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Article: Aagab is required for zebrafish larval development by regulating neural activity.

Ding, Shihui / Aziz, Tursunjan / Meng, Anming / Jia, Shunji

Journal of genetics and genomics = Yi chuan xue bao

2024

Abstract: Clathrin-mediated endocytosis has been implicated in various physiological processes, including nutrient uptake, signal transduction, synaptic vesicle recycling, maintenance of cell polarity, and antigen presentation. Despite prior knowledge of its ... ...

Abstract	Clathrin-mediated endocytosis has been implicated in various physiological processes, including nutrient uptake, signal transduction, synaptic vesicle recycling, maintenance of cell polarity, and antigen presentation. Despite prior knowledge of its importance as a key regulator in promoting clathrin-mediated endocytosis, the physiological function of α- and γ-adaptin binding protein (aagab) remains elusive. In this study, we investigate the biological function of aagab during zebrafish development. We establish a loss-of-function mutant of the aagab gene in zebrafish, revealing impaired swimming and early larval mortality. Given the high expression level of the aagab gene in the brain, we probe into its physiological role in the nervous system. aagab mutants display subdued calcium responses and local field potential in the optic tectal neurons, aligning with reduced neurotransmitter release (e.g., norepinephrine) in the tectal neuropil of aagab mutants. Overexpressing aagab message RNA (mRNA) or nervous stimulant treatment in mutants restores neurotransmitter release, calcium responses, swimming ability, and survival. Furthermore, our observations show delayed release of FM 1-43 in AAGAB knockdown differentiated neuroblastoma cells, pointing towards a probable link to defective clathrin-mediated synaptic vesicle recycling. In conclusion, our study underscores the significance of Aagab in neurobiology and suggests its potential impacts in neurological disorders.
Language	English
Publishing date	2024-01-20
Publishing country	China
Document type	Journal Article
ZDB-ID	2374568-X
ISSN	1873-5533 ; 1673-8527
ISSN (online)	1873-5533
ISSN	1673-8527
DOI	10.1016/j.jgg.2024.01.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TGFβ family signaling and development.

Jia, Shunji / Meng, Anming

Development (Cambridge, England)

2021 Volume 148, Issue 5

Abstract: The transforming growth factor β (TGFβ) signaling family is evolutionarily conserved in metazoans. The signal transduction mechanisms of TGFβ family members have been expansively investigated and are well understood. During development and homeostasis, ... ...

Abstract	The transforming growth factor β (TGFβ) signaling family is evolutionarily conserved in metazoans. The signal transduction mechanisms of TGFβ family members have been expansively investigated and are well understood. During development and homeostasis, numerous TGFβ family members are expressed in various cell types with temporally changing levels, playing diverse roles in embryonic development, adult tissue homeostasis and human diseases by regulating cell proliferation, differentiation, adhesion, migration and apoptosis. Here, we discuss the molecular mechanisms underlying signal transduction and regulation of the TGFβ subfamily pathways, and then highlight their key functions in mesendoderm induction, dorsoventral patterning and laterality development, as well as in the formation of several representative tissues/organs.
MeSH term(s)	Animals ; Bone Morphogenetic Proteins/metabolism ; Embryonic Development/physiology ; Germ Layers/metabolism ; Nodal Protein/metabolism ; Organogenesis ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta/chemistry ; Transforming Growth Factor beta/metabolism
Chemical Substances	Bone Morphogenetic Proteins ; Nodal Protein ; Receptors, Transforming Growth Factor beta ; Smad Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2021-03-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.188490
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Article ; Online: Epistatic genetic interactions between Insm1 and Ikzf2 during cochlear outer hair cell development

Shuting Li / Shunji He / Ying Lu / Shiqi Jia / Zhiyong Liu

Cell Reports, Vol 42, Iss 5, Pp 112504- (2023)

2023

Abstract: Summary: The cochlea harbors two types of sound receptors, outer hair cells (OHCs) and inner hair cells (IHCs). OHCs transdifferentiate into IHCs in Insm1 mutants, and OHCs in Ikzf2-deficient mice are dysfunctional and maintain partial IHC gene ... ...

Abstract	Summary: The cochlea harbors two types of sound receptors, outer hair cells (OHCs) and inner hair cells (IHCs). OHCs transdifferentiate into IHCs in Insm1 mutants, and OHCs in Ikzf2-deficient mice are dysfunctional and maintain partial IHC gene expression. Insm1 potentially acts as a positive but indirect regulator of Ikzf2, considering that Insm1 is expressed earlier than Ikzf2 and primarily functions as a transcriptional repressor. However, direct evidence of this possibility is lacking. Here, we report the following results: first, Insm1 overexpression in IHCs leads to ectopic Ikzf2 expression. Second, Ikzf2 expression is repressed in Insm1-deficient OHCs, and forced expression of Ikzf2 mitigates the OHC abnormality in Insm1 mutants. Last, dual ablation of Insm1 and Ikzf2 generates a similar OHC phenotype as does Insm1 ablation alone. Collectively, our findings reveal the transcriptional cascade from Insm1 to Ikzf2, which should facilitate future investigation of the molecular mechanisms underlying OHC development and regeneration.
Keywords	CP: Developmental biology ; CP: Neuroscience ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Epistatic genetic interactions between Insm1 and Ikzf2 during cochlear outer hair cell development.

