Extraribosomal functions of ribosomal proteins （RPs） have gained much attention for their implications in tumorigenesis and pro- gression. However, the regulations for transition between the ribosomal and extraribos...Extraribosomal functions of ribosomal proteins （RPs） have gained much attention for their implications in tumorigenesis and pro- gression. However, the regulations for transition between the ribosomal and extraribosomal functions of RPs are rarely reported. Herein, we identified a ribosomal protein S7-interacting partner, BCCIPβ, which modulates the functional conversion of S7. Through the N-terminal acidic domain, BCCIPβ interacts with the central basic region in S7 and regulates the extraribosomal dis- tribution of S7. BCCIPI~ deficiency abrogates the ribosomal accumulation but enhances the ribosome-free location of S7. This translocation further impairs protein synthesis and triggers ribosomal stress. Consequently, BCCIPβ deficiency suppresses the ribosomal function and initiates the extraribosomal function of S7, resulting in restriction of cell proliferation. Moreover, clinically relevant S7 mutations were found to dampen the interaction with BCCIPβ and facilitate the functional transition of S7. In conclu- sion, BCCIPβ, as a S7 modulator, contributes to the regulation of ribosomal and extraribosomai functions of S7 and has implica- tions in cell growth and tumor development.展开更多
文摘Extraribosomal functions of ribosomal proteins （RPs） have gained much attention for their implications in tumorigenesis and pro- gression. However, the regulations for transition between the ribosomal and extraribosomal functions of RPs are rarely reported. Herein, we identified a ribosomal protein S7-interacting partner, BCCIPβ, which modulates the functional conversion of S7. Through the N-terminal acidic domain, BCCIPβ interacts with the central basic region in S7 and regulates the extraribosomal dis- tribution of S7. BCCIPI~ deficiency abrogates the ribosomal accumulation but enhances the ribosome-free location of S7. This translocation further impairs protein synthesis and triggers ribosomal stress. Consequently, BCCIPβ deficiency suppresses the ribosomal function and initiates the extraribosomal function of S7, resulting in restriction of cell proliferation. Moreover, clinically relevant S7 mutations were found to dampen the interaction with BCCIPβ and facilitate the functional transition of S7. In conclu- sion, BCCIPβ, as a S7 modulator, contributes to the regulation of ribosomal and extraribosomai functions of S7 and has implica- tions in cell growth and tumor development.
