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首页> 外文期刊>The international journal of developmental biology >Expression of ADP-ribosylation factor (ARF)-like protein 6 during mouse embryonic development
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Expression of ADP-ribosylation factor (ARF)-like protein 6 during mouse embryonic development

机译:小鼠胚胎发育过程中ADP-核糖基化因子(ARF)样蛋白6的表达

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ADP-ribosylation factor (ARF)-like protein 6 (ARL6) is a member of the ARF-like protein (ARL) subfamily of small GTPases (Moss, 1995; Chavrier, 1999). ARLs are highly conserved through evolution and most of them possess the consensus sequence required for GTP binding and hydrolysis (Pasquallato, 2002). Among ARLs, ARL6 which was initially isolated from a J2E erythroleukernic cell line is divergent in its consensus sequences and its expression has been shown to be limited to the brain and kidney in adult mouse (Ingley, 1999). Recently, it was reported that mutations of the ARL6 gene cause type 3 Bardet-Biedl syndrome in humans and that ARL6 is involved in ciliary transport in C. elegans (Chiang, 2004; Fan, 2004). Here, we investigated the expression pat-tern of ARL6 during early mouse development by whole-mount in situ hybridization and found that interestingly, ARL6mRNA was localized around the node at 7.0-7.5 days post coitum (dpc) embryos, while weak expression was also found in the ectoderm. At the later stage (8.5 dpc) ARL6 was expressed in the neural plate and probably in the somites. Based on these results, a possible role of ARL6 in early development is discussed in relation to the findings in human and C. elegans (Chiang, 2004; Fan, 2004).
机译:ADP-核糖基化因子(ARF)样蛋白6(ARL6)是小GTPase的ARF样蛋白(ARL)亚家族的成员(Moss,1995; Chavrier,1999)。 ARL通过进化高度保守,并且大多数具有GTP结合和水解所需的共有序列(Pasquallato,2002)。在ARL中,最初从J2E红白血病细胞系中分离出的ARL6在共有序列上存在差异,并且已证明其表达仅限于成年小鼠的大脑和肾脏(Ingley,1999)。最近,据报道,ARL6基因的突变引起人类3型Bardet-Biedl综合征,而ARL6参与秀丽隐杆线虫的纤毛运输(Chiang,2004; Fan,2004)。在这里,我们通过整装原位杂交研究了小鼠早期发育过程中ARL6的表达模式,发现有趣的是,ARL6mRNA的位置是在Coitum(dpc)胚胎后7.0-7.5天,位于结节周围。在外胚层中发现。在后期(8.5 dpc),ARL6在神经板中以及可能在体节中表达。基于这些结果,与人类和秀丽隐杆线虫的发现相关,讨论了ARL6在早期发育中的可能作用(Chiang,2004; Fan,2004)。

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