Delta regulates keratinocyte spreading and motility independently of differentiation
Delta regulates keratinocyte spreading and motility independently of differentiation
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DOI：
10.1016/s0925-4773(01)00459-2
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发表时间：
2001-09-01
影响因子：
2.6
通讯作者：
Watt, FM
中科院分区：
文献类型：
--
作者：
Lowell, S;Watt, FM
在人类滤泡间表皮干细胞中，干细胞成簇分布，周围环绕着它们分化的子代细胞，即转运放大细胞，这种排列反映了细胞内聚性和运动性的差异。角化细胞表达显性负性Delta1突变体Delta（T），缺乏大部分胞质结构域，获得了转运细胞的运动行为，同时保留了它们的干细胞身份。相反，Delta1的过度表达促进角质形成细胞的凝聚力。Delta1和Delta（T）的粘附作用不依赖于SuH依赖性Notch信号传导。Delta（T）增加单个角质形成细胞的运动性和伸展性，并刺激板状伪足形成。Delta和Delta（T）与皮质肌动蛋白共定位，并在Latrunculin治疗后重新分布。我们建议，三角洲促进角质形成细胞的凝聚力，通过限制运动和讨论潜在的机制，三角洲可以与肌动蛋白细胞骨架相互作用。(C)2001爱思唯尔科学爱尔兰有限公司保留所有权利。
In human interfollicular epidermis stem cells lie in clusters surrounded by their differentiated daughters, transit amplifying cells, an arrangement that reflects differences in cell cohesiveness and motility. Keratinocytes expressing a dominant negative Delta1 mutant, Delta(T), lacking most of the cytoplasmic domain, acquired the motile behaviour of transit cells while retaining their stem cell identity. Conversely, overexpression of Delta1 promoted keratinocyte cohesiveness. The adhesive effects of Delta1 and Delta(T) were independent of SuH-dependent Notch signalling. Delta(T) increased motility and spreading of individual keratinocytes and stimulated lamellipodia formation. Delta and Delta(T) colocalised with cortical actin and redistributed on Latrunculin treatment. We propose that Delta promotes keratinocyte cohesiveness by restricting motility and discuss potential mechanisms by which Delta could interact with the actin cytoskeleton. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.