Takada Tatsuyuki, Iida Keiko, Sasaki Hiroshi, Taira Masanori, Kimura Hiroshi
Department of Experimental Radiology, Shiga University of Medical Science, Ohtsu, Japan.
Int J Dev Biol. 2005;49(7):891-4. doi: 10.1387/ijdb.052031tt.
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 erythroleukemic 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 pattern of ARL6 during early mouse development by whole-mount in situ hybridization and found that interestingly, ARL6 mRNA 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).
ADP核糖基化因子(ARF)样蛋白6(ARL6)是小GTP酶的ARF样蛋白(ARL)亚家族的成员(莫斯,1995;沙维耶,1999)。ARL在进化过程中高度保守,其中大多数具有GTP结合和水解所需的共有序列(帕斯夸拉托,2002)。在ARL中,最初从J2E红白血病细胞系中分离出来的ARL6在其共有序列上存在差异,并且已证明其表达在成年小鼠中仅限于脑和肾(英格利,1999)。最近,有报道称ARL6基因的突变会导致人类3型巴德-比德尔综合征,并且ARL6参与秀丽隐杆线虫的纤毛运输(蒋,2004;范,2004)。在此,我们通过全胚胎原位杂交研究了ARL6在小鼠早期发育过程中的表达模式,有趣的是发现,在交配后7.0 - 7.5天(dpc)的胚胎中,ARL6 mRNA定位于节点周围,而在外胚层中也发现了微弱表达。在后期阶段(8.5 dpc),ARL6在神经板中表达,可能也在体节中表达。基于这些结果,结合人类和秀丽隐杆线虫的研究结果(蒋,2004;范,2004),讨论了ARL6在早期发育中的可能作用。