Lai Keane K Y, Hu Xiaohui, Chosa Keisuke, Nguyen Cu, Lin David P, Lai Keith K, Kato Nobuo, Higuchi Yusuke, Highlander Sarah K, Melendez Elizabeth, Eriguchi Yoshihiro, Fueger Patrick T, Ouellette Andre J, Chimge Nyam-Osor, Ono Masaya, Kahn Michael
Department of Molecular Medicine, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.
Cancers (Basel). 2021 Mar 14;13(6):1288. doi: 10.3390/cancers13061288.
Differential usage of Kat3 coactivators, CBP and p300, by β-catenin is a fundamental regulatory mechanism in stem cell maintenance and initiation of differentiation and repair. Based upon our earlier pharmacologic studies, p300 serine 89 (S89) is critical for controlling differential coactivator usage by β-catenin via post-translational phosphorylation in stem/progenitor populations, and appears to be a target for a number of kinase cascades. To further investigate mechanisms of signal integration effected by this domain, we generated p300 S89A knock-in mice. We show that S89A mice are extremely sensitive to intestinal insult resulting in colitis, which is known to significantly increase the risk of developing colorectal cancer. We demonstrate cell intrinsic differences, and microbiome compositional differences and differential immune responses, in intestine of S89A versus wild type mice. Genomic and proteomic analyses reveal pathway differences, including lipid metabolism, oxidative stress response, mitochondrial function and oxidative phosphorylation. The diverse effects on fundamental processes including epithelial differentiation, metabolism, immune response and microbiome colonization, all brought about by a single amino acid modification S89A, highlights the critical role of this region in p300 as a signaling nexus and the rationale for conservation of this residue and surrounding region for hundreds of million years of vertebrate evolution.
β-连环蛋白对Kat3共激活因子CBP和p300的差异性利用是干细胞维持、分化起始和修复过程中的一种基本调控机制。基于我们早期的药理学研究,p300丝氨酸89(S89)对于通过干细胞/祖细胞群体中的翻译后磷酸化来控制β-连环蛋白对共激活因子的差异性利用至关重要,并且似乎是许多激酶级联反应的靶点。为了进一步研究该结构域影响信号整合的机制,我们构建了p300 S89A基因敲入小鼠。我们发现S89A小鼠对导致结肠炎的肠道损伤极其敏感,而结肠炎已知会显著增加患结直肠癌的风险。我们证明了S89A小鼠与野生型小鼠在肠道中的细胞内在差异、微生物群组成差异以及免疫反应差异。基因组和蛋白质组分析揭示了通路差异,包括脂质代谢、氧化应激反应、线粒体功能和氧化磷酸化。单个氨基酸修饰S89A对包括上皮分化、代谢、免疫反应和微生物群定殖在内的基本过程产生的多种影响,突出了p300中该区域作为信号枢纽的关键作用,以及该残基和周围区域在数亿年脊椎动物进化过程中保守的原理。