Liver tetraploidization is controlled by a new process of incomplete cytokinesis
Liver tetraploidization is controlled by a new process of incomplete cytokinesis
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DOI：
10.1242/jcs.016907
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发表时间：
2007-10-15
影响因子：
4
通讯作者：
Desdouets, Chantal
中科院分区：
文献类型：
--
作者：
Margall-Ducos, Germain;Celton-Morizur, Severine;Desdouets, Chantal
胞质分裂在时间和空间上都得到了精确的控制，以确保遗传物质在子细胞之间的均匀分布。胞质分裂不完全可能与发育或病理细胞分裂程序有关，导致四倍体后代。在这项研究中，我们破译了在出生后肝脏生长过程中肝细胞发生不完全胞质分裂的新机制。这一过程是在断奶后在体内启动的，与后期细胞伸长的缺失有关。在这个过程中，没有观察到功能性收缩肌球蛋白环的形成；事实上，沿着皮质展开的肌动蛋白细丝并没有集中在假定的皱纹位置。由Rho-Kinase控制的肌球蛋白II向大脑皮层的募集功能受损。星体微管无法接触赤道皮质并传递其分子信号，从而阻止了RhoA途径的激活。这些发现揭示了肝脏中一种新的发育细胞分裂程序，它阻止了卵裂面的规范。
Cytokinesis is precisely controlled in both time and space to ensure equal distribution of the genetic material between daughter cells. Incomplete cytokinesis can be associated with developmental or pathological cell division programs leading to tetraploid progenies. In this study we decipher a new mechanism of incomplete cytokinesis taking place in hepatocytes during post-natal liver growth. This process is initiated in vivo after weaning and is associated with an absence of anaphase cell elongation. In this process, formation of a functional contractile actomyosin ring was never observed; indeed, actin filaments spread out along the cortex were not concentrated to the putative site of furrowing. Recruitment of myosin II to the cortex, controlled by Rho-kinase, was impaired. Astral microtubules failed to contact the equatorial cortex and to deliver their molecular signal, preventing activation of the RhoA pathway. These findings reveal a new developmental cell division program in the liver that prevents cleavage-plane specification.