4.7 Article

Regulation of centrosome movements by Numb and the Collapsin Response Mediator Protein during Drosophila sensory progenitor asymmetric division

期刊

DEVELOPMENT
卷 140, 期 13, 页码 2657-2668

出版社

COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.087338

关键词

Notch signalling; Asymmetric cell division; Centrosome; Drosophila; Cytokinesis; Rab11

资金

  1. Fondation pour la recherche medicale [26329]
  2. Institut National du Cancer [4731]
  3. l'Association pour la recherche sur le cancer (ARC) [ARC 4830]
  4. L'Agence nationale de la recherche [BLAN07-3-207540]
  5. L'Agence nationale de la recherche [MorphoDro]
  6. European Research Council [CePoDro 209718]
  7. Ministere de l'enseignement superieur et de la recherche
  8. ARC [1185]
  9. Erwin Schrodinger fellowship of the Austrian Science Fund
  10. European Molecular Biology Organization long-term fellowship ALTF [42-2009]

向作者/读者索取更多资源

Asymmetric cell division generates cell fate diversity during development and adult life. Recent findings have demonstrated that during stem cell divisions, the movement of centrosomes is asymmetric in prophase and that such asymmetry participates in mitotic spindle orientation and cell polarization. Here, we have investigated the dynamics of centrosomes during Drosophila sensory organ precursor asymmetric divisions and find that centrosome movements are asymmetric during cytokinesis. We demonstrate that centrosome movements are controlled by the cell fate determinant Numb, which does not act via its classical effectors, Sanpodo and alpha-Adaptin, but via the Collapsin Response Mediator Protein (CRMP). Furthermore, we find that CRMP is necessary for efficient Notch signalling and that it regulates the duration of the pericentriolar accumulation of Rab11-positive endosomes, through which the Notch ligand, Delta is recycled. Our work characterizes an additional mode of asymmetric centrosome movement during asymmetric divisions and suggests a model whereby the asymmetry in centrosome movements participates in differential Notch activation to regulate cell fate specification.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据