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Article ; Online: The origin and evolution of gene targeting.

Capecchi, Mario R

2021 Volume 481, Page(s) 179–187

MeSH term(s)	Animals ; Gene Targeting/history ; Gene Targeting/trends ; History, 20th Century ; History, 21st Century
Language	English
Publishing date	2021-10-30
Publishing country	United States
Document type	Historical Article ; Journal Article
ZDB-ID	1114-9
ISSN	1095-564X ; 0012-1606
ISSN (online)	1095-564X
ISSN	0012-1606
DOI	10.1016/j.ydbio.2021.10.007
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Article ; Online: Lrig1 expression identifies quiescent stem cells in the ventricular-subventricular zone from postnatal development to adulthood and limits their persistent hyperproliferation.

Nam, Hyung-Song / Capecchi, Mario R

Neural development

2023 Volume 18, Issue 1, Page(s) 1

Abstract: Background: We previously identified Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) as a marker of long-term neurogenic stem cells in the lateral wall of the adult mouse brain. The morphology of the stem cells thus identified differed ... ...

Abstract	Background: We previously identified Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) as a marker of long-term neurogenic stem cells in the lateral wall of the adult mouse brain. The morphology of the stem cells thus identified differed from the canonical B1 type stem cells, raising a question about their cellular origin. Thus, we investigated the development of these stem cells in the postnatal and juvenile brain. Furthermore, because Lrig1 is a known regulator of quiescence, we also investigated the effect(s) of its deletion on the cellular proliferation in the lateral wall. Methods: To observe the development of the Lrig1-lineage stem cells, genetic inducible fate mapping studies in combination with thymidine analog administration were conducted using a previously published Lrig1 Results: We observed the Lrig1-lineage labeled cells with morphologies consistent with neurogenic stem cell identity in postnatal, juvenile, and adult mouse brains. Interestingly, when induced at postnatal or juvenile ages, morphologically distinct cells were revealed, including cells with the canonical B1 type stem cell morphology. Almost all of the presumptive stem cells labeled were non-proliferative at these ages. In the old Lrig1 germline knock-out mice, increased proliferation was observed compared to wildtype littermates without concomitant increase in apoptosis. Conclusions: Once set aside during embryogenesis, the Lrig1-lineage stem cells remain largely quiescent during postnatal and juvenile development until activation in adult age. The absence of premature proliferative exhaustion in the Lrig1 knock-out stem cell niche during aging is likely due to a complex cascade of effects on the adult stem cell pool. Thus, we suggest that the adult stem cell pool size may be genetically constrained via Lrig1.
MeSH term(s)	Animals ; Mice ; Adult Stem Cells/metabolism ; Cell Proliferation ; Lateral Ventricles/growth & development ; Membrane Glycoproteins/genetics ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism
Chemical Substances	Lrig1 protein, mouse ; Membrane Glycoproteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-01-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2254847-6
ISSN	1749-8104 ; 1749-8104
ISSN (online)	1749-8104
ISSN	1749-8104
DOI	10.1186/s13064-022-00169-1
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Article ; Online: Correction: Lrig1 expression prospectively identifies stem cells in the ventricular-subventricular zone that are neurogenic throughout adult life.

Nam, Hyung-Song / Capecchi, Mario R

Neural development

2023 Volume 18, Issue 1, Page(s) 3

Language	English
Publishing date	2023-05-19
Publishing country	England
Document type	Published Erratum
ZDB-ID	2254847-6
ISSN	1749-8104 ; 1749-8104
ISSN (online)	1749-8104
ISSN	1749-8104
DOI	10.1186/s13064-023-00171-1
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Article ; Online: Correction: Lrig1 expression identifies quiescent stem cells in the ventricular‑subventricular zone from postnatal development to adulthood and limits their persistent hyperproliferation.

Nam, Hyung-Song / Capecchi, Mario R

Neural development

2023 Volume 18, Issue 1, Page(s) 4

Language	English
Publishing date	2023-05-23
Publishing country	England
Document type	Published Erratum
ZDB-ID	2254847-6
ISSN	1749-8104 ; 1749-8104
ISSN (online)	1749-8104
ISSN	1749-8104
DOI	10.1186/s13064-023-00172-0
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Article ; Online: Optogenetic stimulation of mouse Hoxb8 microglia in specific regions of the brain induces anxiety, grooming, or both.

