Von Stetina Stephen E, Mango Susan E
Department of Molecular and Cellular Biology, Harvard University, Boston, MA 02138, USA.
Dev Biol. 2015 Jul 1;403(1):5-14. doi: 10.1016/j.ydbio.2015.03.002. Epub 2015 Mar 12.
Cell polarity is a fundamental characteristic of epithelial cells. Classical cell biological studies have suggested that establishment and orientation of polarized epithelia depend on outside-in cues that derive from interactions with either neighboring cells or the substratum (Akhtar and Streuli, 2013; Chen and Zhang, 2013; Chung and Andrew, 2008; McNeill et al., 1990; Nejsum and Nelson, 2007; Nelson et al., 2013; Ojakian and Schwimmer, 1994; Wang et al., 1990; Yu et al., 2005). This paradigm has been challenged by examples of epithelia generated in the absence of molecules that mediate cell-cell or cell-matrix interactions, notably E-cadherin and integrins (Baas et al., 2004; Choi et al., 2013; Costa et al., 1998; Harris and Peifer, 2004; Raich et al., 1999; Roote and Zusman, 1995; Vestweber et al., 1985; Williams and Waterston, 1994; Wu et al., 2009). Here we explore an alternative hypothesis, that cadherins and integrins function redundantly to substitute for one another during epithelium formation (Martinez-Rico et al., 2010; Ojakian et al., 2001; Rudkouskaya et al., 2014; Weber et al., 2011). We use C. elegans, which possesses a single E-cadherin (Costa et al., 1998; Hardin et al., 2013; Tepass, 1999) and a single β-integrin (Gettner et al., 1995; Lee et al., 2001), and analyze the arcade cells, which generate an epithelium late in embryogenesis (Portereiko and Mango, 2001; Portereiko et al., 2004), after most maternal factors are depleted. Loss of E-cadherin(HMR-1) in combination with β-integrin(PAT-3) had no impact on the onset or formation of the arcade cell epithelium, nor the epidermis or digestive tract. Moreover, ß-integrin(PAT-3) was not enriched at the basal surface of the arcades, and the candidate PAT-3 binding partner β-laminin(LAM-1) was not detected until after arcade cell polarity was established and exhibited no obvious polarity defect when mutated. Instead, the polarity protein par-6 (Chen and Zhang, 2013; Watts et al., 1996) was required to polarize the arcade cells, and par-6 mutants exhibited mislocalized or absent apical and junctional proteins. We conclude that the arcade cell epithelium polarizes by a PAR-6-mediated pathway that is independent of E-cadherin, β-integrin and β-laminin.
细胞极性是上皮细胞的一个基本特征。经典细胞生物学研究表明,极化上皮细胞的建立和定向依赖于从与相邻细胞或基底的相互作用中获得的由外向内的信号(Akhtar和Streuli,2013年;Chen和Zhang,2013年;Chung和Andrew,2008年;McNeill等人,1990年;Nejsum和Nelson,2007年;Nelson等人,2013年;Ojakian和Schwimmer,1994年;Wang等人,1990年;Yu等人,2005年)。这种模式受到了在缺乏介导细胞-细胞或细胞-基质相互作用的分子(特别是E-钙黏蛋白和整合素)的情况下产生上皮细胞的例子的挑战(Baas等人,2004年;Choi等人,2013年;Costa等人,1998年;Harris和Peifer,2004年;Raich等人,1999年;Roote和Zusman,1995年;Vestweber等人,1985年;Williams和Waterston,1994年;Wu等人,2009年)。在这里,我们探讨另一种假说,即钙黏蛋白和整合素在上皮形成过程中功能冗余,可以相互替代(Martinez-Rico等人,2010年;Ojakian等人,2001年;Rudkouskaya等人2014年;Weber等人,2011年)。我们使用秀丽隐杆线虫,它具有单一的E-钙黏蛋白(Costa等人,1998年;Hardin等人,2013年;Tepass,1999年)和单一的β-整合素(Gettner等人,1995年;Lee等人,2001年),并分析拱廊细胞,这些细胞在胚胎发育后期(Portereiko和Mango,2001年;Portereiko等人,2004年),在大多数母体因子耗尽后产生上皮细胞。E-钙黏蛋白(HMR-1)与β-整合素(PAT-3)的缺失对拱廊细胞上皮的起始或形成没有影响,对表皮或消化道也没有影响。此外,β-整合素(PAT-3)在拱廊细胞的基底表面没有富集,候选的PAT-3结合伴侣β-层粘连蛋白(LAM-1)直到拱廊细胞极性建立后才被检测到,并且在突变时没有表现出明显的极性缺陷。相反,极性蛋白par-6(Chen和Zhang,2013年;Watts等人,1996年)是使拱廊细胞极化所必需的,par-6突变体表现出顶端和连接蛋白定位错误或缺失。我们得出结论,拱廊细胞上皮通过一条独立于E-钙黏蛋白、β-整合素和β-层粘连蛋白的PAR-6介导的途径极化。