Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development
The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the...
Ausführliche Beschreibung
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| Autor*in: |
Goto, Masanori [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
12 |
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| Übergeordnetes Werk: |
Enthalten in: DNA methylation mediates gonadal development via regulating the expression levels of - Su, Junxiao ELSEVIER, 2023, an international multidisciplinary journal devoted to fundamental research in the brain sciences, Amsterdam |
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| Übergeordnetes Werk: |
volume:1625 ; year:2015 ; day:2 ; month:11 ; pages:206-217 ; extent:12 |
| Links: |
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| DOI / URN: |
10.1016/j.brainres.2015.08.045 |
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| 520 | |a The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. | ||
| 520 | |a The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. | ||
| 650 | 7 | |a Hes1 |2 Elsevier | |
| 650 | 7 | |a Hes5 |2 Elsevier | |
| 650 | 7 | |a Pituicyte |2 Elsevier | |
| 650 | 7 | |a Pituitary development |2 Elsevier | |
| 650 | 7 | |a Neurohypophysis |2 Elsevier | |
| 700 | 1 | |a Hojo, Masato |4 oth | |
| 700 | 1 | |a Ando, Mitsushige |4 oth | |
| 700 | 1 | |a Kita, Aya |4 oth | |
| 700 | 1 | |a Kitagawa, Masashi |4 oth | |
| 700 | 1 | |a Ohtsuka, Toshiyuki |4 oth | |
| 700 | 1 | |a Kageyama, Ryoichiro |4 oth | |
| 700 | 1 | |a Miyamoto, Susumu |4 oth | |
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10.1016/j.brainres.2015.08.045 doi GBVA2015020000030.pica (DE-627)ELV029297400 (ELSEVIER)S0006-8993(15)00696-4 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Goto, Masanori verfasserin aut Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. Hes1 Elsevier Hes5 Elsevier Pituicyte Elsevier Pituitary development Elsevier Neurohypophysis Elsevier Hojo, Masato oth Ando, Mitsushige oth Kita, Aya oth Kitagawa, Masashi oth Ohtsuka, Toshiyuki oth Kageyama, Ryoichiro oth Miyamoto, Susumu oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1625 year:2015 day:2 month:11 pages:206-217 extent:12 https://doi.org/10.1016/j.brainres.2015.08.045 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1625 2015 2 1102 206-217 12 045F 150 |
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10.1016/j.brainres.2015.08.045 doi GBVA2015020000030.pica (DE-627)ELV029297400 (ELSEVIER)S0006-8993(15)00696-4 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Goto, Masanori verfasserin aut Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. Hes1 Elsevier Hes5 Elsevier Pituicyte Elsevier Pituitary development Elsevier Neurohypophysis Elsevier Hojo, Masato oth Ando, Mitsushige oth Kita, Aya oth Kitagawa, Masashi oth Ohtsuka, Toshiyuki oth Kageyama, Ryoichiro oth Miyamoto, Susumu oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1625 year:2015 day:2 month:11 pages:206-217 extent:12 https://doi.org/10.1016/j.brainres.2015.08.045 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1625 2015 2 1102 206-217 12 045F 150 |
| allfields_unstemmed |
10.1016/j.brainres.2015.08.045 doi GBVA2015020000030.pica (DE-627)ELV029297400 (ELSEVIER)S0006-8993(15)00696-4 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Goto, Masanori verfasserin aut Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. Hes1 Elsevier Hes5 Elsevier Pituicyte Elsevier Pituitary development Elsevier Neurohypophysis Elsevier Hojo, Masato oth Ando, Mitsushige oth Kita, Aya oth Kitagawa, Masashi oth Ohtsuka, Toshiyuki oth Kageyama, Ryoichiro oth Miyamoto, Susumu oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1625 year:2015 day:2 month:11 pages:206-217 extent:12 https://doi.org/10.1016/j.brainres.2015.08.045 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1625 2015 2 1102 206-217 12 045F 150 |
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10.1016/j.brainres.2015.08.045 doi GBVA2015020000030.pica (DE-627)ELV029297400 (ELSEVIER)S0006-8993(15)00696-4 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Goto, Masanori verfasserin aut Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. Hes1 Elsevier Hes5 Elsevier Pituicyte Elsevier Pituitary development Elsevier Neurohypophysis Elsevier Hojo, Masato oth Ando, Mitsushige oth Kita, Aya oth Kitagawa, Masashi oth Ohtsuka, Toshiyuki oth Kageyama, Ryoichiro oth Miyamoto, Susumu oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1625 year:2015 day:2 month:11 pages:206-217 extent:12 https://doi.org/10.1016/j.brainres.2015.08.045 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1625 2015 2 1102 206-217 12 045F 150 |
| allfieldsSound |
