CYTOPLASM AND CELLULAR FUNCTION

细胞质和细胞功能

• 批准号: 8170845
• 负责人: ERNST-LUDWIG FLORIN
• 金额: $ 3.74万
• 依托单位: UNIVERSITY OF COLORADO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8170845
• 关键词: Affect; Cell Communication; Cell physiology; Cells; Computer Retrieval of Information on Scientific Projects Database; Cytoplasm; Data; Electron Microscopy; Filament; Fission Yeast; Freezing; Funding; Grant; Immobilization; Institution; Intracellular Transport; Liquid substance; Mediating; Nutrient; Phase Transition; Polymers; Protein Family; Proteins; Research; Research Personnel; Resources; Solid; Source; Starvation; Structure; Time; United States National Institutes of Health; Yeasts; cell motility; interest

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The cytoplasm of a cell mediates important cellular functions such as intracellular transport, cell communication and cell motility. We are interested in how the organization of the cytoplasm affects or controls these functions. Specifically, it has been shown that the cytoplasm of fission yeast cells undergoes a kind of "phase transition" depending on external control parameters. Yeast cells enter a solid-like state when grown in nutrient deficient conditions. We are interested in the mechanism that leads to this "freezing" of cells. The only apparent way that the cell can cause the immobilization of all structure is to form some kind of rigid polymer network. A family of proteins (septins) has been identified as filament forming and is the most likely candidate to cause the transition from the fluid- to the solid-like state. Preliminary data leads to the hypothesis that the septin protein Spn1 forms a rigid network in cells grown in starvation conditions. We will use electron microscopy of such cells to visualize, for the first time, a septin protein network.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 细胞的细胞质介导了重要的细胞功能，例如细胞内转运，细胞通信和细胞运动。 我们对细胞质的组织如何影响或控制这些功能感兴趣。具体而言，已经表明，根据外部控制参数，裂变酵母细胞的细胞质会经历一种“相变”。 酵母细胞在营养不足的条件下生长时进入固态状态。 我们对导致这种细胞“冷冻”的机制感兴趣。 细胞可能导致所有结构固定的唯一明显方式是形成某种刚性聚合物网络。 蛋白质（Septins）家族已被确定为丝状形成，是最有可能导致从液体转变为固体状态的候选者。 初步数据导致了以下假设：Septin蛋白SPN1在饥饿条件下生长的细胞中形成一个刚性网络。 我们将使用此类细胞的电子显微镜来首次可视化Septin蛋白网络。