A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila

Summary: Neuroprotection is essential for the maintenance of normal physiological functions in the nervous system. This is especially true under stress conditions. Here, we demonstrate a novel protective function of PRL-1 against CO2 stimulation in Drosophila. In the absence of PRL-1, flies exhibit...

Full description

Bibliographic Details
Main Authors: Pengfei Guo, Xiao Xu, Fang Wang, Xin Yuan, Yinqi Tu, Bei Zhang, Huimei Zheng, Danqing Yu, Wanzhong Ge, Zhefeng Gong, Xiaohang Yang, Yongmei Xi
Format: Article
Language:English
Published: Elsevier 2019-09-01
Series:iScience
Online Access:http://www.sciencedirect.com/science/article/pii/S2589004219302512
id doaj-c25288663c244259a1433e3f2fcd4acf
record_format Article
collection DOAJ
language English
format Article
sources DOAJ
author Pengfei Guo
Xiao Xu
Fang Wang
Xin Yuan
Yinqi Tu
Bei Zhang
Huimei Zheng
Danqing Yu
Wanzhong Ge
Zhefeng Gong
Xiaohang Yang
Yongmei Xi
spellingShingle Pengfei Guo
Xiao Xu
Fang Wang
Xin Yuan
Yinqi Tu
Bei Zhang
Huimei Zheng
Danqing Yu
Wanzhong Ge
Zhefeng Gong
Xiaohang Yang
Yongmei Xi
A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
iScience
author_facet Pengfei Guo
Xiao Xu
Fang Wang
Xin Yuan
Yinqi Tu
Bei Zhang
Huimei Zheng
Danqing Yu
Wanzhong Ge
Zhefeng Gong
Xiaohang Yang
Yongmei Xi
author_sort Pengfei Guo
title A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
title_short A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
title_full A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
title_fullStr A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
title_full_unstemmed A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila
title_sort novel neuroprotective role of phosphatase of regenerating liver-1 against co2 stimulation in drosophila
publisher Elsevier
series iScience
issn 2589-0042
publishDate 2019-09-01
description Summary: Neuroprotection is essential for the maintenance of normal physiological functions in the nervous system. This is especially true under stress conditions. Here, we demonstrate a novel protective function of PRL-1 against CO2 stimulation in Drosophila. In the absence of PRL-1, flies exhibit a permanent held-up wing phenotype upon CO2 exposure. Knockdown of the CO2 olfactory receptor, Gr21a, suppresses the phenotype. Our genetic data indicate that the wing phenotype is due to a neural dysfunction. PRL-1 physically interacts with Uex and controls Uex expression levels. Knockdown of Uex alone leads to a similar wing held-up phenotype to that of PRL-1 mutants. Uex acts downstream of PRL-1. Elevated Uex levels in PRL-1 mutants prevent the CO2-induced phenotype. PRL-1 and Uex are required for a wide range of neurons to maintain neuroprotective functions. Expression of human homologs of PRL-1 could rescue the phenotype in Drosophila, suggesting a similar function in humans. : Molecular Genetics; Molecular Neuroscience Subject Areas: Molecular Genetics, Molecular Neuroscience
url http://www.sciencedirect.com/science/article/pii/S2589004219302512
work_keys_str_mv AT pengfeiguo anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xiaoxu anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT fangwang anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xinyuan anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT yinqitu anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT beizhang anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT huimeizheng anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT danqingyu anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT wanzhongge anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT zhefenggong anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xiaohangyang anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT yongmeixi anovelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT pengfeiguo novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xiaoxu novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT fangwang novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xinyuan novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT yinqitu novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT beizhang novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT huimeizheng novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT danqingyu novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT wanzhongge novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT zhefenggong novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT xiaohangyang novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
AT yongmeixi novelneuroprotectiveroleofphosphataseofregeneratingliver1againstco2stimulationindrosophila
_version_ 1725814359226056704
spelling doaj-c25288663c244259a1433e3f2fcd4acf2020-11-24T22:08:51ZengElsevieriScience2589-00422019-09-0119291302A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in DrosophilaPengfei Guo0Xiao Xu1Fang Wang2Xin Yuan3Yinqi Tu4Bei Zhang5Huimei Zheng6Danqing Yu7Wanzhong Ge8Zhefeng Gong9Xiaohang Yang10Yongmei Xi11Institute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; College of Life Sciences, Zhejiang University, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; College of Life Sciences, Zhejiang University, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaCollege of Life Sciences, Zhejiang University, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; College of Life Sciences, Zhejiang University, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; College of Life Sciences, Zhejiang University, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaThe Second Affiliated Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaDepartment of Neurobiology, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Key Laboratory of Neurobiology, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, ChinaInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; Joint Institute of Genetics and Genomic Medicine between Zhejiang University and University of Toronto, Zhejiang University, Hangzhou, Zhejiang Province 310058, China; Corresponding authorInstitute of Genetics and Department of Genetics, Division of Human Reproduction and Developmental Genetics of the Women's Hospital, Zhejiang University School of Medicine, Yuhangtang Road 866, Xihu District, Hangzhou, Zhejiang Province 310058, China; Corresponding authorSummary: Neuroprotection is essential for the maintenance of normal physiological functions in the nervous system. This is especially true under stress conditions. Here, we demonstrate a novel protective function of PRL-1 against CO2 stimulation in Drosophila. In the absence of PRL-1, flies exhibit a permanent held-up wing phenotype upon CO2 exposure. Knockdown of the CO2 olfactory receptor, Gr21a, suppresses the phenotype. Our genetic data indicate that the wing phenotype is due to a neural dysfunction. PRL-1 physically interacts with Uex and controls Uex expression levels. Knockdown of Uex alone leads to a similar wing held-up phenotype to that of PRL-1 mutants. Uex acts downstream of PRL-1. Elevated Uex levels in PRL-1 mutants prevent the CO2-induced phenotype. PRL-1 and Uex are required for a wide range of neurons to maintain neuroprotective functions. Expression of human homologs of PRL-1 could rescue the phenotype in Drosophila, suggesting a similar function in humans. : Molecular Genetics; Molecular Neuroscience Subject Areas: Molecular Genetics, Molecular Neurosciencehttp://www.sciencedirect.com/science/article/pii/S2589004219302512