10.1016/j.brainres.2015.08.045 doi GBVA2015020000030.pica (DE-627)ELV029297400 (ELSEVIER)S0006-8993(15)00696-4 DE-627 ger DE-627 rakwb eng 150 610 150 DE-600 610 DE-600 540 570 VZ BIODIV DE-30 fid 35.80 bkl 58.30 bkl Goto, Masanori verfasserin aut Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development 2015transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. Hes1 Elsevier Hes5 Elsevier Pituicyte Elsevier Pituitary development Elsevier Neurohypophysis Elsevier Hojo, Masato oth Ando, Mitsushige oth Kita, Aya oth Kitagawa, Masashi oth Ohtsuka, Toshiyuki oth Kageyama, Ryoichiro oth Miyamoto, Susumu oth Enthalten in Elsevier Su, Junxiao ELSEVIER DNA methylation mediates gonadal development via regulating the expression levels of 2023 an international multidisciplinary journal devoted to fundamental research in the brain sciences Amsterdam (DE-627)ELV010071113 volume:1625 year:2015 day:2 month:11 pages:206-217 extent:12 https://doi.org/10.1016/j.brainres.2015.08.045 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.80 Makromolekulare Chemie VZ 58.30 Biotechnologie VZ AR 1625 2015 2 1102 206-217 12 045F 150 |
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Hes1 and Hes5 are required for differentiation of pituicytes and formation of the neurohypophysis in pituitary development |
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The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. |
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The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. |
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The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development. |
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In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The pituitary gland is a critical endocrine organ regulating diverse physiological functions, including homeostasis, metabolism, reproduction, and growth. It is composed of two distinct entities: the adenohypophysis, including the anterior and intermediate lobes, and the neurohypophysis known as the posterior lobe. The neurohypophysis is composed of pituicytes (glial cells) and axons projected from hypothalamic neurons. The adenohypophysis derives from Rathke's pouch, whereas the neurohypophysis derives from the infundibulum, an evagination of the ventral diencephalon. Molecular mechanisms of adenohypophysis development are much better understood, but little is known about mechanisms that regulate neurohypophysis development. Hes genes, known as Notch effectors, play a crucial role in specifying cellular fates during the development of various tissues and organs. Here, we report that the ventral diencephalon fails to evaginate resulting in complete loss of the posterior pituitary lobe in Hes1 −/−; Hes5 +/− mutant embryos. In these mutant mice, progenitor cells are differentiated into neurons at the expense of pituicytes in the ventral diencephalon. In the developing neurohypophysis, the proliferative zone is located at the base of the infundibulum. Thus, Hes1 and Hes5 modulate not only maintenance of progenitor cells but also pituicyte versus neuron fate specification during neurohypophysis development.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Hes1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Hes5</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pituicyte</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pituitary development</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurohypophysis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hojo, Masato</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ando, Mitsushige</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kita, Aya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kitagawa, Masashi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ohtsuka, Toshiyuki</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kageyama, Ryoichiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Miyamoto, Susumu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Su, Junxiao ELSEVIER</subfield><subfield code="t">DNA methylation mediates gonadal development via regulating the expression levels of</subfield><subfield code="d">2023</subfield><subfield code="d">an international multidisciplinary journal devoted to fundamental research in the brain sciences</subfield><subfield code="g">Amsterdam</subfield><subfield code="w">(DE-627)ELV010071113</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:1625</subfield><subfield code="g">year:2015</subfield><subfield code="g">day:2</subfield><subfield code="g">month:11</subfield><subfield code="g">pages:206-217</subfield><subfield code="g">extent:12</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.brainres.2015.08.045</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-BIODIV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">35.80</subfield><subfield code="j">Makromolekulare Chemie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">58.30</subfield><subfield code="j">Biotechnologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">1625</subfield><subfield code="j">2015</subfield><subfield code="b">2</subfield><subfield code="c">1102</subfield><subfield code="h">206-217</subfield><subfield code="g">12</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">150</subfield></datafield></record></collection>
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