Nagarajan, Naveen / Capecchi, Mario R

Molecular psychiatry

2023

Abstract: Previously, we have shown that either disruption of the Hoxb8 gene or ablation of a microglial subpopulation, Hoxb8 microglia, results in mice exhibiting both chronic anxiety and OCSD-like behavior, compulsive pathological hair pulling (trichotillomania), ...

Abstract	Previously, we have shown that either disruption of the Hoxb8 gene or ablation of a microglial subpopulation, Hoxb8 microglia, results in mice exhibiting both chronic anxiety and OCSD-like behavior, compulsive pathological hair pulling (trichotillomania), to the point of showing lesions at the sites of overgrooming. Herein we show, that optogenetic stimulation of Hoxb8 microglia in specific regions of the brain induces elevated anxiety, grooming or both. Optogenetic stimulation of Hoxb8 microglia within the dorsomedial striatum (DMS) or the medial prefrontal cortex (mPFC) induces grooming, whereas stimulation of Hoxb8 microglia in the basolateral amygdala (BLA) or central amygdala (CeA) produces elevated anxiety. Optogenetic stimulation of Hoxb8 microglia in the ventral CA1 region of the hippocampus (vCA1) induces both behaviors as well as freezing. In vitro we directly demonstrate that optogenetic stimulation of Hoxb8 microglia in specific regions of the brain activate neighboring neural activity through the induction of the c-fos-immediate early response. These experiments connect outputs from optogenetically stimulated Hoxb8 microglia, within specific regions of the brain, to the activation of neurons and neural circuits that in turn enable induction of these behaviors. These experiments suggest that Hoxb8 microglia are likely to be among, or the main, first responders to signals that evoke these behaviors. The same regions of the brain (DMS, mPFC, BLA, CeA and vCA1) have previously been defined at the neuronal level, by optogenetics, to control anxiety in mice. Intriguingly, the optogenetic experiments in microglia suggest that the two populations of microglia, canonical non-Hoxb8 and Hoxb8 microglia, function in opposition rather than in parallel to each other, providing a biological reason for the presence of two microglial subpopulations in mice.
Language	English
Publishing date	2023-04-10
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-023-02019-w
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Article ; Online: Lrig1 expression prospectively identifies stem cells in the ventricular-subventricular zone that are neurogenic throughout adult life.

Nam, Hyung-Song / Capecchi, Mario R

Neural development

2020 Volume 15, Issue 1, Page(s) 3

Abstract: Background: Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) regulates stem cell quiescence. As a marker, it identifies stem cells in multiple organs of the mouse. We had detected Lrig1 expression in cultured Id1: Methods: Publicly ... ...

Abstract	Background: Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) regulates stem cell quiescence. As a marker, it identifies stem cells in multiple organs of the mouse. We had detected Lrig1 expression in cultured Id1 Methods: Publicly available single cell RNA sequencing datasets were analyzed with Seurat and Monocle. The Lrig1+ cells were lineage traced in vivo with a novel non-disruptive co-translational Lrig1 Results: Analysis of single cell RNA sequencing datasets suggested Lrig1 was highly expressed in the most primitive stem cells of the neurogenic lineage in the lateral wall of the adult mouse brain. In support of their neurogenic stem cell identity, cell cycle entry was only observed in two morphologically distinguishable Lrig1+ cells that could also be induced into activation by Ara-C infusion. The Lrig1+ neurogenic stem cells were observed throughout the lateral wall. Neuroblasts and neurons were lineage traced from Lrig1+ neurogenic stem cells at 1 year after labeling. Conclusions: We identified Lrig1 as a marker of long-term neurogenic stem cells in the lateral wall of the mouse brain. Lrig1 expression revealed two morphotypes of the Lrig1+ cells that function as long-term neurogenic stem cells. The spatial distribution of the Lrig1+ neurogenic stem cells suggested all subtypes of the adult neurogenic stem cells were labeled.
MeSH term(s)	Adult Stem Cells ; Animals ; Cells, Cultured ; Databases, Genetic ; Datasets as Topic ; Embryo, Mammalian ; Lateral Ventricles/cytology ; Lateral Ventricles/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/physiology ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Neural Stem Cells/metabolism ; Neurogenesis/genetics ; Neurogenesis/physiology ; Sequence Analysis, RNA
Chemical Substances	Lrig1 protein, mouse ; Membrane Glycoproteins ; Nerve Tissue Proteins
Language	English
Publishing date	2020-03-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2254847-6
ISSN	1749-8104 ; 1749-8104
ISSN (online)	1749-8104
ISSN	1749-8104
DOI	10.1186/s13064-020-00139-5
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Article ; Online: ASPM regulates symmetric stem cell division by tuning Cyclin E ubiquitination.

