...
首页> 外文期刊>Developmental cell >Actin Filament Elongation in Arp2/3-Derived Networks Is Controlled by Three Distinct Mechanisms
【24h】

Actin Filament Elongation in Arp2/3-Derived Networks Is Controlled by Three Distinct Mechanisms

机译:Arp2 / 3衍生网络中的肌动蛋白丝伸长受三种不同机制的控制。

获取原文
获取原文并翻译 | 示例

摘要

Spatial and temporal control of actin filament barbed end elongation is crucial for force generation by actin networks. In this study, genetics, cell biology, and biochemistry were used to reveal three complementary mechanisms that regulate actin filament barbed end elongation in Arp2/3-derived networks. Aip1 inhibits elongation of aged ADP-actin filaments decorated with cofilin and, together with capping protein (CP), maintains a high level of assembly-competent actin species. We identified Abp1 and Aim3 as two additional proteins that work together to inhibit barbed end elongation. Abp1/Aim3 collaborates with CP to control elongation of newly assembled ATP-actin filaments to organize filament polarity within actin networks. Thus, three distinct mechanisms control filament elongation in different regions of Arp2/3 networks, maintaining pools of assembly-competent actin species while ensuring proper filament polarity and facilitating force production. Michelot et al. uncover three complementary mechanisms that control actin filament elongation in different regions of Arp2/3 networks. Inhibition of ADP-actin filaments by Aip1/Cofilin and capping protein (CP) acting in conjunction with Abp1/Aim3/CP-mediated ATP-actin filament elongation maintains pools of assembly-competent actin species while ensuring filament polarity and facilitating force production.
机译:肌动蛋白丝带刺末端伸长的时空控制对于肌动蛋白网络产生力至关重要。在这项研究中,遗传学,细胞生物学和生物化学被用来揭示在Arp2 / 3衍生的网络中调节肌动蛋白丝倒刺末端伸长的三种互补机制。 Aip1抑制装饰有cofilin的ADP-actin老化丝的伸长,并与封端蛋白(CP)一起保持高水平的装配能力肌动蛋白。我们确定Abp1和Aim3为两个额外的蛋白,它们共同抑制带刺的末端延长。 Abp1 / Aim3与CP合作控制新组装的ATP-肌动蛋白丝的伸长,从而在肌动蛋白网络内组织丝的极性。因此,三种不同的机制可控制Arp2 / 3网络不同区域中的细丝伸长,在确保适当的细丝极性和促进力产生的同时,保持具有装配能力的肌动蛋白种类的集合。 Michelot等。揭示了控制Arp2 / 3网络不同区域中肌动蛋白丝伸长的三种互补机制。 Aip1 / Cofilin对ADP-肌动蛋白丝的抑制作用以及与Abp1 / Aim3 / CP介导的ATP-肌动蛋白丝伸长作用共同作用的封端蛋白(CP)可以维持具有装配能力的肌动蛋白种类,同时确保细丝极性并促进产生力。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号