PRMT5 regulates Golgi apparatus structure through methylation of the golgin GM130

Maintenance of the Golgi apparatus （GA） structure and function depends on Golgi matrix proteins. The posttranslational modification of Golgi proteins such as phosphorylation of members of the golgin and GRASP families is important for determining Golgi architecture. Some Golgi proteins including golgin-84 are also known to be methylated, but the function of golgin methylation remains unclear. Here, we show that the protein arginine methyltransferase 5 （PRMT5） localizes to the GA and forms complexes with several components involved in GA ribbon formation and vesicle tethering. PRMT5 interacts with the golgin GM130, and depletion of PRMT5 causes defects in Golgi ribbon formation. Furthermore, PRMT5 methylates N-terminal arginines in GM130, and such arginine methylation appears critical for GA ribbon formation. Our findings reveal a molecular mechanism by which PRMT5-dependent arginine methylation of GM130 controls the maintenance of GA architecture.

Neighborhood Modularization‑based Artificial Bee Colony Algorithm for Disassembly Planning with Operation Attributes

The recycling and remanufacturing of end-of-life products are significant for environmental protection and resource conservation.Disassembly is an essential process of remanufacturing end-of-life products.Effective disassembly plans help improve disassembly efficiency and reduce disassembly costs.This paper studies a disassembly planning problem with operation attributes,in which an integrated decision of the disassembly sequence,disassembly directions,and disassembly tools are made.Besides,a mathematical model is formulated with the objective of minimizing the penalty cost caused by the changing of operation attributes.Then,a neighborhood modularization-based artificial bee colony algorithm is developed,which contains a modular optimized design.Finally,two case studies with different scales and complexities are used to verify the performance of the proposed approach,and experimental results show that the proposed algorithm outperforms the two existing methods within an acceptable computational time.

Autophagy receptor CCDC50 tunes the STING-mediated interferon response in viral infections and autoimmune diseases

DNA sensing and timely activation of interferon(IFN)-mediated innate immunity are crucial for the defense against DNA virus infections and the clearance of abnormal cells.However,overactivation of immune responses may lead to tissue damage and autoimmune diseases;therefore,these processes must be intricately regulated.STING is the key adaptor protein,which is activated by cyclic GMP-AMP,the second messenger derived from cGAS-mediated DNA sensing.Here,we report that CCDC50,a newly identified autophagy receptor,tunes STING-directed type I IFN signaling activity by delivering K63-polyubiquitinated STING to autolysosomes for degradation.Knockout of CCDC50 significantly increases herpes simplex virus 1(HSV-1)-or DNA ligand-induced production of type I IFN and proinflammatory cytokines.Ccdc50-deficient mice show increased production of IFN,decreased viral replication,reduced cell infiltration,and improved survival rates compared with their wild-type littermates when challenged with HSV-1.Remarkably,the expression of CCDC50 is downregulated in systemic lupus erythematosus(SLE),a chronic autoimmune disease.CCDC50 levels are negatively correlated with IFN signaling pathway activation and disease severity in human SLE patients.CCDC50 deficiency potentiates the cGAS-STING-mediated immune response triggered by SLE serum.Thus,our findings reveal the critical role of CCDC50 in the immune regulation of viral infections and autoimmune diseases and provide insights into the therapeutic implications of CCDC50 manipulation.

Correction: Autophagy receptor CCDC50 modulates STING-mediated interferon response in viral infection and autoimmune disease

Correction to:Cellular&Molecular Immunology https://doi.org/10.1038/s41423-021-00758-w In the version of this article initially published,one unintended error was made during manuscript editing.The title of the article was not in accordance with that of the original manuscript,and the correct statement is“Autophagy receptor CCDC50 modulates STING-mediated interferon response in viral infection and autoimmune disease”.The results and conclusions are not affected.