Capecchi, Mario R / Pozner, Amir

Nature communications

2015 Volume 6, Page(s) 8763

Abstract: We generate a mouse model for the human microcephaly syndrome by mutating the ASPM locus, and demonstrate a premature exhaustion of the neuronal progenitor pool due to dysfunctional self-renewal processes. Earlier studies have linked ASPM mutant ... ...

Abstract	We generate a mouse model for the human microcephaly syndrome by mutating the ASPM locus, and demonstrate a premature exhaustion of the neuronal progenitor pool due to dysfunctional self-renewal processes. Earlier studies have linked ASPM mutant progenitor excessive cell cycle exit to a mitotic orientation defect. Here, we demonstrate a mitotic orientation-independent effect of ASPM on cell cycle duration. We pinpoint the cell fate-determining factor to the length of time spent in early G1 before traversing the restriction point. Characterization of the molecular mechanism reveals an interaction between ASPM and the Cdk2/Cyclin E complex, regulating the Cyclin activity by modulating its ubiquitination, phosphorylation and localization into the nucleus, before the cell is fated to transverse the restriction point. Thus, we reveal a novel function of ASPM in mediating the tightly coordinated Ubiquitin- Cyclin E- Retinoblastoma- E2F bistable-signalling pathway controlling restriction point progression and stem cell maintenance.
MeSH term(s)	Animals ; Calmodulin-Binding Proteins/genetics ; Calmodulin-Binding Proteins/metabolism ; Cell Cycle ; Cell Division ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cyclin E/genetics ; Cyclin E/metabolism ; Cyclin-Dependent Kinase 2/genetics ; Cyclin-Dependent Kinase 2/metabolism ; E2F Transcription Factors/genetics ; E2F Transcription Factors/metabolism ; G1 Phase ; Humans ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Phosphorylation ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism ; Stem Cells/cytology ; Stem Cells/enzymology ; Stem Cells/metabolism ; Ubiquitination
Chemical Substances	ASPM protein, mouse ; Calmodulin-Binding Proteins ; Cyclin E ; E2F Transcription Factors ; Nerve Tissue Proteins ; Retinoblastoma Protein ; Cyclin-Dependent Kinase 2 (EC 2.7.11.22)
Language	English
Publishing date	2015-11-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms9763
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Article ; Online: Hoxc8 initiates an ectopic mammary program by regulating Fgf10 and Tbx3 expression and Wnt/β-catenin signaling.

Carroll, Lara S / Capecchi, Mario R

Development (Cambridge, England)

2015 Volume 142, Issue 23, Page(s) 4056–4067

Abstract: The role of Hox genes in the formation of cutaneous accessory organs such as hair follicles and mammary glands has proved elusive, a likely consequence of overlapping function and expression among various homeobox factors. Lineage and immunohistochemical ...

Abstract	The role of Hox genes in the formation of cutaneous accessory organs such as hair follicles and mammary glands has proved elusive, a likely consequence of overlapping function and expression among various homeobox factors. Lineage and immunohistochemical analysis of Hoxc8 in mice revealed that this midthoracic Hox gene has transient but strong regional expression in ventrolateral surface ectoderm at E10.5, much earlier than previously reported. Targeted mice were generated to conditionally misexpress Hoxc8 from the Rosa locus using select Cre drivers, which significantly expanded the domain of thoracic identity in mutant embryos. Accompanying this expansion was the induction of paired zones of ectopic mammary development in the cervical region, which generated between three and five pairs of mammary placodes anterior to the first wild-type mammary rudiment. These rudiments expressed the mammary placode markers Wnt10b and Tbx3 and were labeled by antibodies to the mammary mesenchyme markers ERα and androgen receptor. Somitic Fgf10 expression, which is required for normal mammary line formation, was upregulated in mutant cervical somites, and conditional ablation of ectodermal Tbx3 expression eliminated all normally positioned and ectopic mammary placodes. We present evidence that Hoxc8 participates in regulating the initiation stages of mammary placode morphogenesis, and suggest that this and other Hox genes are likely to have important roles during regional specification and initiation of these and other cutaneous accessory organs.
MeSH term(s)	Animals ; Body Patterning ; Cell Lineage ; Ectoderm/metabolism ; Female ; Fibroblast Growth Factor 10/genetics ; Fibroblast Growth Factor 10/metabolism ; Gene Expression Regulation, Developmental ; Genotype ; Green Fluorescent Proteins/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Immunohistochemistry ; In Situ Hybridization ; Lac Operon ; Male ; Mesoderm/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Time Factors ; Up-Regulation ; Wnt Signaling Pathway
Chemical Substances	Fgf10 protein, mouse ; Fibroblast Growth Factor 10 ; Homeodomain Proteins ; Hoxc8 protein, mouse ; T-Box Domain Proteins ; Tbx3 protein, mouse ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2015-12-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.128298
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Article ; Online: Defining the Hoxb8 cell lineage during murine definitive hematopoiesis.

