Detail of Fig1C_E17
Project
Title
Immunostaining image of embryonic lungs at E17 with anti-E-cadherin(green)and anti-a-catenin(red) and a18(gray) antibodies
Description
NA
Release, Updated
2018-11-14
License
CC BY
Kind
Image data
based on Experiment
File Formats
Data size
3.0 MB
Protein names
E-cadherin, a-catenin
Reporter
anti-E-cadherin, anti-a-catenin
Datatype
organ formation
Molecular Function (MF)
Biological Process (BP)
lung development
(
GO:0030324
)
Cellular Component (CC)
cytoskeleton
(
GO:005856
)
Biological Imaging Method
XYZ Scale
XY: 0.2075 micrometer/pixel, Z: NA
T scale
-
Image Acquisition
Experiment type
Immunofluorescence
Microscope type
FluorescenceMicroscope
Acquisition mode
Other
Contrast method
Fluorescence
Microscope model
Carl Zeiss, LSM880
Detector model
-
Objective model
-
Filter set
-
Summary of Methods
See details in Fumoto et al. (2017) Development, 144(1): 151-162.
Related paper(s)
Katsumi Fumoto, Hisako Takigawa-Imamura, Kenta Sumiyama, Tomoyuki Kaneiwa, Akira Kikuchi (2017) Modulation of apical constriction by Wnt signaling is required for lung epithelial shape transition., Development (Cambridge, England), Volume 144, Number 1, pp. 151-162
Published in 2017 Jan 1 (Electronic publication in Dec. 2, 2016, midnight )
- doi: 10.1242/dev.141325
-
pmid: 27913639
(Abstract) In lung development, the apically constricted columnar epithelium forms numerous buds during the pseudoglandular stage. Subsequently, these epithelial cells change shape into the flat or cuboidal pneumocytes that form the air sacs during the canalicular and saccular (canalicular-saccular) stages, yet the impact of cell shape on tissue morphogenesis remains unclear. Here, we show that the expression of Wnt components is decreased in the canalicular-saccular stages, and that genetically constitutive activation of Wnt signaling impairs air sac formation by inducing apical constriction in the epithelium as seen in the pseudoglandular stage. Organ culture models also demonstrate that Wnt signaling induces apical constriction through apical actomyosin cytoskeletal organization. Mathematical modeling reveals that apical constriction induces bud formation and that loss of apical constriction is required for the formation of an air sac-like structure. We identify MAP/microtubule affinity-regulating kinase 1 (Mark1) as a downstream molecule of Wnt signaling and show that it is required for apical cytoskeletal organization and bud formation. These results suggest that Wnt signaling is required for bud formation by inducing apical constriction during the pseudoglandular stage, whereas loss of Wnt signaling is necessary for air sac formation in the canalicular-saccular stages.(MeSH Terms)
- Animals
- Cell Differentiation
- Cell Polarity/physiology
- Cell Shape
- Cytoskeleton/physiology
- Embryo, Mammalian
- Lung/embryology[major]
- Mice
- Mice, Inbred ICR
- Mice, Transgenic
- Models, Theoretical
- Organ Size
- Organogenesis/genetics[major]
- Pulmonary Alveoli/cytology[major]
- Pulmonary Alveoli/embryology[major]
- Wnt Signaling Pathway/physiology[major]
Contact
Akira Kikuchi
, Departments of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita 565-0871, Japan.
, Graduate School of Medicine
, Departments of Molecular Biology and Biochemistry
Contributors
Katsumi Fumoto, Hisako Takigawa-Imamura, Kenta Sumiyama, Tomoyuki Kaneiwa, Akira Kikuchi
OMERO Dataset
OMERO Project
Source