科研速览 · Science Skim继续刷下去 · Keep skimming →
◆ Cell reports2026-09-11

TRRAP enables MMB-dependent mitotic transcription and determines sensitivity to CHK1 inhibition.

Franziska Liss, Dörthe Gertzmann, Devi Bala Murugan, Leonie Bohn, Wiebke Brethauer, Phil Kuhn, Lara Wenzel, Ann-Sophie Hopff, Christina Schülein-Völk, Carsten P Ade, Grit Weinstock, Elmar Wolf, Martin Eilers, Björn von Eyss, Stefan Gaubatz

原始摘要(英文原文)· Original abstract
Precise temporal activation of mitotic genes is essential for proper cell-cycle progression, yet the chromatin-based mechanisms coordinating this process remain incompletely understood. The B-MYB-MuvB (MMB) complex is a key regulator of mitotic gene expression and becomes hyperactivated following inhibition of the ATR-CHK1 pathway, resulting in MMB-dependent premature mitotic entry, replication catastrophe, and cell death. Here, we combine proximity-dependent proteomics with a targeted siRNA screen of chromatin regulators using CHK1 inhibitor-induced premature mitosis and DNA damage as functional readouts. We identify TRRAP as a critical regulator of MMB-dependent mitotic transcription. TRRAP physically associates with B-MYB, occupies MMB target promoters, and is required for expression of mitotic genes during both normal G2/M progression and CHK1 inhibitor-induced premature mitosis. Although activation of YAP signaling bypasses the G1 requirement for TRRAP, TRRAP remains essential for G2/M gene expression and mitotic progression. Together, these findings link TRRAP-dependent chromatin regulation to MMB activity and checkpoint sensitivity.
读原文 · Read the paper ↗

AI 追问PRO

登录后使用 AI 追问

讨论区

登录后参与讨论

相关论文 · Related

TRRAP enables MMB-dependent mitotic transcription and determines sensitivity to CHK1 inhibition. — 科研速览 Science Skim