Van Deren, Donn A / De, Shrutokirti / Xu, Ben / Eschenbacher, Kayla M / Zhang, Shuhua / Capecchi, Mario R

Development (Cambridge, England)

2022 Volume 149, Issue 8

Abstract: Previously, we have demonstrated that a subpopulation of microglia, known as Hoxb8 microglia, is derived from the Hoxb8 lineage during the second wave (E8.5) of yolk sac hematopoiesis, whereas canonical non-Hoxb8 microglia arise from the first wave (E7.5) ...

Abstract	Previously, we have demonstrated that a subpopulation of microglia, known as Hoxb8 microglia, is derived from the Hoxb8 lineage during the second wave (E8.5) of yolk sac hematopoiesis, whereas canonical non-Hoxb8 microglia arise from the first wave (E7.5). Hoxb8 microglia have an ontogeny distinct from non-Hoxb8 microglia. Dysfunctional Hoxb8 microglia cause the acquisition of chronic anxiety and an obsessive-compulsive spectrum-like behavior, trichotillomania, in mice. The nature and fate of the progenitors generated during E8.5 yolk sac hematopoiesis have been controversial. Herein, we use the Hoxb8 cell lineage reporter to define the ontogeny of hematopoietic cells arising during the definitive waves of hematopoiesis initiated in the E8.5 yolk sac and aorta-gonad-mesonephros (AGM) region. Our murine cell lineage analysis shows that the Hoxb8 cell lineage reporter robustly marks erythromyeloid progenitors, hematopoietic stem cells and their progeny, particularly monocytes. Hoxb8 progenitors and microglia require Myb function, a hallmark transcription factor for definitive hematopoiesis, for propagation and maturation. During adulthood, all immune lineages and, interestingly, resident macrophages in only hematopoietic/lymphoid tissues are derived from Hoxb8 precursors. These results illustrate that the Hoxb8 lineage exclusively mirrors murine definitive hematopoiesis.
MeSH term(s)	Animals ; Cell Lineage ; Hematopoiesis ; Hematopoietic Stem Cells ; Homeodomain Proteins/genetics ; Mesonephros ; Mice ; Yolk Sac
Chemical Substances	Homeodomain Proteins ; Hoxb8 protein, mouse
Language	English
Publishing date	2022-04-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.200200
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Book: Molecular genetics of early drosophila and mouse development

Capecchi, Mario R.

(Current communications in molecular biology)

1989

Institution	Meeting on Molecular Genetic Analysis of Early Drosophila and Mouse Development
Author's details	[Meeting on Molecular Genetic Analysis of Early Drosophila and Mouse Development]. Ed. by Mario R. Capecchi
Series title	Current communications in molecular biology
Keywords	Drosophila / genetics / congresses ; Mice / genetics / congresses ; Drosophila ; Entwicklungsphysiologie ; Genregulation ; Maus
Subject	Genetische Regulation ; Transkription ; Genaktivität ; Entwicklungsmechanik ; Kausalmorphologie ; Kausale Morphologie ; Labormaus ; Weiße Maus
Size	XIII, 141 S. : Ill., graph. Darst.
Publisher	Cold Spring Harbor Laboratory Pr
Publishing place	Cold Spring Habor, NY
Publishing country	United States
Document type	Book
HBZ-ID	HT003525593
ISBN	0-87969-339-8 ; 978-0-87969-339-8
Database	Catalogue ZB MED Medicine, Health

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