Paolini Alessio, Duchemin Anne-Laure, Albadri Shahad, Patzel Eva, Bornhorst Dorothee, González Avalos Paula, Lemke Steffen, Machate Anja, Brand Michael, Sel Saadettin, Di Donato Vincenzo, Del Bene Filippo, Zolessi Flavio R, Ramialison Mirana, Poggi Lucia
Department of Developmental Biology/Physiology, Centre for Organismal Studies (COS) Heidelberg, Im Neuenheimer Feld 230, Heidelberg 69120, Germany.
Department of Developmental Biology/Physiology, Centre for Organismal Studies (COS) Heidelberg, Im Neuenheimer Feld 230, Heidelberg 69120, Germany Department of Ophthalmology, University of Heidelberg, Heidelberg 69120, Germany.
Development. 2015 Mar 1;142(5):832-9. doi: 10.1242/dev.118612. Epub 2015 Feb 5.
Divisions that generate one neuronal lineage-committed and one self-renewing cell maintain the balance of proliferation and differentiation for the generation of neuronal diversity. The asymmetric inheritance of apical domains and components of the cell division machinery has been implicated in this process, and might involve interactions with cell fate determinants in regulatory feedback loops of an as yet unknown nature. Here, we report the dynamics of Anillin - an essential F-actin regulator and furrow component - and its contribution to progenitor cell divisions in the developing zebrafish retina. We find that asymmetrically dividing retinal ganglion cell progenitors position the Anillin-rich midbody at the apical domain of the differentiating daughter. anillin hypomorphic conditions disrupt asymmetric apical domain inheritance and affect daughter cell fate. Consequently, the retinal cell type composition is profoundly affected, such that the ganglion cell layer is dramatically expanded. This study provides the first in vivo evidence for the requirement of Anillin during asymmetric neurogenic divisions. It also provides insights into a reciprocal regulation between Anillin and the ganglion cell fate determinant Ath5, suggesting a mechanism whereby the balance of proliferation and differentiation is accomplished during progenitor cell divisions in vivo.
产生一个神经元谱系定向细胞和一个自我更新细胞的细胞分裂维持了神经元多样性产生过程中增殖与分化的平衡。顶端结构域和细胞分裂机制成分的不对称遗传与这一过程有关，并且可能涉及与细胞命运决定因子在性质尚不清楚的调节反馈回路中的相互作用。在此，我们报告了膜收缩环蛋白（一种重要的F-肌动蛋白调节因子和沟成分）的动态变化及其对斑马鱼发育视网膜中祖细胞分裂的贡献。我们发现，不对称分裂的视网膜神经节细胞祖细胞将富含膜收缩环蛋白的中间体定位在分化子代的顶端结构域。膜收缩环蛋白低表达状态会破坏顶端结构域的不对称遗传，并影响子代细胞命运。因此，视网膜细胞类型组成受到深远影响，神经节细胞层显著扩张。这项研究为膜收缩环蛋白在不对称神经源性分裂过程中的需求提供了首个体内证据。它还为膜收缩环蛋白与神经节细胞命运决定因子Ath5之间的相互调节提供了见解，提示了一种在体内祖细胞分裂过程中实现增殖与分化平衡的机制。
