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Article ; Online: Increased RET Activity Coupled with a Reduction in the

Okamoto, Mitsumasa / Uesaka, Toshihiro / Ito, Keisuke / Enomoto, Hideki

2021 Volume 8, Issue 3

Abstract: Mutations of the gene encoding ... ...

Abstract	Mutations of the gene encoding the
MeSH term(s)	Animals ; Gene Dosage ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Hirschsprung Disease/genetics ; Humans ; Mice ; Mutation/genetics ; Proto-Oncogene Proteins c-ret/genetics
Chemical Substances	Glial Cell Line-Derived Neurotrophic Factor ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1)
Language	English
Publishing date	2021-06-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0534-20.2021
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Article ; Online: Live visualization of a functional RET-EGFP chimeric receptor in homozygous knock-in mice.

Sunardi, Mukhamad / Ito, Keisuke / Enomoto, Hideki

Development, growth & differentiation

2021 Volume 63, Issue 6, Page(s) 285–294

Abstract: The GDNF Family Ligands (GFLs) regulate neural development and kidney organogenesis by activating the RET receptor tyrosine kinase. Many RET-dependent developmental processes involve long-distance cell-cell communications or cell polarity, which includes ...

Abstract	The GDNF Family Ligands (GFLs) regulate neural development and kidney organogenesis by activating the RET receptor tyrosine kinase. Many RET-dependent developmental processes involve long-distance cell-cell communications or cell polarity, which includes cell migration and axon guidance. This suggests that spatiotemporally regulated subcellular localization of RET protein and appropriate propagation of RET signaling in cells are essential for the physiological function of the GFLs. Little is known, however, about the dynamics of RET protein in cells. Addressing this issue requires development of a system that allows visualization of RET in living cells. In this study, we report generation of a novel knock-in mouse line in which the RET-EGFP chimeric receptor is expressed under the Ret promoter. Unlike Ret-deficient mice that die after birth due to the absence of the enteric nervous system (ENS) and kidneys, Ret
MeSH term(s)	Animals ; Cell Movement ; Enteric Nervous System ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Mice ; Neurons ; Signal Transduction
Chemical Substances	Glial Cell Line-Derived Neurotrophic Factor
Language	English
Publishing date	2021-08-10
Publishing country	Japan
Document type	Journal Article
ZDB-ID	280433-5
ISSN	1440-169X ; 0012-1592
ISSN (online)	1440-169X
ISSN	0012-1592
DOI	10.1111/dgd.12740
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Article: Uts2b is a microbiota-regulated gene expressed in vagal afferent neurons connected to enteroendocrine cells producing cholecystokinin

Yoshioka, Yuta / Tachibana, Yoshihisa / Uesaka, Toshihiro / Hioki, Hiroyuki / Sato, Yuya / Fukumoto, Takumi / Enomoto, Hideki

Biochemical and biophysical research communications. 2022 June 11, v. 608

2022

Abstract: Enteroendocrine cells (EECs) are the primary sensory cells that sense the gut luminal environment and secret hormones to regulate organ function. Recent studies revealed that vagal afferent neurons are connected to EECs and relay sensory information from ...

