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C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis
Mei, Jie1; Zhang, Qi-Ya1; Li, Zhi1; Lin, Shuo2; Gui, Jian-Fang1; Gui, JF, Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China
2008-07-15
Source PublicationDEVELOPMENTAL BIOLOGY
ISSN0012-1606
Volume319Issue:2Pages:273-284
AbstractExcept for the complement C1q, the immunological functions of other C1q family members have remained unclear. Here we describe zebrafish C1q-like, whose transcription and translation display a uniform distribution in early embryos, and are restricted to mid-hind brain and eye in later embryos. In vitro studies showed that C1q-like could inhibit the apoptosis induced by ActD and CHX in EPC cells, through repressing caspase 3/9 activities. Moreover, its physiological roles were studied by morpholino-mediated knockdown in zebrafish embryogenesis. In comparison with control embryos, the C1q-like knockdown embryos display obvious defects in the head and cramofacial development mediated through p53-induced apoptosis, which was confirmed by the in vitro transcribed C1q-like mRNA or p53 MO co-injection. TUNEL assays revealed extensive cell death, and caspase 3/9 activity measurement also revealed about two folds increase in C1q-like morphant embryos, which was inhibited by p53 MO co-injection. Real-time quantitative PCR showed the up-regulation expression of several apoptosis regulators such as p53, mdm2, p21, Box and caspase 3, and down-regulation expression of hbae1 in the C1q-like morphant embryos. Knockdown of C1q-like in zebrafish embryos decreased hemoglobin production and impaired the organization of mesencephalic vein and other brain blood vessels. Interestingly, exposure of zebrafish embryos to UV resulted in an increase in mRNA expression of C1q-like, whereas over-expression of C1q-like was not enough resist to the damage. Furthermore, C1q-like transcription was up-regulated in response to pathogen Aeromonas hydrophila, and embryo survival significantly decreased in the C1q-like morphants after exposure to the bacteria. The data suggested that C1q-like might play an antiapoptotic and protective role in inhibiting p53-dependent and caspase 3/9-mediated apoptosis during embryogenesis, especially in the brain development, and C1q-like should be a novel regulator of cell survival during zebrafish embryogenesis. (c) 2008 Elsevier Inc. All rights reserved.; Except for the complement C1q, the immunological functions of other C1q family members have remained unclear. Here we describe zebrafish C1q-like, whose transcription and translation display a uniform distribution in early embryos, and are restricted to mid-hind brain and eye in later embryos. In vitro studies showed that C1q-like could inhibit the apoptosis induced by ActD and CHX in EPC cells, through repressing caspase 3/9 activities. Moreover, its physiological roles were studied by morpholino-mediated knockdown in zebrafish embryogenesis. In comparison with control embryos, the C1q-like knockdown embryos display obvious defects in the head and cramofacial development mediated through p53-induced apoptosis, which was confirmed by the in vitro transcribed C1q-like mRNA or p53 MO co-injection. TUNEL assays revealed extensive cell death, and caspase 3/9 activity measurement also revealed about two folds increase in C1q-like morphant embryos, which was inhibited by p53 MO co-injection. Real-time quantitative PCR showed the up-regulation expression of several apoptosis regulators such as p53, mdm2, p21, Box and caspase 3, and down-regulation expression of hbae1 in the C1q-like morphant embryos. Knockdown of C1q-like in zebrafish embryos decreased hemoglobin production and impaired the organization of mesencephalic vein and other brain blood vessels. Interestingly, exposure of zebrafish embryos to UV resulted in an increase in mRNA expression of C1q-like, whereas over-expression of C1q-like was not enough resist to the damage. Furthermore, C1q-like transcription was up-regulated in response to pathogen Aeromonas hydrophila, and embryo survival significantly decreased in the C1q-like morphants after exposure to the bacteria. The data suggested that C1q-like might play an antiapoptotic and protective role in inhibiting p53-dependent and caspase 3/9-mediated apoptosis during embryogenesis, especially in the brain development, and C1q-like should be a novel regulator of cell survival during zebrafish embryogenesis. (c) 2008 Elsevier Inc. All rights reserved.
SubtypeArticle
KeywordC1q-like Factor P53 Caspase 3/9 Brain Zebrafish Apoptosis G2/m Phase Arrest Hematopoiesis
Department[Mei, Jie; Zhang, Qi-Ya; Li, Zhi; Gui, Jian-Fang] Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China; [Lin, Shuo] Univ Calif Los Angeles, Dept Mol Cell & Dev Biol, Los Angeles, CA 90095 USA
Subject AreaDevelopmental Biology
DOI10.1016/j.ydbio.2008.04.022
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Indexed BySCI
Language英语
WOS Research AreaDevelopmental Biology
WOS SubjectDevelopmental Biology
WOS IDWOS:000257734600011
WOS KeywordCELL-SURVIVAL ; DEATH RECEPTOR ; PRIMITIVE HEMATOPOIESIS ; HUMAN ERYTHROPOIESIS ; PROTEIN-KINASE ; P53 ; PHOSPHORYLATION ; GENES ; C1Q ; BCL-2
Citation statistics
Cited Times:55[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/8060
Collection期刊论文
Corresponding AuthorGui, JF, Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China
Affiliation1.Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China
2.Univ Calif Los Angeles, Dept Mol Cell & Dev Biol, Los Angeles, CA 90095 USA
Recommended Citation
GB/T 7714
Mei, Jie,Zhang, Qi-Ya,Li, Zhi,et al. C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis[J]. DEVELOPMENTAL BIOLOGY,2008,319(2):273-284.
APA Mei, Jie,Zhang, Qi-Ya,Li, Zhi,Lin, Shuo,Gui, Jian-Fang,&Gui, JF, Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China.(2008).C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis.DEVELOPMENTAL BIOLOGY,319(2),273-284.
MLA Mei, Jie,et al."C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis".DEVELOPMENTAL BIOLOGY 319.2(2008):273-284.
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