Li, Shuting / He, Shunji / Lu, Ying / Jia, Shiqi / Liu, Zhiyong

Cell reports

2023 Volume 42, Issue 5, Page(s) 112504

Abstract: The cochlea harbors two types of sound receptors, outer hair cells (OHCs) and inner hair cells (IHCs). OHCs transdifferentiate into IHCs in Insm1 mutants, and OHCs in Ikzf2-deficient mice are dysfunctional and maintain partial IHC gene expression. Insm1 ... ...

Abstract	The cochlea harbors two types of sound receptors, outer hair cells (OHCs) and inner hair cells (IHCs). OHCs transdifferentiate into IHCs in Insm1 mutants, and OHCs in Ikzf2-deficient mice are dysfunctional and maintain partial IHC gene expression. Insm1 potentially acts as a positive but indirect regulator of Ikzf2, considering that Insm1 is expressed earlier than Ikzf2 and primarily functions as a transcriptional repressor. However, direct evidence of this possibility is lacking. Here, we report the following results: first, Insm1 overexpression in IHCs leads to ectopic Ikzf2 expression. Second, Ikzf2 expression is repressed in Insm1-deficient OHCs, and forced expression of Ikzf2 mitigates the OHC abnormality in Insm1 mutants. Last, dual ablation of Insm1 and Ikzf2 generates a similar OHC phenotype as does Insm1 ablation alone. Collectively, our findings reveal the transcriptional cascade from Insm1 to Ikzf2, which should facilitate future investigation of the molecular mechanisms underlying OHC development and regeneration.
MeSH term(s)	Animals ; Mice ; Cochlea/metabolism ; Hair Cells, Auditory, Inner/metabolism ; Hair Cells, Auditory, Outer/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription Factors/metabolism
Chemical Substances	Insm1 protein, mouse ; Repressor Proteins ; Transcription Factors ; Ikzf2 protein, mouse
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112504
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Article ; Online: Molecular basis for bipartite recognition of histone H3 by the PZP domain of PHF14.

Zheng, Shuangping / Bi, Yucong / Chen, Haining / Gong, Bo / Jia, Shunji / Li, Haitao

Nucleic acids research

2021 Volume 49, Issue 15, Page(s) 8961–8973

Abstract: Histone recognition constitutes a key epigenetic mechanism in gene regulation and cell fate decision. PHF14 is a conserved multi-PHD finger protein that has been implicated in organ development, tissue homeostasis, and tumorigenesis. Here we show that ... ...

Abstract	Histone recognition constitutes a key epigenetic mechanism in gene regulation and cell fate decision. PHF14 is a conserved multi-PHD finger protein that has been implicated in organ development, tissue homeostasis, and tumorigenesis. Here we show that PHF14 reads unmodified histone H3(1-34) through an integrated PHD1-ZnK-PHD2 cassette (PHF14PZP). Our binding, structural and HDX-MS analyses revealed a feature of bipartite recognition, in which PHF14PZP utilizes two distinct surfaces for concurrent yet separable engagement of segments H3-Nter (e.g. 1-15) and H3-middle (e.g. 14-34) of H3(1-34). Structural studies revealed a novel histone H3 binding mode by PHD1 of PHF14PZP, in which a PHF14-unique insertion loop but not the core β-strands of a PHD finger dominates H3K4 readout. Binding studies showed that H3-PHF14PZP engagement is sensitive to modifications occurring to H3 R2, T3, K4, R8 and K23 but not K9 and K27, suggesting multiple layers of modification switch. Collectively, our work calls attention to PHF14 as a 'ground' state (unmodified) H3(1-34) reader that can be negatively regulated by active marks, thus providing molecular insights into a repressive function of PHF14 and its derepression.
MeSH term(s)	Allosteric Regulation ; Animals ; Crystallography, X-Ray ; Histones/chemistry ; Histones/metabolism ; Humans ; Models, Molecular ; Mutagenesis ; Nuclear Proteins/chemistry ; Protein Binding ; Protein Interaction Domains and Motifs ; Transcription Factors/chemistry ; Zebrafish Proteins/chemistry ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Histones ; Nuclear Proteins ; PHF14 protein, human ; Transcription Factors ; Zebrafish Proteins
Language	English
Publishing date	2021-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkab670
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Zs.A 1067: Show issues

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Article ; Online: A Golgi-derived vesicle potentiates PtdIns4P to PtdIns3P conversion for endosome fission.

