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首页> 外文期刊>Development >Lef1-dependent Wnt/beta-catenin signalling drives the proliferative engine that maintains tissue homeostasis during lateral line development.
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Lef1-dependent Wnt/beta-catenin signalling drives the proliferative engine that maintains tissue homeostasis during lateral line development.

机译：依赖Lef1的Wnt /β-catenin信号驱动增生引擎，在侧线发育过程中维持组织稳态。

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摘要

During tissue morphogenesis and differentiation, cells must self-renew while contemporaneously generating daughters that contribute to the growing tissue. How tissues achieve this precise balance between proliferation and differentiation is, in most instances, poorly understood. This is in part due to the difficulties in dissociating the mechanisms that underlie tissue patterning from those that regulate proliferation. In the migrating posterior lateral line primordium (PLLP), proliferation is predominantly localised to the leading zone. As cells emerge from this zone, they periodically organise into rosettes that subsequently dissociate from the primordium and differentiate as neuromasts. Despite this reiterative loss of cells, the primordium maintains its size through regenerative cell proliferation until it reaches the tail. In this study, we identify a null mutation in the Wnt-pathway transcription factor Lef1 and show that its activity is required to maintain proliferation in the progenitor pool of cells that sustains the PLLP as it undergoes migration, morphogenesis and differentiation. In absence of Lef1, the leading zone becomes depleted of cells during its migration leading to the collapse of the primordium into a couple of terminal neuromasts. We show that this behaviour resembles the process by which the PLLP normally ends its migration, suggesting that suppression of Wnt signalling is required for termination of neuromast production in the tail. Our data support a model in which Lef1 sustains proliferation of leading zone progenitors, maintaining the primordium size and defining neuromast deposition rate.
机译：在组织形态发生和分化过程中，细胞必须自我更新，同时生成有助于组织生长的子代。在大多数情况下，人们对组织如何在增殖与分化之间达到这种精确的平衡还知之甚少。这部分是由于难以将组织图案形成基础的机制与调节增殖的机制分离。在移行的后侧原基（PLLP）中，增殖主要位于前导区。当细胞从该区域出现时，它们会定期组织成玫瑰花结，随后从原基上解离并分化为神经浆。尽管存在这种细胞的重复性损失，但原基通过再生性细胞增殖维持其大小，直至到达尾巴。在这项研究中，我们确定Wnt途径转录因子Lef1中的无效突变，并表明其活性是维持PLLP经历迁移，形态发生和分化的细胞祖细胞中维持增殖所必需的。在没有Lef1的情况下，前导区在迁移过程中会耗尽细胞，从而导致原基塌陷成两个末端神经瘤。我们表明，这种行为类似于PLLP正常结束其迁移的过程，这表明需要抑制Wnt信号传导才能终止尾部神经肥大的产生。我们的数据支持Lef1维持领先区域祖细胞增殖，维持原基大小并确定神经肥大沉积速率的模型。

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