Abstract	Enteroendocrine cells (EECs) are the primary sensory cells that sense the gut luminal environment and secret hormones to regulate organ function. Recent studies revealed that vagal afferent neurons are connected to EECs and relay sensory information from EECs to the brain stem. To date, however, the identity of vagal afferent neurons connected to a given EEC subtype and the mode of their gene responses to its intestinal hormone have remained unknown. Hypothesizing that EEC-associated vagal afferent neurons change their gene expression in response to the microbiota-related extracellular stimuli, we conducted comparative gene expression analyses of the nodose-petrosal ganglion complex (NPG) using specific pathogen-free (SPF) and germ-free (GF) mice. We report here that the Uts2b gene, which encodes a functionally unknown neuropeptide, urotensin 2B (UTS2B), is expressed in a microbiota-dependent manner in NPG neurons. In cultured NPG neurons, expression of Uts2b was induced by AR420626, the selective agonist for FFAR3. Moreover, distinct gastrointestinal hormones exerted differential effects on Uts2b expression in NPG neurons, where cholecystokinin (CCK) significantly increased its expression. The majority of Uts2b-expressing NPG neurons expressed CCK-A, the receptor for CCK, which comprised approximately 25% of all CCK-A-expressing NPG neurons. Selective fluorescent labeling of Uts2b-expressing NPG neurons revealed a direct contact of their nerve fibers to CCK-expressing EECs. This study identifies the Uts2b as a microbiota-regulated gene, demonstrates that Uts2b-expressing vagal afferent neurons transduce sensory information from CCK-expressing EECs to the brain, and suggests potential involvement of UTS2B in a modality of CCK actions.
Keywords	agonists ; brain stem ; cholecystokinin ; direct contact ; fluorescence ; ganglia ; gene expression ; genes ; intestines ; nerve tissue ; research
Language	English
Dates of publication	2022-0611
Size	p. 66-72.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.03.117
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Article ; Online: A Single RET Mutation in Hirschsprung Disease Induces Intestinal Aganglionosis Via a Dominant-Negative Mechanism.

Sunardi, Mukhamad / Ito, Keisuke / Sato, Yuya / Uesaka, Toshihiro / Iwasaki, Mitsuhiro / Enomoto, Hideki

Cellular and molecular gastroenterology and hepatology

2022 Volume 15, Issue 6, Page(s) 1505–1524

Abstract: Background & aims: Hirschsprung disease (HSCR) is a congenital disorder characterized by the absence of the enteric nervous system (ENS). HSCR potentially involves multiple gene aberrations and displays complex patterns of inheritance. Mutations of the ... ...

Abstract	Background & aims: Hirschsprung disease (HSCR) is a congenital disorder characterized by the absence of the enteric nervous system (ENS). HSCR potentially involves multiple gene aberrations and displays complex patterns of inheritance. Mutations of the RET gene, encoding the RET receptor tyrosine kinase, play a central role in the pathogenesis of HSCR. Although a wide variety of coding RET mutations have been identified, their pathogenetic significance in vivo has remained largely unclear. Methods: We introduced a HSCR-associated RET missense mutation, RET(S811F), into the corresponding region (S812) of the mouse Ret gene. Pathogenetic impact of Ret(S812F) was assessed by histologic and functional analyses of the ENS and by biochemical analyses. Interactions of the Ret(S812F) allele with HSCR susceptibility genes, the RET9 allele and the Ednrb gene, were examined by genetic crossing in mice. Results: Ret Conclusions: This study demonstrates that a single RET missense mutation alone induces intestinal aganglionosis via a dominant-negative mechanism. The Ret
MeSH term(s)	Animals ; Mice ; Hirschsprung Disease/genetics ; Proto-Oncogene Proteins c-ret/genetics ; Proto-Oncogene Proteins c-ret/metabolism ; Mutation/genetics ; Neurons/metabolism ; Enteric Nervous System/metabolism
Chemical Substances	Proto-Oncogene Proteins c-ret (EC 2.7.10.1)
Language	English
Publishing date	2022-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2022.12.003
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Article ; Online: Uts2b is a microbiota-regulated gene expressed in vagal afferent neurons connected to enteroendocrine cells producing cholecystokinin.

Yoshioka, Yuta / Tachibana, Yoshihisa / Uesaka, Toshihiro / Hioki, Hiroyuki / Sato, Yuya / Fukumoto, Takumi / Enomoto, Hideki

