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细胞状态速度对静止-增殖命运决定的惯性效应。

Inertial effect of cell state velocity on the quiescence-proliferation fate decision.

作者信息

Venkatachalapathy Harish, Brzakala Cole, Batchelor Eric, Azarin Samira M, Sarkar Casim A

机构信息

Department of Chemical Engineering and Materials Science, University of Minnesota, Minneapolis, MN, USA.

Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, USA.

出版信息

NPJ Syst Biol Appl. 2024 Oct 2;10(1):111. doi: 10.1038/s41540-024-00428-3.

Abstract

Energy landscapes can provide intuitive depictions of population heterogeneity and dynamics. However, it is unclear whether individual cell behavior, hypothesized to be determined by initial position and noise, is faithfully recapitulated. Using the p21-/Cdk2-dependent quiescence-proliferation decision in breast cancer dormancy as a testbed, we examined single-cell dynamics on the landscape when perturbed by hypoxia, a dormancy-inducing stress. Combining trajectory-based energy landscape generation with single-cell time-lapse microscopy, we found that a combination of initial position and velocity on a p21/Cdk2 landscape, but not position alone, was required to explain the observed cell fate heterogeneity under hypoxia. This is likely due to additional cell state information such as epigenetic features and/or other species encoded in velocity but missing in instantaneous position determined by p21 and Cdk2 levels alone. Here, velocity dependence manifested as inertia: cells with higher cell cycle velocities prior to hypoxia continued progressing along the cell cycle under hypoxia, resisting the change in landscape towards cell cycle exit. Such inertial effects may markedly influence cell fate trajectories in tumors and other dynamically changing microenvironments where cell state transitions are governed by coordination across several biochemical species.

摘要

能量景观可以直观地描绘群体异质性和动态变化。然而,尚不清楚假设由初始位置和噪声决定的单个细胞行为是否能如实地再现。我们以乳腺癌休眠中依赖p21/Cdk2的静止-增殖决定作为测试平台,研究了在缺氧(一种诱导休眠的应激)干扰下景观上的单细胞动态变化。将基于轨迹的能量景观生成与单细胞延时显微镜相结合,我们发现,要解释缺氧条件下观察到的细胞命运异质性,需要p21/Cdk2景观上的初始位置和速度的组合,而不仅仅是位置。这可能是由于额外的细胞状态信息,如表观遗传特征和/或其他编码在速度中但仅由p21和Cdk2水平决定的瞬时位置中缺失的特征。在这里,速度依赖性表现为惯性:缺氧前细胞周期速度较高的细胞在缺氧条件下继续沿着细胞周期进展,抵抗景观向细胞周期退出的变化。这种惯性效应可能会显著影响肿瘤和其他动态变化的微环境中的细胞命运轨迹,在这些微环境中,细胞状态转变由多种生化物质的协同作用控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da60/11447052/fa51b77ba295/41540_2024_428_Fig1_HTML.jpg

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