Kosno Martyna, Currie Simon L, Kumar Ashwani, Xing Chao, Rosen Michael K
Department of Biophysics and Howard Hughes Medical Institute, UT Southwestern Medical Center, Dallas TX, 75390.
Eugene McDermott Center for Human Growth and Development, UT Southwestern Medical Center, Dallas TX, 75390.
bioRxiv. 2023 May 11:2023.05.11.540414. doi: 10.1101/2023.05.11.540414.
Aberrant formation of biomolecular condensates has been proposed to play a role in several cancers. The oncogenic fusion protein BRD4-NUT forms condensates and drives changes in gene expression in Nut Carcinoma (NC). Here we sought to understand the molecular elements of BRD4-NUT and its associated histone acetyltransferase (HAT), p300, that promote these activities. We determined that a minimal fragment of NUT (MIN) in fusion with BRD4 is necessary and sufficient to bind p300 and form condensates. Furthermore, a BRD4-p300 fusion protein also forms condensates and drives gene expression similarly to BRD4-NUT(MIN), suggesting the p300 fusion may mimic certain features of BRD4-NUT. The intrinsically disordered regions, transcription factor-binding domains, and HAT activity of p300 all collectively contribute to condensate formation by BRD4-p300, suggesting that these elements might contribute to condensate formation by BRD4-NUT. Conversely, only the HAT activity of BRD4-p300 appears necessary to mimic the transcriptional profile of cells expressing BRD4-NUT. Our results suggest a model for condensate formation by the BRD4-NUT:p300 complex involving a combination of positive feedback and phase separation, and show that multiple overlapping, yet distinct, regions of p300 contribute to condensate formation and transcriptional regulation.
生物分子凝聚物的异常形成被认为在几种癌症中发挥作用。致癌融合蛋白BRD4-NUT形成凝聚物并驱动核蛋白癌(NC)中的基因表达变化。在这里,我们试图了解BRD4-NUT及其相关组蛋白乙酰转移酶(HAT)p300促进这些活性的分子元件。我们确定与BRD4融合的NUT最小片段(MIN)对于结合p300和形成凝聚物是必要且充分的。此外,BRD4-p300融合蛋白也形成凝聚物并与BRD4-NUT(MIN)类似地驱动基因表达,这表明p300融合可能模拟了BRD4-NUT的某些特征。p300的内在无序区域、转录因子结合结构域和HAT活性共同促成了BRD4-p300的凝聚物形成,这表明这些元件可能促成了BRD4-NUT的凝聚物形成。相反,BRD4-p300的HAT活性似乎是模拟表达BRD4-NUT的细胞转录谱所必需的。我们的结果提出了一个BRD4-NUT:p300复合物凝聚物形成的模型,该模型涉及正反馈和相分离的组合,并表明p300的多个重叠但不同的区域促成了凝聚物形成和转录调控。