to pluripotency. How global H3K9 methylation levels are coupled with the acquisition and loss of pluripotency remains largely unknown. Here, we identify SUV39H1, a major H3K9 di- and tri-methylase, as an indirect target of the pluripotency network of Transcription Factors (TFs). We find that pluripotency TFs, principally OCT4, activate the expression of an uncharacterized antisense long non-coding RNA to Suv39h1, which we name Suv39h1as. In turn, Suv39h1as downregulates Suv39h1 transcription in cis via a mechanism involving the modulation of the chromatin status of the locus. The targeted deletion of the Suv39h1as promoter region triggers increased SUV39H1 expression and H3K9me2 and H3K9me3 levels, leading to accelerated and more efficient commitment into differentiation. We report, therefore, a simple genetic circuitry coupling the global levels of H3K9 methylation to pluripotency in mouse ES cells.

Published
2021

6. The molecular logic of Nanog-induced self-renewal in mouse embryonic stem cells

Author

Philippe Clerc, Agnès Dubois, Victor Heurtier, Nick D.L. Owens, Florian Mueller, Damien Mornico, Pablo Navarro, Caroline Proux, Inma Gonzalez, Epigénétique des Cellules Souches - Epigenetics of Stem Cells, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Imagerie et Modélisation - Imaging and Modeling, Transcriptome et Epigénome (PF2), Institut Pasteur [Paris], Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB, This work was supported by recurrent funding from the Institut Pasteur, the CNRS, and Revive (Investissement d’Avenir, ANR-10-LABX-73). P.N. acknowledges financial support from the Fondation Schlumberger (FRM FSER 2017), the Fondation ARC pour la recherche sur le cancer (ARC NAVARRO CA 14/12/2016), the Agence Nationale de la Recherche (ANR 16 CE12 0004 01 MITMAT), and the Ligue contre le Cancer (LNCC EL2018 NAVARRO). V.H. is supported by the Fondation ARC and Revive. N.O. is supported by Revive., We thank Dr. Pentao Liu and Dr. Di Croce for kindly providing PiggyBack plasmids and Phf19 knock-down vectors, respectively, Dr. Domingos Henrique for fruitful discussions regarding the involvement of Polycomb activity in Nanog function, Carla Mulas for critical reading of the manuscript., ANR-10-LABX-0073,REVIVE,Stem Cells in Regenerative Biology and Medicine(2010), ANR-16-CE12-0004,MitMAT,Mémoire mitotique de l'activité transcriptionnelle dans les cellules ES(2016), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), and Institut Pasteur [Paris] (IP)

Subjects
0301 basic medicine, Homeobox protein NANOG, Science, General Physics and Astronomy, 02 engineering and technology, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Leukemia Inhibitory Factor, Article, General Biochemistry, Genetics and Molecular Biology, Cell Line, Mice, 03 medical and health sciences, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Animals, Gene Regulatory Networks, Cell Self Renewal, Enhancer, lcsh:Science, Transcription factor, reproductive and urinary physiology, Epigenomics, Regulation of gene expression, Otx Transcription Factors, Multidisciplinary, biology, Mouse Embryonic Stem Cells, Nanog Homeobox Protein, General Chemistry, 021001 nanoscience & nanotechnology, Embryonic stem cell, Chromatin, Cell biology, Histone Code, Enhancer Elements, Genetic, 030104 developmental biology, Histone, [SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and Organogenesis, Gene Expression Regulation, embryonic structures, biology.protein, lcsh:Q, 0210 nano-technology
Abstract

Transcription factor networks, together with histone modifications and signalling pathways, underlie the establishment and maintenance of gene regulatory architectures associated with the molecular identity of each cell type. However, how master transcription factors individually impact the epigenomic landscape and orchestrate the behaviour of regulatory networks under different environmental constraints is only partially understood. Here, we show that the transcription factor Nanog deploys multiple distinct mechanisms to enhance embryonic stem cell self-renewal. In the presence of LIF, which fosters self-renewal, Nanog rewires the pluripotency network by promoting chromatin accessibility and binding of other pluripotency factors to thousands of enhancers. In the absence of LIF, Nanog blocks differentiation by sustaining H3K27me3, a repressive histone mark, at developmental regulators. Among those, we show that the repression of Otx2 plays a preponderant role. Our results underscore the versatility of master transcription factors, such as Nanog, to globally influence gene regulation during developmental processes., Transcription factor (TF) networks are essential for the molecular identity of each cell type. Here, the authors show that TF Nanog utilises multiple molecular strategies to enhance embryonic stem cell self-renewal, which include regulation of chromatin accessibility in the presence of LIF or maintenance of H3K27me3 at developmental regulators in its absence.