Gong, Bo / Guo, Yuting / Ding, Shihui / Liu, Xiaohui / Meng, Anming / Li, Dong / Jia, Shunji

Nature cell biology

2021 Volume 23, Issue 7, Page(s) 782–795

Abstract: Endosome fission is essential for cargo sorting and targeting in the endosomal system. However, whether organelles other than the endoplasmic reticulum (ER) participate in endosome fission through membrane contacts is unknown. Here, we characterize a ... ...

Abstract	Endosome fission is essential for cargo sorting and targeting in the endosomal system. However, whether organelles other than the endoplasmic reticulum (ER) participate in endosome fission through membrane contacts is unknown. Here, we characterize a Golgi-derived vesicle, the SEC14L2 compartment, that plays a unique role in facilitating endosome fission through ternary contacts with endosomes and the ER. Localized to the ER-mediated endosome fission site, the phosphatidylinositol transfer protein SEC14L2 promotes phosphatidylinositol 4-phosphate (PtdIns4P) to phosphatidylinositol 3-phosphate (PtdIns3P) conversion before endosome fission. In the absence of SEC14L2, endosome fission is attenuated and more enlarged endosomes arise due to endosomal accumulation of PtdIns4P and reduction in PtdIns3P. Collectively, our data suggest roles of the Golgi network in ER-associated endosome fission and a mechanism involving ER-endosome contacts in the regulation of endosomal phosphoinositide conversion.
MeSH term(s)	Animals ; COS Cells ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Chlorocebus aethiops ; Class III Phosphatidylinositol 3-Kinases/genetics ; Class III Phosphatidylinositol 3-Kinases/metabolism ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/metabolism ; Endosomes/genetics ; Endosomes/metabolism ; Golgi Apparatus/genetics ; Golgi Apparatus/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphatidylinositol Phosphates/metabolism ; Protein Transport ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism ; Mice
Chemical Substances	Carrier Proteins ; Phosphatidylinositol Phosphates ; SEC14L3 protein, human ; Sec14l3 protein, mouse ; Zebrafish Proteins ; phosphatidylinositol 3-phosphate ; phosphatidylinositol 4-phosphate ; Class III Phosphatidylinositol 3-Kinases (EC 2.7.1.137)
Language	English
Publishing date	2021-06-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-021-00704-y
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 12: Show issues

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Article ; Online: Temporospatial inhibition of Erk signaling is required for lymphatic valve formation.

Meng, Yaping / Lv, Tong / Zhang, Junfeng / Shen, Weimin / Li, Lifang / Li, Yaqi / Liu, Xin / Lei, Xing / Lin, Xuguang / Xu, Hanfang / Meng, Anming / Jia, Shunji

Signal transduction and targeted therapy

2023 Volume 8, Issue 1, Page(s) 342

Abstract: Intraluminal lymphatic valves (LVs) and lymphovenous valves (LVVs) are critical to ensure the unidirectional flow of lymphatic fluid. Morphological abnormalities in these valves always cause lymph or blood reflux, and result in lymphedema. However, the ... ...

Abstract	Intraluminal lymphatic valves (LVs) and lymphovenous valves (LVVs) are critical to ensure the unidirectional flow of lymphatic fluid. Morphological abnormalities in these valves always cause lymph or blood reflux, and result in lymphedema. However, the underlying molecular mechanism of valve development remains poorly understood. We here report the implication of Efnb2-Ephb4-Rasa1 regulated Erk signaling axis in lymphatic valve development with identification of two new valve structures. Dynamic monitoring of phospho-Erk activity indicated that Erk signaling is spatiotemporally inhibited in some lymphatic endothelial cells (LECs) during the valve cell specification. Inhibition of Erk signaling via simultaneous depletion of zygotic erk1 and erk2 or treatment with MEK inhibitor selumetinib causes lymphatic vessel hypoplasia and lymphatic valve hyperplasia, suggesting opposite roles of Erk signaling during these two processes. ephb4b mutants, efnb2a;efnb2b or rasa1a;rasa1b double mutants all have defective LVs and LVVs and exhibit blood reflux into lymphatic vessels with an edema phenotype. Importantly, the valve defects in ephb4b or rasa1a;rasa1b mutants are mitigated with high-level gata2 expression in the presence of MEK inhibitors. Therefore, Efnb2-Ephb4 signaling acts to suppress Erk activation in valve-forming cells to promote valve specification upstream of Rasa1. Not only do our findings reveal a molecular mechanism of lymphatic valve formation, but also provide a basis for the treatment of lymphatic disorders.
MeSH term(s)	Endothelial Cells ; Lymphatic Vessels ; Signal Transduction/genetics ; Phosphorylation ; Mitogen-Activated Protein Kinase Kinases
Chemical Substances	Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2023-09-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2886872-9
ISSN	2059-3635 ; 2095-9907
ISSN (online)	2059-3635
ISSN	2095-9907
DOI	10.1038/s41392-023-01571-9
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Article ; Online: Silibinin inhibits ethanol- or acetaldehyde-induced ferroptosis in liver cell lines.

