Umebayashi Kyohei, Stenmark Harald, Yoshimori Tamotsu
Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Mol Biol Cell. 2008 Aug;19(8):3454-62. doi: 10.1091/mbc.e07-10-0988. Epub 2008 May 28.
c-Cbl is the E3 ubiquitin ligase that ubiquitinates the epidermal growth factor (EGF) receptor (EGFR). On the basis of localization, knockdown, and in vitro activity analyses, we have identified the E2 ubiquitin-conjugating enzyme that cooperates with c-Cbl as Ubc4/5. Upon EGF stimulation, both Ubc4/5 and c-Cbl were relocated to the plasma membrane and then to Hrs-positive endosomes, strongly suggesting that EGFR continues to be ubiquitinated after internalization. Our time-course experiment showed that EGFR undergoes polyubiquitination, which seemed to be facilitated during the transport to Hrs-positive endosomes. Use of a conjugation-defective ubiquitin mutant suggested that receptor polyubiquitination is required for efficient interaction with Hrs and subsequent sorting to lysosomes. Abrupt inhibition of the EGFR kinase activity resulted in dissociation of c-Cbl from EGFR. Concomitantly, EGFR was rapidly deubiquitinated and its degradation was delayed. We propose that sustained tyrosine phosphorylation of EGFR facilitates its polyubiquitination in endosomes and counteracts rapid deubiquitination, thereby ensuring Hrs-dependent lysosomal sorting.
c-Cbl是一种E3泛素连接酶,可使表皮生长因子(EGF)受体(EGFR)发生泛素化。基于定位、敲低及体外活性分析,我们已确定与c-Cbl协同作用的E2泛素结合酶为Ubc4/5。在EGF刺激后,Ubc4/5和c-Cbl均重新定位于质膜,然后定位于Hrs阳性的内体,这强烈表明EGFR内化后仍持续发生泛素化。我们的时间进程实验表明,EGFR发生多聚泛素化,这在向Hrs阳性内体的转运过程中似乎得到促进。使用一种结合缺陷型泛素突变体表明,受体多聚泛素化是与Hrs有效相互作用及随后分选至溶酶体所必需的。EGFR激酶活性的突然抑制导致c-Cbl与EGFR解离。与此同时,EGFR迅速去泛素化,其降解延迟。我们提出,EGFR持续的酪氨酸磷酸化促进其在内体中的多聚泛素化,并抵消快速去泛素化,从而确保依赖Hrs的溶酶体分选。