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4 results on '"FuDe Huang"'

1. Efr3b is essential for social recognition by modulating the excitability of CA2 pyramidal neurons.

Author

Xiaojie Wei, Jing Wang, Enlu Yang, Yiping Zhang, Qi Qian, Xuekun Li, Fude Huang, and Binggui Sun

Subjects
PYRAMIDAL neurons, RECOGNITION (Psychology), LABORATORY mice, CELL membranes, HIPPOCAMPUS (Brain)
Abstract

CA2 pyramidal neurons (PNs) are associated with social behaviors. The mechanisms, however, remain to be fully investigated. Here, we report that Efr3b, a protein essential for phospholipid metabolism at the plasma membrane, is widely expressed in the brain, especially in the hippocampal CA2/CA3 areas. To assess the functional significance of Efr3b in the brain, we generated Efr3bf/f mice and crossed them with Nestin-cre mice to delete Efr3b specifically in the brain. We find that Efr3b deficiency in the brain leads to deficits of social novelty recognition and hypoexcitability of CA2 PNs. We then knocked down the expression of Efr3b specifically in CA2 PNs of C57BL/6J mice, and our results showed that reducing Efr3b in CA2 PNs also resulted in deficits of social novelty recognition and hypoexcitability of CA2 PNs. More interestingly, restoring the expression of Efr3b in CA2 PNs enhances their excitability and improves social novelty recognition in Efr3b-deficient mice. Furthermore, direct activation of CA2 PNs with chemogenetics improves social behaviors in Efr3b-deficient mice. Together, our data suggest that Efr3b is essential for social novelty by modulating the excitability of CA2 PNs. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Hyccin/FAM126A deficiency reduces glial enrichment and axonal sheath, which are rescued by overexpression of a plasma membrane-targeting PI4KIIIα in Drosophila

Author

Qichao Zhang, Baozhu Zhang, Nastasia.K.H. Lim, Xiao Zhang, Shiquan Meng, Jens R. Nyengaard, Fude Huang, and Wen-An Wang

Subjects
TTC7, Cell Membrane, Green Fluorescent Proteins, Biophysics, Cell Biology, Phosphatidylinositols, Biochemistry, Axons, Minor Histocompatibility Antigens, FAM126A, Phosphotransferases (Alcohol Group Acceptor), Drosophila melanogaster, FAM126B, Hyccin, PI4KIIIα, Gene Knockdown Techniques, Multiprotein Complexes, Glia, Animals, Drosophila Proteins, Visual Pathways, Molecular Biology, Neuroglia, Protein Binding
Abstract

Hyccin/FAM126A mutations are linked to hypomyelination and congenital cataract disease (HCC), but whether and how Hyccin/FAM126A deficiency causes hypomyelination remains undetermined. This study shows Hyccin/FAM126A expression was necessary for the expression of other components of the PI4KIIIα complex in Drosophila. Knockdown of Hyccin/FAM126A in glia reduced the enrichment of glial cells, disrupted axonal sheaths and visual ability in the visual system, and these defects could be fully rescued by overexpressing either human FAM126A or FAM126B, and partially rescued by overexpressing a plasma membrane-targeting recombinant mouse PI4KIIIα. Additionally, PI4KIIIα knockdown in glia phenocopied Hyccin/FAM126A knockdown, and this was partially rescued by overexpressing the recombinant PI4KIIIα, but not human FAM126A or FAM126B. This study establishes an animal model of HCC and indicates that Hyccin/FAM126A plays an essential role in glial enrichment and axonal sheath in a cell-autonomous manner in the visual system via controlling the expression and stabilization of the PI4KIIIα complex at the plasma membrane.

Published
2022
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3. Efr3a Insufficiency Attenuates the Degeneration of Spiral Ganglion Neurons after Hair Cell Loss.

Author

Haixia Hu, Bin Ye, Le Zhang, Quan Wang, Zhiwei Liu, Suying Ji, Qiuju Liu, Jingrong Lv, Yan Ma, Ying Xu, Hao Wu, Fude Huang, and Mingliang Xiang

Subjects
RISK of deafness, HAIR cells, NEURAL physiology, NEURODEGENERATION, HIPPOCAMPUS (Brain), NEONATAL anatomy
Abstract

Sensorineural hearing loss (SNHL) is caused by an irreversible impairment of cochlear hair cells and subsequent progressive degeneration of spiral ganglion neurons (SGNs). Eighty-five requiring 3 (Efr3) is a plasma membrane protein conserved from yeast to human, and knockout of Efr3a was reported to facilitate the survival of hippocampal newborn neurons in adult mice. Previously, we found Efr3a expression in the auditory neural pathway is upregulated soon after the destruction of hair cells. Here we conducted a time-course analysis of drug-caused damage to hearing ability, hair cells and SGNs in Efr3a knocking down mice (Efr3a-/+, Efr3a KD) and their wild type littermates. Functional examination showed that both groups of mice suffered from serious hearing loss with a higher level of severity in wild type (WT) mice. Morphologic observation following drugs administration showed that both WT and Efr3a KD mice went through progressive loss of hair cells and SGNs, in association with degenerative changes in the perikarya, intracellular organelles, cell body conformation in SGNs, and the changes of SGNs in WT mice were more severe than in Efr3a KD mice. These beneficial effects of Efr3a KD could be ascribed to an increase in the expression of some neurotrophic factors and their receptors in Efr3a KD mice. Our results indicate that Efr3a insufficiency suppresses drug-caused SNHL neurodegeneration in association with an increase in the expression of some neurotrophic factors and their receptors, which may be targeted in the treatment of neurodegeneration. [ABSTRACT FROM AUTHOR]