Published
2019

7. The molecular logic of Nanog-induced self-renewal

Author

Pablo Navarro, Agnès Dubois, Nick D.L. Owens, Inma Gonzalez, Damien Mornico, Victor Heurtier, Philippe Clerc, Caroline Proux, Florian Mueller, Epigénétique des Cellules Souches - Epigenetics of Stem Cells, Centre National de la Recherche Scientifique ( CNRS ) -Institut Pasteur [Paris], Collège doctoral [Sorbonne universités], Imagerie et Modélisation, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Transcriptome et Epigénome ( PF2 ), Institut Pasteur [Paris], Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB, P.N. acknowledges financial support from the Fondation Schlumberger (FRM FSER 2017), theFondation ARC pour la recherche sur le cancer (ARC NAVARRO CA 14/12/2016), the Agence Nationale de la Recherche (ANR 16 CE12 0004 01 MITMAT), and the Ligue contre le Cancer(LNCC EL2018 NAVARRO). V.H is supported by the Fondation ARC and Revive.N.O. is supported by Revive., and ANR-16-CE12-0004,MitMAT,Mémoire mitotique de l'activité transcriptionnelle dans les cellules ES ( 2016 )

Subjects
Homeobox protein NANOG, H3K27me3, Biology, Pluripotency Network, Nanog, [ SDV.BDD ] Life Sciences [q-bio]/Development Biology, Enhancer, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Transcription factor, reproductive and urinary physiology, Epigenomics, Regulation of gene expression, [ SDV ] Life Sciences [q-bio], [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, [ SDV.BC.BC ] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], ES cells, Embryonic stem cell, Chromatin, Cell biology, Histone, [ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Differentiation, [ SDV.BDD.EO ] Life Sciences [q-bio]/Development Biology/Embryology and Organogenesis, embryonic structures, biology.protein, Self-renewal, Otx2
Abstract

This article is a preprint: it has not been peer-reviewed.; Transcription factor networks, together with histone modifications and signalling pathways, underlie the establishment and maintenance of gene regulatory architectures associated with the molecular identity of each cell type. However, how master transcription factors individually impact the epigenomic landscape and orchestrate the behaviour of regulatory networks under different environmental constraints is only very partially understood. Here, we show that the transcription factor Nanog deploys multiple distinct mechanisms to enhance embryonic stem cell self-renewal. In the presence of LIF, which fosters self-renewal, Nanog rewires the pluripotency network by promoting chromatin accessibility and binding of other pluripo-tency factors to thousands of enhancers. In the absence of LIF, Nanog blocks differentiation by sustaining H3K27me3, a repressive histone mark, at developmental regulators. Among those, we show that the repression of Otx2 plays a preponderant role. Our results underscore the versatility of master transcription factors, such as Nanog, to globally influence gene regulation during developmental processes.

Published
2018
Full Text
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8. IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