Biochemical and biophysical research communications

2022 Volume 608, Page(s) 66–72

Abstract	Enteroendocrine cells (EECs) are the primary sensory cells that sense the gut luminal environment and secret hormones to regulate organ function. Recent studies revealed that vagal afferent neurons are connected to EECs and relay sensory information from EECs to the brain stem. To date, however, the identity of vagal afferent neurons connected to a given EEC subtype and the mode of their gene responses to its intestinal hormone have remained unknown. Hypothesizing that EEC-associated vagal afferent neurons change their gene expression in response to the microbiota-related extracellular stimuli, we conducted comparative gene expression analyses of the nodose-petrosal ganglion complex (NPG) using specific pathogen-free (SPF) and germ-free (GF) mice. We report here that the Uts2b gene, which encodes a functionally unknown neuropeptide, urotensin 2B (UTS2B), is expressed in a microbiota-dependent manner in NPG neurons. In cultured NPG neurons, expression of Uts2b was induced by AR420626, the selective agonist for FFAR3. Moreover, distinct gastrointestinal hormones exerted differential effects on Uts2b expression in NPG neurons, where cholecystokinin (CCK) significantly increased its expression. The majority of Uts2b-expressing NPG neurons expressed CCK-A, the receptor for CCK, which comprised approximately 25% of all CCK-A-expressing NPG neurons. Selective fluorescent labeling of Uts2b-expressing NPG neurons revealed a direct contact of their nerve fibers to CCK-expressing EECs. This study identifies the Uts2b as a microbiota-regulated gene, demonstrates that Uts2b-expressing vagal afferent neurons transduce sensory information from CCK-expressing EECs to the brain, and suggests potential involvement of UTS2B in a modality of CCK actions.
MeSH term(s)	Animals ; Cholecystokinin/genetics ; Cholecystokinin/metabolism ; Enteroendocrine Cells/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Microbiota ; Neurons, Afferent/metabolism ; Nodose Ganglion/metabolism ; Peptide Hormones/genetics ; Peptide Hormones/metabolism ; Vagus Nerve/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Peptide Hormones ; Uts2b protein, mouse ; Cholecystokinin (9011-97-6)
Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.03.117
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Article ; Online: Pcgf1 gene disruption reveals primary involvement of epigenetic mechanism in neuronal subtype specification in the enteric nervous system.

Putra, Bayu Pratama / Ito, Keisuke / Cirillo, Carla / Sunardi, Mukhamad / Koseki, Haruhiko / Uesaka, Toshihiro / Enomoto, Hideki

Development, growth & differentiation

2023 Volume 65, Issue 8, Page(s) 461–469

Abstract: The enteric nervous system (ENS) regulates gut functions independently from the central nervous system (CNS) by its highly autonomic neural circuit that integrates diverse neuronal subtypes. Although several transcription factors are shown to be ... ...

Abstract	The enteric nervous system (ENS) regulates gut functions independently from the central nervous system (CNS) by its highly autonomic neural circuit that integrates diverse neuronal subtypes. Although several transcription factors are shown to be necessary for the generation of some enteric neuron subtypes, the mechanisms underlying neuronal subtype specification in the ENS remain elusive. In this study, we examined the biological function of Polycomb group RING finger protein 1 (PCGF1), one of the epigenetic modifiers, in the development and differentiation of the ENS by disrupting the Pcgf1 gene selectively in the autonomic-lineage cells. Although ENS precursor migration and enteric neurogenesis were largely unaffected, neuronal differentiation was impaired in the Pcgf1-deficient mice, with the numbers of neurons expressing somatostatin (Sst
MeSH term(s)	Animals ; Mice ; Neurons ; Cell Differentiation/genetics ; Transcription Factors/metabolism ; Enteric Nervous System/metabolism ; Epigenesis, Genetic ; Polycomb Repressive Complex 1/genetics ; Polycomb Repressive Complex 1/metabolism
Chemical Substances	Transcription Factors ; Pcgf1 protein, mouse ; Polycomb Repressive Complex 1 (EC 2.3.2.27)
Language	English
Publishing date	2023-08-18
Publishing country	Japan
Document type	Journal Article
ZDB-ID	280433-5
ISSN	1440-169X ; 0012-1592
ISSN (online)	1440-169X
ISSN	0012-1592
DOI	10.1111/dgd.12880
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Article ; Online: Retrograde transport of neurotrophic factor signaling: implications in neuronal development and pathogenesis.

Ito, Keisuke / Enomoto, Hideki

Journal of biochemistry

2016 Volume 160, Issue 2, Page(s) 77–85

Abstract: Neurotrophic factors and their receptors play a central role in neuronal survival. Since neurons have a highly polarized morphology, target-derived neurotrophic factor signaling is transported retrogradely along the axon to the cell body. A body of ... ...

