Novel growth factor supporting survival of murine primordial germ cells: evidence from conditioned medium of ter fetal gonadal somatic cells
Novel growth factor supporting survival of murine primordial germ cells: evidence from conditioned medium of ter fetal gonadal somatic cells
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DOI：
10.1002/mrd.1101
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发表时间：
2001-11
影响因子：
2.5
通讯作者：
Shuji Takabayashi;Yumiko Sasaoka;M. Yamashita;T. Tokumoto;K. Ishikawa;M. Noguchi
中科院分区：
文献类型：
--
作者：
Shuji Takabayashi;Yumiko Sasaoka;M. Yamashita;T. Tokumoto;K. Ishikawa;M. Noguchi
ter（畸胎瘤，18号染色体）突变导致在交配后8.0天（dpc）来自ter同类系小鼠品系的ter/ter胚胎中原始生殖细胞（PGCs）缺乏。为了分析ter基因的功能，在此我们检测了来自+/+、+/ter或ter/ter基因型的14.5 dpc睾丸和卵巢体细胞的条件培养基（CM）对在饲养细胞上与自身体细胞“混合培养”的小鼠PGCs的影响。结果表明，+/+和+/ter CM支持9.5和11.5 dpc ICR PGC的存活，但ter/ter CM不能挽救PGC中TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）阳性凋亡，尽管其不影响PGC中的5-溴-2-脱氧尿苷掺入。+/+ CM（而非ter/ter CM）中的这种支持性物质被表征为可溶性、热不稳定且大于30 kDa。我们还发现，一些已知的PGCs及其受体的生长因子表达在ter/ter睾丸以及+/+睾丸，这表明ter功能是独立的。因此，可以得出结论，胎儿性腺体细胞表达一种新的PGC生长因子（称为TER因子），支持PGC而不是体细胞的存活，并且ter/ter睾丸中的PGC缺乏是由该因子的缺失引起的。摩尔Reprod. Dev. 60：384 - 396，© 2001 Wiley利斯公司。
The ter (teratoma, chromosome 18) mutation causes a deficiency of primordial germ cells (PGCs) in ter/ter embryos from the ter congenic mouse strain at 8.0 days post coitum (dpc). In order to analyse the function of the ter gene, here we examined effects of conditioned medium (CM) from 14.5 dpc testicular and ovarian somatic cells of +/+, +/ter, or ter/ter genotype on mouse PGCs “mixed‐cultured” with own somatic cells on feeder cells. The results showed that +/+ and +/ter CM supported survival in 9.5 and 11.5 dpc ICR PGCs but ter/ter CM did not rescue TUNEL (terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling)‐positive apoptosis in the PGCs though it did not affect 5‐bromo‐2‐deoxyuridine incorporation in PGCs. This supportive substance in +/+ CM, not ter/ter CM, was characterized as soluble, heat labile, and larger than 30 kDa. We also found that several known growth factors for PGCs and their receptors were expressed in ter/ter testes as well as +/+ testes, suggesting the ter function is independent. Thus, it was concluded that fetal gonadal somatic cells express a novel PGC growth factor (designated as TER Factor) supporting survival of PGCs not somatic cells and that the PGC deficiency in ter/ter testes is caused by a loss of this factor. Mol. Reprod. Dev. 60:384‐396, © 2001 Wiley‐Liss, Inc.