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ATAC-Seq of WT and Nedd4L-cKO Muscle stem cells

ABSTRACT: ATAC-Seq of WT and Nedd4L-cKO Muscle stem cells

PROVIDER: PRJNA962016 | ENA |

REPOSITORIES: ENA

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ATAC-Seq of WT and Nedd4L-cKO Muscle stem cells

Project description:Muscle stem cell quiescence is a complex and dynamic state. In this study we examined the role of the Ubiquitin Protease System in muscle stem cell function and quiescence. Using a genetic mouse model where Nedd4L is selectively deleted in myogenic cells, we characterized the effect of the loss of Nedd4L on muscle stem cells. With RNA-Seq we determined that the genetic deletion of Nedd4L resulted in the transition of the muscle stem cells out of deep quiescence and into Galert. Characterized by the upregulation of cell cycle genes and differentiation genes and loss of expression in numerous known quiescence genes. Nedd4L-cKO muscle stem cells are more prone to differentiation and fail to expand properly in vitro.

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Project description:SAGA and ATAC are two related transcriptional coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development but the precise role of the two complexes in RNA polymerase II transcription in mammals is less understood. To determine whether SAGA and ATAC have redundant or specific functions dependent on their HAT activities, we compared the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC subunits are required for complex assembly, mouse ESC growth and self-renewal. Additionally, ATAC, but not SAGA subunits are required for ESC viability by regulating the transcription of translation-related genes. Surprisingly, depletion of specific or shared HAT module subunits caused a global decrease in histone H3K9 acetylation, but did not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for viability and self-renewal of mouse ESCs by regulating transcription through different pathways, in a HAT-independent manner.

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