Published
2017
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4. Genetic diseases and molecular genetics - 2

Author

Kenneth I. Glassberg, David G. Motto, Chong Zhang, Valeriy Nosikov, E.I. Christensen, Mikhail Shvetsov, Bin Zhu, Ana Paula Rodrigues Melo, Manuela Cuccurullo, Ryszard Grenda, Vladimir Tesar, Guido Gatti, Boris Utsch, Susanna Tomasoni, Nan Chen, A. Schirinzi, Nobuaki Takagi, Maria Roszkowska-Blaim, Semiramis Jamil Adad do Monte, Eric Wise, Federica Mezzabotta, Fabien Nevo, Wolf H. Fridman, Véronique Frémeaux-Bacchi, Angela D'Angelo, Joseph H. Lee, Christian Becker, Monica Ceol, Andrea Emmert, Elena Kamyshova, Dorothee Schönfeld, Dali Dalia, Adile Akdas, Peter Nürnberg, Fatiu A Arogundade, Franca Anglani, Frank Bienaimé, Carsten A. Wagner, Céline Becker, Zhaohui Wang, Maja Krzysztalowska, Kálmán Tory, João Bosco, Ali G. Gharavi, Piera Trionfini, Malgorzata Panczyk-Tomaszewska, Maria Bracale, Martijn J. Wilmer, Abubakr Sanusi, M Merta, Vera Krane, Bruno Ranchin, Marie-Agnes Dragon-Durey, Ellen Shapiro, Andrzej Ciechanowicz, Aleksey Shestakov, Karolina Skonieczna, Rémi Salomon, Pierre Ronco, Ahmet Nayir, Dominik N. Müller, Elena Ranieri, Ilenia Bernascone, Giuseppe Remuzzi, QiuJu Liu, Faddi Fakhouri, Irina Kutyrina, Patricia L. Weng, Corinne Antignac, Massimo Attanasio, Celin Schaeffer, Jitka Stekrova, Vinay Sakhuja, Jean-Luc Andre, Sidarth Kumar Sethi, Laura Zagato, Giorgio Casari, Pauling Chu, Frank Breunig, L Salawu, Olivier Gribouval, I. Meij, Leo A. H. Monnens, Dorella Del Prete, Mustafa Solak, Mieczyslaw Litwin, Loreto Gesualdo, Nazim Denizli, P. Cerullo, Lambertus P. van den Heuvel, Christoph Wanner, Shih-Hua Lin, W. van't Hoff, P. Deen, Muheez A. Durosinmi, Christian Noel, Frank Weidemann, G. Messina, Lorena Longaretti, Pinar Ata Eren, Veronika Elisakova, Emilia Tiralongo, Ling Qin, Stanislava Svobodova, Gian Marco Ghiggeri, Marta Drozdzynska, Anne-Laure Sellier-Leclerc, Sung-Sen Yang, Jarosław Peregud-Pogorzelski, José Adail Fonseca de Castro, Chiara Lanzani, Lino Merlino, Fabrizio Dal Piaz, Cristina Malaventura, Chantal Loirat, Wen Zhang, Monica Dagnino, Marco Simonini, Vivekanand Jha, Lina Artifoni, Lorena Citterio, Gudrun Nürnberg, Grażyna Adler, Friedhelm Hildebrandt, Elisa Benetti, Lorenzo A. Calò, Michael Zirbs, Terry W. Hensle, Eduardo Machuca, Arnaud Garnier, Solmaz Erdem, Andrzej Brodkiewicz, Caroline Blanc, Audrey Pawtowski, Miriam Galbusera, Muzzamil Hassan, M. Belingheri, Hong Ren, Anita Konka, Reiterová J, Jackeline Larissa Mendes de Sousa, Yasaswi Paruchuri, Luca Rampoldi, N.V. Knoers, Milada Kohoutová, L. Rampoldi, Simona Delli Carpini, Francesco Scolari, H. Mehmet Sokmen, Annalisa Vilasi, Maddalena Gigante, O. Devuyst, Antonio Malorni, Elena Levtchenko, Nirupama Chandel, Leo A. J. Kluijtmans, Giovambattista Capasso, Sam Werzberger, Zeynep Acar, Simone Sanna-Cherchi, José Tibúrcio do Monte Neto, L. Ghio, Weiming Wang, Sophie Saunier, Xavier Jeunemaitre, Robert D. Burk, FuDe Huang, Elena Brioni, Paolo Manunta, Luisa Murer, G.M. Ghiggeri, P. K. Aggarwal, Daniela Corna, Yi-Fen Lo, Ana Maria Martins, Edgar A. Otto, Adewale Akinsola, Anatália de Brito Ribeiro da Silva, Roberto Ravazzolo, Enrica Tosetto, Dorothee Schoenfeld, Yu-Juei Hsu, Claudia Izzi, Ariela Benigni, Alan Werzberger, Matthias T.F. Wolf, Gianluca Caridi, Giuseppe Bianchi, Vânia D'Almeida, Irina Davydenko, and E.N. Levtchenko

Subjects
Genetics, Transplantation, medicine.medical_specialty, Nephrology, business.industry, Molecular genetics, medicine, business, Human genetics
Published
2009
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