Song, Xiao-Yu / Liu, Peng-Cheng / Liu, Wei-Wei / Zhou, Jia / Hayashi, Toshihiko / Mizuno, Kazunori / Hattori, Shunji / Fujisaki, Hitomi / Ikejima, Takashi

Toxicology in vitro : an international journal published in association with BIBRA

2022 Volume 82, Page(s) 105388

Abstract: Alcoholic liver disease has become one of the main causes of liver injury, and its prevention and cure are important medical tasks. Silibinin, a natural flavonoid glycoside, is a conventional hepatic protectant. This study elucidates the modulation of ... ...

Abstract	Alcoholic liver disease has become one of the main causes of liver injury, and its prevention and cure are important medical tasks. Silibinin, a natural flavonoid glycoside, is a conventional hepatic protectant. This study elucidates the modulation of ferroptosis in silibinin's protective effects on ethanol- or acetaldehyde-induced liver cell damage by using human carcinomatous liver HepG2 cells and immortalized liver HL7702 cells. Our results show that ferroptosis is induced in the cells treated with ethanol or acetaldehyde, as evidenced by the increased ROS stress and iron level. Silibinin resolves the oxidative stress and reduces iron level. Ferroptosis induced by ethanol- or acetaldehyde involving nuclear receptor co-activator 4 (NCOA4)-dependent autophagic degradation of ferritin, a protein for storing iron is rescued by silibinin. PINK1 and Parkin-mediated mitophagy is arrested in ethanol- or acetaldehyde-treated cells but reversed by silibinin. Ferritin degradation and ROS level are further increased when PINK1 or Parkin is silenced in the cells treated with ethanol or acetaldehyde. Collectively, our study reveals that silibinin inhibits ethanol- or acetaldehyde-induced ferroptosis in two liver cell lines, HepG2 and HL7702 cells, providing new therapeutic strategies for alcoholic liver injury.
MeSH term(s)	Acetaldehyde/toxicity ; Cell Line ; Ethanol/toxicity ; Ferritins ; Ferroptosis ; Humans ; Iron ; Liver ; Protein Kinases ; Reactive Oxygen Species ; Silybin/pharmacology ; Ubiquitin-Protein Ligases
Chemical Substances	Reactive Oxygen Species ; Ethanol (3K9958V90M) ; Silybin (4RKY41TBTF) ; Ferritins (9007-73-2) ; Iron (E1UOL152H7) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; Acetaldehyde (GO1N1ZPR3B)
Language	English
Publishing date	2022-05-18
Publishing country	England
Document type	Journal Article
ZDB-ID	639064-x
ISSN	1879-3177 ; 0887-2333
ISSN (online)	1879-3177
ISSN	0887-2333
DOI	10.1016/j.tiv.2022.105388
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Article ; Online: Sec14l3 potentiates VEGFR2 signaling to regulate zebrafish vasculogenesis

Bo Gong / Zhihao Li / Wanghua Xiao / Guangyuan Li / Shihui Ding / Anming Meng / Shunji Jia

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 16

Abstract: The growth factor VEGF is known to regulate vasculogenesis but the downstream pathways activated are unclear. Here, the authors report that Sec14l3, a member of the PITP (phosphatidyl inositol transfer proteins) family regulates the formation of ... ...

Abstract	The growth factor VEGF is known to regulate vasculogenesis but the downstream pathways activated are unclear. Here, the authors report that Sec14l3, a member of the PITP (phosphatidyl inositol transfer proteins) family regulates the formation of zebrafish vasculature by promoting VEGFR2 endocytic trafficking.
Keywords	Science ; Q
Language	English
Publishing date	2019-04-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Sec14l3 potentiates VEGFR2 signaling to regulate zebrafish vasculogenesis

Bo Gong / Zhihao Li / Wanghua Xiao / Guangyuan Li / Shihui Ding / Anming Meng / Shunji Jia

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 16

Abstract	The growth factor VEGF is known to regulate vasculogenesis but the downstream pathways activated are unclear. Here, the authors report that Sec14l3, a member of the PITP (phosphatidyl inositol transfer proteins) family regulates the formation of zebrafish vasculature by promoting VEGFR2 endocytic trafficking.
Keywords	Science ; Q
Language	English
Publishing date	2019-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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