Abstract	Neurotrophic factors and their receptors play a central role in neuronal survival. Since neurons have a highly polarized morphology, target-derived neurotrophic factor signaling is transported retrogradely along the axon to the cell body. A body of evidence suggests that retrograde transport of the neurotrophic factors and their receptors is required for signal propagation. Retrograde transport of neurotrophic factor signaling is crucial not only for neuronal development, but also for preventing neuronal degeneration. Thus, elucidating the mechanism of retrograde transport will lead to insights into the developmental mechanisms of the nervous system as well as contribute to the establishment of novel therapies for neurodegenerative diseases. In this article, we will review the recent progress made in research of retrograde trafficking and discuss its physiological significance.
MeSH term(s)	Animals ; Central Nervous System/embryology ; Central Nervous System/pathology ; Humans ; Nerve Growth Factors/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Signal Transduction
Chemical Substances	Nerve Growth Factors
Language	English
Publishing date	2016-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	218073-x
ISSN	1756-2651 ; 0021-924X
ISSN (online)	1756-2651
ISSN	0021-924X
DOI	10.1093/jb/mvw037
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Article ; Online: Enhanced enteric neurogenesis by Schwann cell precursors in mouse models of Hirschsprung disease.

Uesaka, Toshihiro / Okamoto, Mitsumasa / Nagashimada, Mayumi / Tsuda, Yoshihiro / Kihara, Miho / Kiyonari, Hiroshi / Enomoto, Hideki

Glia

2021 Volume 69, Issue 11, Page(s) 2575–2590

Abstract: Hirschsprung disease (HSCR) is characterized by congenital absence of enteric neurons in distal portions of the gut. Although recent studies identified Schwann cell precursors (SCPs) as a novel cellular source of enteric neurons, it is unknown how SCPs ... ...

Abstract	Hirschsprung disease (HSCR) is characterized by congenital absence of enteric neurons in distal portions of the gut. Although recent studies identified Schwann cell precursors (SCPs) as a novel cellular source of enteric neurons, it is unknown how SCPs contribute to the disease phenotype of HSCR. Using Schwann cell-specific genetic labeling, we investigated SCP-derived neurogenesis in two mouse models of HSCR; Sox10 haploinsufficient mice exhibiting distal colonic aganglionosis and Ednrb knockout mice showing small intestinal aganglionosis. We also examined Ret dependency in SCP-derived neurogenesis using mice displaying intestinal aganglionosis in which Ret expression was conditionally removed in the Schwann cell lineage. SCP-derived neurons were abundant in the transition zone lying between the ganglionated and aganglionic segments, although SCP-derived neurogenesis was scarce in the aganglionic region. In the transition zone, SCPs mainly gave rise to nitrergic neurons that are rarely observed in the SCP-derived neurons under the normal condition. Enhanced SCP-derived neurogenesis was also detected in the transition zone of mice lacking RET expression in the Schwann cell lineage. Increased SCP-derived neurogenesis in the transition zone suggests that reduction in the vagal neural crest-derived enteric neurons promotes SCP-derived neurogenesis. SCPs may adopt a neuronal subtype by responding to changes in the gut environment. Robust SCP-derived neurogenesis can occur in a Ret-independent manner, which suggests that SCPs are a cellular source to compensate for missing enteric neurons in HSCR.
MeSH term(s)	Animals ; Enteric Nervous System/metabolism ; Hirschsprung Disease/genetics ; Hirschsprung Disease/metabolism ; Mice ; Mice, Knockout ; Neural Crest/metabolism ; Neurogenesis/genetics ; Schwann Cells/metabolism
Language	English
Publishing date	2021-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24059
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Article ; Online: Generation of conditional ALK F1174L mutant mouse models for the study of neuroblastoma pathogenesis.

Ono, Sachie / Saito, Takeshi / Terui, Keita / Yoshida, Hideo / Enomoto, Hideki

Genesis (New York, N.Y. : 2000)

2019 Volume 57, Issue 10, Page(s) e23323

Abstract: Neuroblastoma, an embryonal tumor arising from the sympathetic ganglia and adrenal medulla, is among the most intractable pediatric cancers. Although a variety of genetic changes have been identified in neuroblastoma, how they contribute to its ... ...

