Detail of ActbKO1_DAPI
Project
Title
Immunofluorescence images of DAPI staining of Actb kncokout-nueral progenitor cells (NPCs)
Description
NA
Release, Updated
2018-11-14
License
CC BY
Kind
Image data
based on Experiment
File Formats
Data size
5.6 MB
Gene symbols
Actb
Datatype
gene expression
Molecular Function (MF)
Biological Process (BP)
gene expression
(
GO:0010467
)
Cellular Component (CC)
nucleus
(
GO:0005634
)
Biological Imaging Method
XYZ Scale
XY: 353 micrometer/pixel, Z: NA
T scale
-
Image Acquisition
Experiment type
Immunofluorescence
Microscope type
FluorescenceMicroscope
Acquisition mode
WideField
Contrast method
Fluorescence
Microscope model
Olympus IX73
Detector model
Olympus DP73
Objective model
Olympus LUCPlanFL N 40x
Filter set
Summary of Methods
See details in Ikeda et al. (2018) Nat Commun, 9(1): 605-614.
Related paper(s)
Takashi Ikeda, Takafusa Hikichi, Hisashi Miura, Hirofumi Shibata, Kanae Mitsunaga, Yosuke Yamada, Knut Woltjen, Kei Miyamoto, Ichiro Hiratani, Yasuhiro Yamada, Akitsu Hotta, Takuya Yamamoto, Keisuke Okita, Shinji Masui (2018) Srf destabilizes cellular identity by suppressing cell-type-specific gene expression programs., Nature communications, Volume 9, Number 1, pp. 1387
Published in 2018 Apr 11 (Electronic publication in April 11, 2018, midnight )
- doi: 10.1038/s41467-018-03748-1
-
pmid: 29643333
(Abstract) Multicellular organisms consist of multiple cell types. The identity of these cells is primarily maintained by cell-type-specific gene expression programs; however, mechanisms that suppress these programs are poorly defined. Here we show that serum response factor (Srf), a transcription factor that is activated by various extracellular stimuli, can repress cell-type-specific genes and promote cellular reprogramming to pluripotency. Manipulations that decrease beta-actin monomer quantity result in the nuclear accumulation of Mkl1 and the activation of Srf, which downregulate cell-type-specific genes and alter the epigenetics of regulatory regions and chromatin organization. Mice overexpressing Srf exhibit various pathologies including an ulcerative colitis-like symptom and a metaplasia-like phenotype in the pancreas. Our results demonstrate an unexpected function of Srf via a mechanism by which extracellular stimuli actively destabilize cell identity and suggest Srf involvement in a wide range of diseases.(MeSH Terms)
- Actins/genetics
- Actins/metabolism
- Animals
- Cell Differentiation
- Cellular Reprogramming/genetics
- Chromatin/chemistry[major]
- Chromatin/metabolism
- Colitis, Ulcerative/genetics[major]
- Colitis, Ulcerative/metabolism
- Colitis, Ulcerative/pathology
- Disease Models, Animal
- Female
- Gene Expression Regulation
- Induced Pluripotent Stem Cells/cytology
- Induced Pluripotent Stem Cells/metabolism[major]
- Male
- Metaplasia/genetics[major]
- Metaplasia/metabolism
- Metaplasia/pathology
- Mice
- Mice, Transgenic
- Neural Stem Cells/cytology
- Neural Stem Cells/metabolism[major]
- Pancreas/metabolism[major]
- Pancreas/pathology
- Serum Response Factor/genetics[major]
- Serum Response Factor/metabolism
- Signal Transduction
- Trans-Activators/genetics
- Trans-Activators/metabolism
Contact
Takashi Ikeda, Keisuke Okita, Shinji Masui
, Kyoto University
, Department of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA)
, Okita Lab
Contributors
Takashi Ikeda, Takafusa Hikichi, Hisashi Miura, Hirofumi Shibata, Kanae Mitsunaga, Yosuke Yamada, Knut Woltjen, Kei Miyamoto, Ichiro Hiratani, Yasuhiro Yamada, Akitsu Hotta, Takuya Yamamoto, Keisuke Okita, Shinji Masui
OMERO Dataset
OMERO Project
Source