Effect of MCM8 deficiency on gene expression of mouse embryo fibroblasts
MCM8 is essential in the replication stress response to maintain genome stability during mitosis. The deficiency of MCM8 results in impaired proliferation and a prolonged cell cycle, which can decrease cell populations. To investigate the effect of MCM8 deficiency on gene expression, we conducted the RNA-seq in wildtype and Mcm8 knockout mouse embryo fibroblasts. We found that the majority of genes were co-expressed and the gene expression distribution was comparable between WT and KO MEFs, suggesting that the global transcription activity was not obviously affected after MCM8 deficiency. Analysis of differentially expressed genes (DEGs) showed they were enriched in pathways including stem cell differentiation and cell fate commitment. In addition, to determine whether MCM8 is potentially involved in regulating splicing, as strongly suggested by the MCM8 interactome, we also performed alternative splicing (AS) analysis on RNA-seq data. Our data suggested that MCM8 may not function in splicing. Overall design: To investigate the function of MCM8 in the regulation of cell growth, we acquired and cultured wildtype and Mcm8 knockout mouse embryo fibroblasts from embryo at embryonic day 13.5. Comparative gene expression profiling analysis of RNA-seq data for wildtype and Mcm8 knockout mouse embryo fibroblasts.