Abstract	Neuroblastoma, an embryonal tumor arising from the sympathetic ganglia and adrenal medulla, is among the most intractable pediatric cancers. Although a variety of genetic changes have been identified in neuroblastoma, how they contribute to its pathogenesis remains largely unclear. Recent studies have identified alterations of the anaplastic lymphoma kinase (ALK) gene in neuroblastoma; ALK F1174L (a phenylalanine-to-leucine substitution at codon 1174) represents one of the most frequent of these somatic mutations, and is associated with amplification of the MYCN gene, the most reliable marker for the poor survival. We engineered the mouse Alk locus so that ALK F1174L is expressed by its endogenous promoter and can be induced in a spatiotemporally controlled fashion using Cre-loxP system. Although expression of ALK F1174L resulted in enhanced proliferation of sympathetic ganglion progenitors and increased the size of the sympathetic ganglia, it was insufficient to cause neuroblastoma. However, lethal neuroblastoma frequently developed in mice co-expressing ALK F1174L and MYCN, even in a genetic background where MYCN alone does not cause overt tumors. These data reveal that physiological expression of ALK F1174L significantly potentiates the oncogenic ability of MYCN in vivo. Our conditional mutant mice provide a valuable platform for investigating the pathogenesis of neuroblastoma.
MeSH term(s)	Anaplastic Lymphoma Kinase/genetics ; Animals ; Carcinogenesis/genetics ; Female ; Ganglia, Sympathetic/growth & development ; Genetic Engineering ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains/genetics ; Mutagenesis, Insertional ; N-Myc Proto-Oncogene Protein/biosynthesis ; Neoplasms, Experimental/enzymology ; Neoplasms, Experimental/etiology ; Neoplasms, Experimental/genetics ; Neuroblastoma/enzymology ; Neuroblastoma/etiology ; Neuroblastoma/genetics
Chemical Substances	MYCN protein, mouse ; N-Myc Proto-Oncogene Protein ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1)
Language	English
Publishing date	2019-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2004544-X
ISSN	1526-968X ; 1526-954X
ISSN (online)	1526-968X
ISSN	1526-954X
DOI	10.1002/dvg.23323
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Article: Regulation of neural development by glial cell line-derived neurotrophic factor family ligands.

Enomoto, Hideki

Anatomical science international

2005 Volume 80, Issue 1, Page(s) 42–52

Abstract: Glial cell line-derived neurotrophic factor (GDNF) and its three relatives constitute a novel family of neurotrophic factors, the GDNF family ligands. These factors signal through a multicomponent receptor complex comprising a ... ...

Abstract	Glial cell line-derived neurotrophic factor (GDNF) and its three relatives constitute a novel family of neurotrophic factors, the GDNF family ligands. These factors signal through a multicomponent receptor complex comprising a glycosylphosphatidylinositol-anchored cell surface molecule (GDNF family receptor (GFR) alpha) and RET tyrosine kinase, triggering the activation of multiple signaling pathways in responsive cells. Recent gene-targeting studies have demonstrated that GDNF family ligands are essential for the development of a diverse set of neuronal populations and we have now started to understand how these ligands uniquely regulate the formation and sculpting of the nervous system. Recent studies have also revealed interactions by multiple extracellular signals during neural development. The deciphering of GDNF family ligand signaling in neural cells promises to provide vital new insights into the development and pathology of the nervous system.
MeSH term(s)	Animals ; Cell Differentiation ; Gene Expression Regulation, Developmental ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Humans ; Ligands ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Nervous System/embryology ; Nervous System/metabolism ; Neuroglia/cytology ; Neuroglia/metabolism ; Neurons/cytology ; Neurons/metabolism ; Organogenesis/physiology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction
Chemical Substances	GDNF protein, human ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Ligands ; Nerve Growth Factors ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2005-03
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2079994-9
ISSN	1447-6959 ; 0022-7722
ISSN	1447-6959 ; 0022-7722
DOI	10.1111/j.1447-073x.2005.00099.x
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