Details

Autor(en) / Beteiligte

• Fischer, Veronique
• Plassard, Damien
• Ye, Tao
• Reina-San-Martin, Bernardo
• Stierle, Matthieu
• Tora, Laszlo
• Devys, Didier

Titel

The related coactivator complexes SAGA and ATAC control embryonic stem cell self-renewal through acetyltransferase-independent mechanisms

Ist Teil von

• Cell reports (Cambridge), 2021-08, Vol.36 (8), p.109598-109598, Article 109598

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2021

Quelle

MEDLINE

Beschreibungen/Notizen

• SAGA (Spt-Ada-Gcn5 acetyltransferase) and ATAC (Ada-two-A-containing) are two related coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development, but the role of these complexes in RNA polymerase II transcription is less understood. To determine whether SAGA and ATAC have redundant or specific functions, we compare 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 are required for complex assembly and mouse ESC growth and self-renewal. Surprisingly, depletion of HAT module subunits causes a global decrease in histone H3K9 acetylation, but does not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for self-renewal of mouse ESCs by regulating transcription through different pathways in a HAT-independent manner. [Display omitted] •SAGA and ATAC are required for mouse ESC growth and self-renewal•SAGA and ATAC predominantly regulate different sets of genes•SAGA and ATAC have a mild global effect on Pol II transcription•SAGA and ATAC effects on Pol II transcription and cell growth are HAT independent Fischer et al. analyze the role of SAGA and ATAC coactivator complexes that share a histone acetyltransferase (HAT) subunit in mouse embryonic stem cells (ESCs). The authors separate the core and HAT activities of these complexes to show that they play non-redundant roles in maintaining ESCs, through HAT-independent pathways.