Sato Miyuki, Sato Ken, Liou Willisa, Pant Saumya, Harada Akihiro, Grant Barth D
Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ, USA.
EMBO J. 2008 Apr 23;27(8):1183-96. doi: 10.1038/emboj.2008.54. Epub 2008 Mar 20.
Using Caenorhabditis elegans genetic screens, we identified receptor-mediated endocytosis (RME)-4 and RME-5/RAB-35 as important regulators of yolk endocytosis in vivo. In rme-4 and rab-35 mutants, yolk receptors do not accumulate on the plasma membrane as would be expected in an internalization mutant, rather the receptors are lost from cortical endosomes and accumulate in dispersed small vesicles, suggesting a defect in receptor recycling. Consistent with this, genetic tests indicate the RME-4 and RAB-35 function downstream of clathrin, upstream of RAB-7, and act synergistically with recycling regulators RAB-11 and RME-1. We find that RME-4 is a conserved DENN domain protein that binds to RAB-35 in its GDP-loaded conformation. GFP-RME-4 also physically interacts with AP-2, is enriched on clathrin-coated pits, and requires clathrin but not RAB-5 for cortical association. GFP-RAB-35 localizes to the plasma membrane and early endocytic compartments but is lost from endosomes in rme-4 mutants. We propose that RME-4 functions on coated pits and/or vesicles to recruit RAB-35, which in turn functions in the endosome to promote receptor recycling.
通过秀丽隐杆线虫遗传筛选,我们确定受体介导的内吞作用(RME)-4和RME-5/RAB-35是体内卵黄内吞作用的重要调节因子。在rme-4和rab-35突变体中,卵黄受体不像内化突变体中预期的那样在质膜上积累,而是从皮质内体丢失并在分散的小泡中积累,这表明受体回收存在缺陷。与此一致的是,遗传学测试表明RME-4和RAB-35在网格蛋白下游、RAB-7上游发挥作用,并与回收调节因子RAB-11和RME-1协同作用。我们发现RME-4是一种保守的DENN结构域蛋白,它以GDP负载的构象与RAB-35结合。GFP-RME-4也与AP-2发生物理相互作用,在网格蛋白包被小窝上富集,并且在皮质区域定位时需要网格蛋白而不是RAB-5。GFP-RAB-35定位于质膜和早期内吞区室,但在rme-4突变体中从内体丢失。我们提出RME-4在包被小窝和/或小泡上发挥作用以招募RAB-35,而RAB-35反过来在内体中发挥作用以促进受体回收。