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导致ter/ter同源近交系小鼠生殖细胞缺陷但不导致睾丸或卵巢畸胎癌发生的ter突变。

The ter mutation responsible for germ cell deficiency but not testicular nor ovarian teratocarcinogenesis in ter / ter congenic mice.

作者信息

Noguchi Motoko, Watanabe Chiaki, Kobayashi Takashi, Kuwashima Miho, Sakurai Takayuki, Katoh Hideki, Moriwaki Kazuo

机构信息

Department of Biology, Faculty of Science, Shizuoka University, Ohya 836, Shizuoka 422, Japan.

Department of Genetics, Central Institute for Experimental Animals, Kawasaki 216, Japan.

出版信息

Dev Growth Differ. 1996 Feb;38(1):59-69. doi: 10.1046/j.1440-169X.1996.00008.x.

DOI:10.1046/j.1440-169X.1996.00008.x
PMID:37282297
Abstract

The ter (teratoma) gene causes germ cell deficiency and a high incidence of congenital testicular teratomas derived from primordial germ cells in 129/Sv-ter strain mice. Ovarian teratomas in LTXBJ mice originate from ovarian parthenotes. In order to study the function of the ter gene in germ cell development and teratocarcinogenesis, we examined the influence of a foreign genetic background on the ter action by introducing the ter gene of 129/Sv-ter strain mice into C57BL/6J, LTXBJ and C3H/HeJ genetic backgrounds by the backcross method and by thus establishing B6-ter, LTXBJ-ter and C3H-ter ter congenic strains, respectively. Histological analysis showed that germ cell deficiency occurred in both sexes of the ter mutants, through the fetal stages to adulthood, but that congenital testicular teratocarcinogenesis did not occur after the fifth backcross generation. The ter/ter gonads were smaller than normal (+/+ or +/ter). Experimental testicular teratomas never developed from intratesticular grafts of B6-ter genital ridges. LTXBJ-ter/ter females had no ovarian teratomas. It is concluded that the ter gene is solely responsible for germ cell deficiency, but not testicular teratocarcinogenesis, in ter congenic strains having background genes other than 129/Sv-ter and that the ter gene is not involved in ovarian teratocarcinogenesis.

摘要

ter(畸胎瘤)基因会导致生殖细胞缺陷,并使129/Sv-ter品系小鼠中源自原始生殖细胞的先天性睾丸畸胎瘤发病率很高。LTXBJ小鼠的卵巢畸胎瘤起源于卵巢孤雌生殖细胞。为了研究ter基因在生殖细胞发育和畸胎癌发生中的作用,我们通过回交法将129/Sv-ter品系小鼠的ter基因导入C57BL/6J、LTXBJ和C3H/HeJ遗传背景中,从而分别建立了B6-ter、LTXBJ-ter和C3H-ter ter同源近交系,以此来检测外来遗传背景对ter基因作用的影响。组织学分析表明,ter突变体的两性从胎儿期到成年期均出现生殖细胞缺陷,但在第五代回交后未发生先天性睾丸畸胎癌。ter/ter性腺比正常的(+/+或+/ter)小。B6-ter生殖嵴的睾丸内移植从未形成实验性睾丸畸胎瘤。LTXBJ-ter/ter雌性小鼠没有卵巢畸胎瘤。得出的结论是,在具有129/Sv-ter以外背景基因的ter同源近交系中,ter基因是生殖细胞缺陷的唯一原因,但不是睾丸畸胎癌发生的原因,并且ter基因不参与卵巢畸胎癌的发生。

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1
The ter mutation responsible for germ cell deficiency but not testicular nor ovarian teratocarcinogenesis in ter / ter congenic mice.导致ter/ter同源近交系小鼠生殖细胞缺陷但不导致睾丸或卵巢畸胎癌发生的ter突变。
Dev Growth Differ. 1996 Feb;38(1):59-69. doi: 10.1046/j.1440-169X.1996.00008.x.
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MC4R mutant mice develop ovarian teratomas.MC4R 突变小鼠会发展出卵巢畸胎瘤。
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A recessive mutation (ter) causing germ cell deficiency and a high incidence of congenital testicular teratomas in 129/Sv-ter mice.一种隐性突变(ter)导致129/Sv-ter小鼠生殖细胞缺乏以及先天性睾丸畸胎瘤的高发病率。
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The ter mutation first causes primordial germ cell deficiency in ter/ter mouse embryos at 8 days of gestation.ter突变首先在妊娠8天时导致ter/ter小鼠胚胎中的原始生殖细胞缺乏。
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The ter primordial germ cell deficiency mutation maps near Grl-1 on mouse chromosome 18.该原始生殖细胞缺陷突变位于小鼠第18号染色体上Grl-1附近。
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Identification of genomic locus responsible for experimentally induced testicular teratoma 1 (ett1) on mouse Chr 18.鉴定小鼠18号染色体上与实验诱导性睾丸畸胎瘤1(ett1)相关的基因组位点。
Mamm Genome. 2014 Aug;25(7-8):317-26. doi: 10.1007/s00335-014-9529-8. Epub 2014 Jul 5.
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Experimental production of testicular teratomas in the mouse.小鼠睾丸畸胎瘤的实验性生成
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BAX-mediated cell death affects early germ cell loss and incidence of testicular teratomas in Dnd1(Ter/Ter) mice.BAX介导的细胞死亡影响Dnd1(Ter/Ter)小鼠早期生殖细胞丢失及睾丸畸胎瘤的发生率。
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[Important roles of oocytes, follicles and corpora lutea in ovarian teratocarcino-genesis in mice].[卵母细胞、卵泡和黄体在小鼠卵巢畸胎癌发生中的重要作用]
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The ter mutation in the rat Dnd1 gene initiates gonadal teratomas and infertility in both genders.大鼠 Dnd1 基因中的 ter 突变会导致两性性腺生殖细胞瘤和不育。
PLoS One. 2012;7(5):e38001. doi: 10.1371/journal.pone.0038001. Epub 2012 May 24.