Author

Patrice Mollard, Jacques Epelbaum, Sonia Garel, Michael J. Meaney, Tatiana Ledent, Yves Le Bouc, Laurent Kappeler, Victor Heurtier, Lyvianne Decourtye, Erik Mire, Maud Clemessy, Iain C. A. F. Robinson, Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), MRC National Institute for Medical Research, Institut de Génomique Fonctionnelle - Montpellier GenomiX (IGF MGX), Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Mécanismes Adaptatifs et Evolution (MECADEV), Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS), Institut de psychiatrie et neurosciences (U894 / UMS 1266), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Douglas Mental Health University Institute [Montréal], McGill University = Université McGill [Montréal, Canada], Institut de biologie de l'ENS Paris (UMR 8197/1024) (IBENS), Département de Biologie - ENS Paris, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), This study was supported by the Institut National de la Santé et de la Recherche Médicale (INSERM), l’Université Pierre et Marie Curie (Sorbonne Universités, UPMC Univ Paris 06), the institute of Cardiometabolism and Nutrition (IHU ICAN), Sandoz-France laboratories, and the Premup foundation., HAL-UPMC, Gestionnaire, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-BioCampus (BCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de biologie de l'ENS Paris (IBENS), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Centre de Psychiatrie et Neurosciences (U894), Centre de Recherche Saint-Antoine ( CR Saint-Antoine ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de Génomique Fonctionnelle - Montpellier GenomiX ( IGF MGX ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Mécanismes adaptatifs : des organismes aux communautés ( MECADEV ), Muséum National d'Histoire Naturelle ( MNHN ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Psychiatrie et Neurosciences ( CPN - U894 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), McGill University, Institut de biologie de l'ENS Paris (UMR 8197/1024) ( IBENS ), École normale supérieure - Paris ( ENS Paris ) -École normale supérieure - Paris ( ENS Paris ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Département de Biologie - ENS Paris, and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, 0301 basic medicine, Pituitary gland, Peptide Hormones, medicine.medical_treatment, lcsh:Medicine, Growth Hormone-Releasing Hormone, Nervous System, Biochemistry, Explant Cultures, Mice, Nerve Fibers, Animal Cells, Arcuate Nucleus, Medicine and Health Sciences, Insulin-Like Growth Factor I, Axon, lcsh:Science, Neurons, 2. Zero hunger, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Multidisciplinary, Brain, Growth hormone–releasing hormone, medicine.anatomical_structure, Hypothalamus, Pituitary Gland, Median eminence, Female, Growth and Development, Biological Cultures, Cellular Types, Anatomy, Research Article, medicine.medical_specialty, Somatotropic cell, Neuronal Outgrowth, Mice, Transgenic, Endocrine System, Biology, Research and Analysis Methods, 03 medical and health sciences, Arcuate nucleus, [ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology, Internal medicine, medicine, Animals, Immunohistochemistry Techniques, Growth factor, lcsh:R, Correction, Biology and Life Sciences, Cell Biology, Axons, Hormones, Mice, Inbred C57BL, Histochemistry and Cytochemistry Techniques, Neuroanatomy, 030104 developmental biology, Endocrinology, Animals, Newborn, Cellular Neuroscience, Growth Hormone, Immunologic Techniques, lcsh:Q, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Neuroscience
Abstract

International audience; Nutrition during the perinatal period programs body growth. Growth hormone (GH) secretion from the pituitary regulates body growth and is controlled by Growth Hormone Releasing Hormone (GHRH) neurons located in the arcuate nucleus of the hypothalamus. We observed that dietary restriction during the early postnatal period (i.e. lactation) in mice influences postnatal growth by permanently altering the development of the somatotropic axis in the pituitary gland. This alteration may be due to a lack of GHRH signaling during this critical developmental period. Indeed, underfed pups showed decreased insulin-like growth factor I (IGF-I) plasma levels, which are associated with lower innervation of the median eminence by GHRH axons at 10 days of age relative to normally fed pups. IGF-I preferentially stimulated axon elongation of GHRH neurons in in vitro arcuate explant cultures from 7 day-old normally fed pups. This IGF-I stimulating effect was selective since other arcuate neurons visualized concomitantly by neurofilament labeling, or AgRP immunochemistry, did not significantly respond to IGF-I stimulation. Moreover, GHRH neurons in explants from age-matched underfed pups lost the capacity to respond to IGF-I stimulation. Molecular analyses indicated that nutritional restriction was associated with impaired activation of AKT. These results highlight a role for IGF-I in axon elongation that appears to be cell selective and participates in the complex cellular mechanisms that link underfeeding during the early postna-tal period with programming of the growth trajectory.

Published
2017

9. Correction: IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

Author

Patrice Mollard, Michael J. Meaney, Jacques Epelbaum, Lyvianne Decourtye, Erik Mire, Yves Le Bouc, Maud Clemessy, Victor Heurtier, Sonia Garel, Iain C. A. F. Robinson, Tatiana Ledent, and Laurent Kappeler

Subjects
0301 basic medicine, medicine.medical_specialty, Multidisciplinary, lcsh:R, lcsh:Medicine, Anatomy, Biology, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Endocrinology, medicine.anatomical_structure, Internal medicine, medicine, lcsh:Q, Axon, Elongation, lcsh:Science, 030217 neurology & neurosurgery
Abstract

[This corrects the article DOI: 10.1371/journal.pone.0170083.].

Published
2017

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