A direct role for SNX9 in the biogenesis of filopodia.
A direct role for SNX9 in the biogenesis of filopodia.
复制标题
SNX9 在丝状伪足生物发生中的直接作用。
DOI：
10.1083/jcb.201909178
复制
发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Jarsch IK
中科院分区：
文献类型：
--
作者：
Jarsch IK
丝状伪足是指状的富含肌动蛋白的突起，从细胞表面延伸，对细胞间通讯和病原体内化非常重要。丝状伪足的小尺寸和瞬时性质与细胞内肌动蛋白调节剂的共同使用相结合，混淆了鉴定丝状伪足蛋白的尝试。在这里，我们使用噬菌体展示表型筛选分离抗体，改变肌动蛋白形态的丝状伪足样结构（FLS）在体外。我们发现，所有导致较短FLS的抗体都与SNX9相互作用，SNX9是一种肌动蛋白调节剂，在胞吞作用期间和侵入伪足结合磷酸肌醇。在细胞中，我们发现SNX9位于Xenopus发育中的特化丝状伪足，并且SNX9是被衣原体入侵劫持的丝状伪足的内源性成分。我们展示了使用抗体技术来鉴定丝状伪足样结构中使用的蛋白质，以及SNX9在丝状伪足中的作用。
Filopodia are finger-like actin-rich protrusions that extend from the cell surface and are important for cell–cell communication and pathogen internalization. The small size and transient nature of filopodia combined with shared usage of actin regulators within cells confounds attempts to identify filopodial proteins. Here, we used phage display phenotypic screening to isolate antibodies that alter the actin morphology of filopodia-like structures (FLS) in vitro. We found that all of the antibodies that cause shorter FLS interact with SNX9, an actin regulator that binds phosphoinositides during endocytosis and at invadopodia. In cells, we discover SNX9 at specialized filopodia inXenopusdevelopment and that SNX9 is an endogenous component of filopodia that are hijacked byChlamydiaentry. We show the use of antibody technology to identify proteins used in filopodia-like structures, and a role for SNX9 in filopodia.