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Rala and the exocyst control Pvr trafficking and signaling to ensure lymph gland homeostasis in Drosophila melanogaster
bioRxiv - Developmental Biology Pub Date : 2020-05-26 , DOI: 10.1101/2020.05.26.086140
Helene Knævelsrud , Caroline Baril , Gwenaëlle Gavory , Jorrit M. Enserink , Marc Therrien

The balance between hematopoietic progenitors and differentiated hemocytes is finely tuned during development. In the larval hematopoietic organ of Drosophila, called the lymph gland, the receptor tyrosine kinase Pvr signals from differentiated cells to maintain a pool of undifferentiated progenitors. However, little is known about the processes that support Pvr function. The small GTPase Ral is involved in the regulation of several membrane trafficking events. Drosophila has a single Ral protein, Rala, which has been implicated in the development of various tissues. Here, we investigated the involvement of Rala in the larval fly hematopoietic system. We discovered that the loss of Rala activity phenocopies Pvr loss of function by promoting hemocyte progenitor differentiation. Moreover, using epistasis analysis, we found that the guanine exchange factor RalGPS lies upstream of Rala in this event, whereas the exocyst and Rab11 are acting downstream. Strikingly, the loss of Rala activity leads to a considerable accumulation of Pvr at the plasma membrane, hence suggesting a trafficking defect and reduced Pvr function. Consistent with this hypothesis, Rala loss of function phenotype in the lymph gland is fully suppressed by constitutive STAT activity, which normally mediates Pvr function in the lymph gland. Together, our findings unravel a novel RalGPS-Rala-exocyst-Rab11 axis for the maintenance of lymph gland homeostasis through Pvr.

中文翻译:

拉拉和囊泡控制果蝇的运输和信号传递,以确保果蝇的淋巴腺稳态。

造血祖细胞和分化的血细胞之间的平衡在发育过程中进行了微调。在果蝇的幼虫造血器官(称为淋巴腺)中,受体酪氨酸激酶Pvr从分化的细胞发出信号,以维持未分化祖细胞的集合。但是,对于支持Pvr功能的过程知之甚少。小的GTPase Ral参与了几种膜运输事件的调控。果蝇只有一种Ral蛋白Rala,与多种组织的发育有关。在这里,我们调查了拉拉在幼虫造血系统中的参与。我们发现,通过促进血细胞祖细胞分化,Rala活性的丧失表现出Pvr功能的丧失。而且,使用上位性分析 我们发现鸟嘌呤交换因子RalGPS在这种情况下位于Rala的上游,而囊泡和Rab11在下游。引人注目的是,Rala活性的丧失导致Pvr在质膜上大量积聚,从而提示运输缺陷和Pvr功能降低。与此假设相符,本构STAT活性完全抑制了淋巴腺中Rala功能表型的丧失,而STAT活性通常会在淋巴腺中介导Pvr功能。在一起,我们的发现揭开了一个新的RalGPS-Rala-exocyst-Rab11轴,用于通过Pvr维持淋巴腺稳态。因此暗示了运输缺陷和降低的Pvr功能。与此假设相符,本构STAT活性完全抑制了淋巴腺中Rala功能表型的丧失,而STAT活性通常会在淋巴腺中介导Pvr功能。在一起,我们的发现揭开了一个新的RalGPS-Rala-exocyst-Rab11轴,用于通过Pvr维持淋巴腺稳态。因此暗示了运输缺陷和降低的Pvr功能。与此假设相符,本构STAT活性完全抑制了淋巴腺中Rala功能表型的丧失,而STAT活性通常会在淋巴腺中介导Pvr功能。在一起,我们的发现揭开了一个新的RalGPS-Rala-exocyst-Rab11轴,用于通过Pvr维持淋巴腺稳态。
更新日期:2020-05-26
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