Seiler S, Nargang F E, Steinberg G, Schliwa M
Adolf-Butenandt-Institut, Zellbiologie, University of Munich, Germany.
EMBO J. 1997 Jun 2;16(11):3025-34. doi: 10.1093/emboj/16.11.3025.
Kinesin is a force-generating molecule that is thought to translocate organelles along microtubules, but its precise cellular function is still unclear. To determine the role of kinesin in vivo, we have generated a kinesin-deficient strain in the simple cell system Neurospora crassa. Null cells exhibit severe alterations in cell morphogenesis, notably hyphal extension, morphology and branching. Surprisingly, the movement of organelles visualized by video microscopy is hardly affected, but apical hyphae fail to establish a Spitzenkörper, an assemblage of secretory vesicles intimately linked to cell elongation and morphogenesis in Neurospora and other filamentous fungi. As cell morphogenesis depends on polarized secretion, our findings demonstrate that a step in the secretory pathway leading to cell shape determination and cell elongation cannot tolerate a loss of kinesin function. The defect is suggested to affect the transport of small, secretory vesicles to the site involved in protrusive activity, resulting in the uncoordinated insertion of new cell wall material over much of the cell surface. These observations have implications for the presumptive function of kinesin in more complex cell systems.
驱动蛋白是一种能产生力的分子，被认为可沿微管转运细胞器，但其确切的细胞功能仍不清楚。为了确定驱动蛋白在体内的作用，我们在简单细胞系统粗糙脉孢菌中构建了一个驱动蛋白缺陷型菌株。缺失驱动蛋白的细胞在细胞形态发生上表现出严重改变，尤其是菌丝延伸、形态和分支。令人惊讶的是，通过视频显微镜观察到的细胞器运动几乎未受影响，但顶端菌丝无法形成顶体，顶体是一种分泌囊泡的集合体，与粗糙脉孢菌及其他丝状真菌的细胞伸长和形态发生密切相关。由于细胞形态发生依赖于极性分泌，我们的研究结果表明，分泌途径中导致细胞形状确定和细胞伸长的一个步骤无法耐受驱动蛋白功能的丧失。这种缺陷被认为会影响小分泌囊泡向参与突出活动部位的运输，导致新细胞壁物质在细胞表面大部分区域无序插入。这些观察结果对驱动蛋白在更复杂细胞系统中的假定功能具有启示意义。