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The Mc4r gene is responsible for the development of experimentally induced testicular teratomas.Mc4r 基因负责实验性诱导的睾丸畸胎瘤的发展。
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Loss of Dead end1 induces testicular teratomas from primordial germ cells that failed to undergo sexual differentiation in embryonic testes.

本文引用的文献

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EXPERIMENTAL PRODUCTION OF TESTICULAR TERATOMAS IN MICE.小鼠睾丸畸胎瘤的实验性产生
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Gene-induced embryological modifications of primordial germ cells in the mouse.基因诱导的小鼠原始生殖细胞胚胎学修饰
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MC4R mutant mice develop ovarian teratomas.MC4R 突变小鼠会发展出卵巢畸胎瘤。
Sci Rep. 2021 Feb 10;11(1):3483. doi: 10.1038/s41598-021-83001-w.
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Mouse dead end1 acts with Nanos2 and Nanos3 to regulate testicular teratoma incidence.鼠标末端 1 与 Nanos2 和 Nanos3 一起作用以调节睾丸生殖细胞瘤的发生率。
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Development. 2011 Jan;138(1):23-32. doi: 10.1242/dev.057000. Epub 2010 Nov 29.
8
BAX-mediated cell death affects early germ cell loss and incidence of testicular teratomas in Dnd1(Ter/Ter) mice.BAX介导的细胞死亡影响Dnd1(Ter/Ter)小鼠早期生殖细胞丢失及睾丸畸胎瘤的发生率。
Dev Biol. 2009 Apr 15;328(2):377-83. doi: 10.1016/j.ydbio.2009.01.041. Epub 2009 Feb 6.
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The identification, origin, and migration of the primordial germ cells in the mouse embryo.小鼠胚胎中原始生殖细胞的识别、起源及迁移。
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Proliferation and migration of primordial germ cells in We/We mouse embryos.We/We小鼠胚胎中原始生殖细胞的增殖与迁移。
Dev Dyn. 1993 Nov;198(3):182-9. doi: 10.1002/aja.1001980304.
6
Apoptosis in mouse primordial germ cells: a study by transmission and scanning electron microscope.小鼠原始生殖细胞中的细胞凋亡:透射电子显微镜和扫描电子显微镜研究
Anat Embryol (Berl). 1994 May;189(5):435-40. doi: 10.1007/BF00185438.
7
The ter primordial germ cell deficiency mutation maps near Grl-1 on mouse chromosome 18.该原始生殖细胞缺陷突变位于小鼠第18号染色体上Grl-1附近。
Mamm Genome. 1994 Jun;5(6):333-6. doi: 10.1007/BF00356550.
8
Follicle-stimulating hormone induction of steel factor (SLF) mRNA in mouse Sertoli cells and stimulation of DNA synthesis in spermatogonia by soluble SLF.促卵泡激素诱导小鼠支持细胞中钢因子(SLF)mRNA的表达以及可溶性钢因子对精原细胞DNA合成的刺激作用。
Dev Biol. 1993 Jan;155(1):68-74. doi: 10.1006/dbio.1993.1007.
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Tumor necrosis factor-alpha (TNF-alpha) stimulates proliferation of mouse primordial germ cells in culture.肿瘤坏死因子-α(TNF-α)可刺激培养中的小鼠原始生殖细胞增殖。
Dev Biol. 1994 Jan;161(1):91-5. doi: 10.1006/dbio.1994.1011.
10
Stem cell factor and leukemia inhibitory factor promote primordial germ cell survival by suppressing programmed cell death (apoptosis).干细胞因子和白血病抑制因子通过抑制程序性细胞死亡(凋亡)来促进原始生殖细胞的存活。
Development. 1993 Aug;118(4):1089-94. doi: 10.1242/dev.118.4.1089.