Plasticity between MyoC- and MyoA-glideosomes: an example of functional compensation in Toxoplasma gondii invasion.
Plasticity between MyoC- and MyoA-glideosomes: an example of functional compensation in Toxoplasma gondii invasion.
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DOI：
10.1371/journal.ppat.1004504
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发表时间：
2014-10
期刊：
影响因子：
6.7
通讯作者：
Soldati-Favre D
中科院分区：
文献类型：
--
作者：
Frénal K;Marq JB;Jacot D;Polonais V;Soldati-Favre D
滑体是一种基于肌动球蛋白的机制，其为顶复门中的运动提供动力，并参与宿主细胞入侵和从感染细胞中排出。肌球蛋白A（MyoA）是滑体的中心成分，是由酰化的滑动相关蛋白GAP 45在表膜上募集的马达。在弓形虫中，GAP 45也有助于在运动牵引期间由内膜复合物（IMC）和质膜组成的表膜的粘附。GAP 70先前被鉴定为GAP 45的一个部分，其被定制为在顶复门球虫亚群的顶帽处募集MyoA。这个家族的第三个成员，GAP 80，在这里被证明组装一个新的滑体，在基底极环招募XIV类肌球蛋白C（MyoC）。MyoC与MyoA共享相同的肌球蛋白轻链，并且还与整合的IMC蛋白GAP 50和GAP 40相互作用。此外，该复合物的一个中心组成部分，IMC相关蛋白1（IAP 1），作为限制MyoC定位到后极的关键决定因素。删除特定组件的MyoC-滑体强调安装补偿机制的组件的MyoA-滑体。相反，去除MyoA导致MyoC沿着表膜和顶帽重新定位，这是残留侵袭的原因。这两个滑动体表现出相当大的可塑性，以确保寄生虫的生存。 弓形虫可感染大多数温血动物，是人类重要的条件致病菌。这种专性细胞内寄生虫能够侵入几乎所有的有核细胞，并且与顶复门的大多数寄生虫一样，依赖于底物依赖性滑动运动来主动渗透到宿主细胞中并从受感染的细胞中排出。为运动提供动力的保守分子机器（称为滑动体）位于寄生虫的外周，并涉及分子马达肌球蛋白A（MyoA）。滑体存在于三种风味，表现出相同的整体组织和共享一些共同的组件，而空间上被限制在中央IMC，顶帽和基底极的寄生虫，分别。中央和顶端的滑体与MyoA（MyoA-滑体）相关，而基底复合体招募肌球蛋白C（MyoC）。删除MyoC-滑体的组分揭示了确保成功建立感染的互补和补偿机制的存在。这项研究突出了滑翔机械的高度复杂性和可塑性。
The glideosome is an actomyosin-based machinery that powers motility in Apicomplexa and participates in host cell invasion and egress from infected cells. The central component of the glideosome, myosin A (MyoA), is a motor recruited at the pellicle by the acylated gliding-associated protein GAP45. In Toxoplasma gondii, GAP45 also contributes to the cohesion of the pellicle, composed of the inner membrane complex (IMC) and the plasma membrane, during motor traction. GAP70 was previously identified as a paralog of GAP45 that is tailored to recruit MyoA at the apical cap in the coccidian subgroup of the Apicomplexa. A third member of this family, GAP80, is demonstrated here to assemble a new glideosome, which recruits the class XIV myosin C (MyoC) at the basal polar ring. MyoC shares the same myosin light chains as MyoA and also interacts with the integral IMC proteins GAP50 and GAP40. Moreover, a central component of this complex, the IMC-associated protein 1 (IAP1), acts as the key determinant for the restricted localization of MyoC to the posterior pole. Deletion of specific components of the MyoC-glideosome underscores the installation of compensatory mechanisms with components of the MyoA-glideosome. Conversely, removal of MyoA leads to the relocalization of MyoC along the pellicle and at the apical cap that accounts for residual invasion. The two glideosomes exhibit a considerable level of plasticity to ensure parasite survival. Toxoplasma gondii can infect most warm-blooded animals, and is an important opportunistic pathogen for humans. This obligate intracellular parasite is able to invade virtually all nucleated cells, and as with most parasites of the Apicomplexa phylum, relies on a substrate-dependent gliding motility to actively penetrate into host cells and egress from infected cells. The conserved molecular machine (named glideosome) powering motility is located at the periphery of the parasite and involves the molecular motor, myosin A (MyoA). The glideosome exists in three flavors, exhibiting the same overall organization and sharing some common components while being spatially restricted to the central IMC, the apical cap and the basal pole of the parasite, respectively. The central and apical glideosomes are associated with MyoA (MyoA-glideosome) whereas the basal complex recruits myosin C (MyoC). Deleting components of the MyoC-glideosome uncovers the existence of complementary and compensatory mechanisms that ensure successful establishment of infection. This study highlights a higher degree of complexity and plasticity of the gliding machinery.
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影响因子：
6.7
作者：
Hu K
通讯作者：
Hu K
影响因子：
7.4
作者：
MAESHIMA, M
通讯作者：
MAESHIMA, M
弓形虫 IMC 蛋白的一个新家族在协调寄生虫分裂中表现出层次结构和功能。
影响因子：
6.7
作者：
Beck, Josh R.;Rodriguez-Fernandez, Imilce A.;de Leon, Jessica Cruz;Huynh, My-Hang;Carruthers, Vern B.;Morrissette, Naomi S.;Bradley, Peter J.
通讯作者：
Bradley, Peter J.
影响因子：
48
作者：
Andenmatten, Nicole;Egarter, Saskia;Jackson, Allison J;Jullien, Nicolas;Herman, Jean-Paul;Meissner, Markus
通讯作者：
Meissner, Markus
影响因子：
3.3
作者：
Håkansson, S;Morisaki, H;Sibley, LD
通讯作者：
Sibley, LD