C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis

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	C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis
	Mei, Jie 1; Zhang, Qi-Ya 1; Li, Zhi 1; Lin, Shuo 2; Gui, Jian-Fang 1
刊名	DEVELOPMENTAL BIOLOGY
	2008-07-15
卷号	319 期号:2 页码:273-284
关键词	C1q-like factor p53 caspase 3/9 brain zebrafish apoptosis G2/M phase arrest hematopoiesis
ISSN号	0012-1606
通讯作者	Gui, JF, Chinese Acad Sci, Grad Sch, Inst Hydrobiol, Ctr Dev Biol,State Key Lab Freshwater Ecol & Biot, Wuhan 430072, Peoples R China
中文摘要	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.
英文摘要	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.
学科主题	Developmental Biology
WOS标题词	Science & Technology ; Life Sciences & Biomedicine
类目[WOS]	Developmental Biology
研究领域[WOS]	Developmental Biology
关键词[WOS]	CELL-SURVIVAL ; DEATH RECEPTOR ; PRIMITIVE HEMATOPOIESIS ; HUMAN ERYTHROPOIESIS ; PROTEIN-KINASE ; P53 ; PHOSPHORYLATION ; GENES ; C1Q ; BCL-2
收录类别	SCI
语种	英语
WOS记录号	WOS:000257734600011
公开日期	2010-10-13
内容类型	期刊论文
源URL	[http://ir.ihb.ac.cn/handle/152342/8060]
专题	水生生物研究所_中科院水生所知识产出（2009年前）_期刊论文
作者单位	1.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
推荐引用方式 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.(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.