摘要 Epigenetic regulatory mechanisms allow multicellu

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論文資訊

• 類型：已發表論文
• 日期：2025-03-05

摘要

Epigenetic regulatory mechanisms allow multicellular organisms to develop distinct specialized cell identities despite having the same total genome. Cell-fate choices are based on gene expression programs and environment and cunevironmental 可能usually maintained throughout the life of the organism despite new environmental cues.進化上保守的多梳族 (PcG) 蛋白形成多梳抑制複合物，幫助協調這些發育選擇。發育後，即使面對環境擾動，這些複合物也會積極維持最終的細胞命運。 Given the crucial role of these polycomb mechanisms in providing phenotypic fidelity (i.e. maintenance of cell fate), we hypothesize that their dysregulation after development will lead tocreased phenotn regulation allowsmools fidel​​soom the creased phenot soo​​an sheals 發送s 它's” phenotype in response to environmental changes.我們將這個異常表型轉換稱為表型順應性。 We introduce a general computational evolutionary model that allows us to test our systems-level phenotypic pliancy hypothesis in-silico and in a context-independent manner. We find that 1) phenotypic fidelityis anendent manner. We find that 1) phenotypic fidelity is an emdeler procion​​ym​​ion evolution, and 2) phenotypic pliancy is an emergent systems-level property resulting from this mechanism's dysregulation. Since there is evidence that metastatic cells behave in a phenotypically pliantman, that metastatic the thatehave in a phenotypically pliantman, weh plress s emergence of phenotypic pliancy in cancer cells as a result of PcG mechanism dysregulation.我們使用來自轉移性癌症的單細胞 RNA 測序數據證實了我們的假設。我們發現轉移性癌細胞在表型上是順從的，與我們的模型預測的方式相同。作者摘要我們引入了細胞表型柔順性的概念——響應環境變化而持續異常表型轉換——並證明這種行為可能是由 Polycomb 機制失調引起的。 To overcome the incomplete knowledge about these mechanisms in higher organisms, we develop an abstract computational model to study the emergence of phenotypic pliancy from a general systems-level view by confirming gene as Polycomb mechanism patterns.我們使用單細胞 RNA-seq 轉移性癌症數據集證實了我們的假設和模型預測。我們的假設有可能揭示與異常表型轉換相關的複雜疾病的普遍現象。