Faculty of Life Sciences, Michael Smith Building, University of Manchester, Oxford Road, Manchester, UK.
Development. 2011 Apr;138(8):1583-93. doi: 10.1242/dev.063800. Epub 2011 Mar 9.
Differential cell motility, which plays a key role in many developmental processes, is perhaps most evident in examples of pattern formation in which the different cell types arise intermingled before sorting out into discrete tissues. This is thought to require heterogeneities in responsiveness to differentiation-inducing signals that result in the activation of cell type-specific genes and 'salt and pepper' patterning. How differential gene expression results in cell sorting is poorly defined. Here we describe a novel gene (hfnA) that provides the first mechanistic link between cell signalling, differential gene expression and cell type-specific sorting in Dictyostelium. HfnA defines a novel group of evolutionarily conserved HECT ubiquitin ligases with an N-terminal filamin domain (HFNs). HfnA expression is induced by the stalk differentiation-inducing factor DIF-1 and is restricted to a subset of prestalk cells (pstO). hfnA(-) pstO cells differentiate but their sorting out is delayed. Genetic interactions suggest that this is due to misregulation of filamin complex activity. Overexpression of filamin complex members phenocopies the hfnA(-) pstO cell sorting defect, whereas disruption of filamin complex function in a wild-type background results in pstO cells sorting more strongly. Filamin disruption in an hfnA(-) background rescues pstO cell localisation. hfnA(-) cells exhibit altered slug phototaxis phenotypes consistent with filamin complex hyperactivity. We propose that HfnA regulates filamin complex activity and cell type-specific motility through the breakdown of filamin complexes. These findings provide a novel mechanism for filamin regulation and demonstrate that filamin is a crucial mechanistic link between responses to differentiation signals and cell movement in patterning based on 'salt and pepper' differentiation and sorting out.
细胞的差异性迁移能力在许多发育过程中起着关键作用,在形态发生过程中表现得最为明显,在这些过程中,不同的细胞类型在分离成离散组织之前是混合在一起的。这被认为需要对分化诱导信号的反应存在异质性,从而导致细胞类型特异性基因的激活和“盐和胡椒”模式的形成。差异性基因表达如何导致细胞分选还没有明确的定义。在这里,我们描述了一种新的基因(hfnA),它为细胞信号转导、差异性基因表达和细胞类型特异性分选之间提供了第一个机制联系,在盘基网柄菌中。HfnA 定义了一组新的进化保守的 HECT 泛素连接酶,具有一个 N 端细丝蛋白结构域(HFNs)。HfnA 的表达受柄分化诱导因子 DIF-1 的诱导,并局限于一小部分前柄细胞(pstO)。hfnA(-) pstO 细胞分化,但它们的分选被延迟。遗传相互作用表明,这是由于细丝蛋白复合物活性的失调。细丝蛋白复合物成员的过表达可模拟 hfnA(-) pstO 细胞分选缺陷,而在野生型背景下破坏细丝蛋白复合物功能则导致 pstO 细胞更强的分选。在 hfnA(-)背景下破坏细丝蛋白可挽救 pstO 细胞的定位。hfnA(-)细胞表现出改变的游走光趋性表型,与细丝蛋白复合物的过度活性一致。我们提出 HfnA 通过细丝蛋白复合物的解体来调节细丝蛋白复合物的活性和细胞类型特异性迁移。这些发现为细丝蛋白的调节提供了一种新的机制,并表明细丝蛋白是基于“盐和胡椒”分化和分选的形态发生中对分化信号的反应和细胞运动之间的关键机制联系。