The mechanical function of the nucleus during epithelial cell shape change and tissue deformation

上皮细胞形状变化和组织变形过程中细胞核的机械功能

• 批准号: 20K15797
• 负责人: Stewart Rachel
• 金额: $ 2.66万
• 依托单位: Institute of Physical and Chemical Research
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Early-Career Scientists
• 财政年份: 2020
• 资助国家: 日本
• 起止时间: 2020-04-01 至 2021-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-20K15797/
• 关键词: Biology; Drosophila; Morphogenesis; Nucleus; Lamina; Embryogenesis; Mechanics; Optogenetics; Epithelium

I screened embryos expressing mutant alleles of cytoskeletal elements/regulators and nuclear components for defects in nuclear positioning/dorsal fold invagination. Based on dorsal fold phenotypes in fixed, immunostained embryos, Shot (spectraplakin), Koi (Sun domain protein), Lamin, Suvar(3-3), and Rtn1 (reticulon) are implicated in dorsal fold invagination/nuclear positioning.The localization and/or expression levels of the polarity protein Par1, known to be involved in dorsal fold invagination, may be perturbed upon disruption of the nuclear lamina, as evidenced by immunostaining, live imaging, and RT-PCR results.I cloned the C-terminus of Klar or the KASH domain alone for the development of a CRY2-CIBN-based optogenetic tool that can move the nucleus along the apical-basal cell axis.

我筛选胚胎表达突变等位基因的细胞骨架元件/调节器和核组件的缺陷，在核定位/背褶内陷。基于固定的免疫染色胚胎的背褶表型，Shot（spectraplakin），锦鲤（Sun结构域蛋白）、核纤层蛋白、Suvar（3-3）和Rtn 1已知参与背褶内陷的极性蛋白质Par 1的定位和/或表达水平可以在核纤层破坏后受到干扰，如免疫染色所证明的，我克隆了Klar的C-末端或单独的KASH结构域，用于开发可以沿着顶部-基底细胞轴沿着移动细胞核的基于KIBN的光遗传学工具。