Live Imaging of Early Mouse Embryos Using Fluorescently Labeled Transgenic Mice

Author(s):  
Takaya Abe ◽  
Shinichi Aizawa ◽  
Toshihiko Fujimori
2009 ◽  
Vol 27 (5) ◽  
pp. 266-276 ◽  
Author(s):  
Sonja Nowotschin ◽  
Guy S. Eakin ◽  
Anna-Katerina Hadjantonakis

2007 ◽  
Vol 15 (2) ◽  
pp. 420-422 ◽  
Author(s):  
M T Fiorenza ◽  
S Torcia ◽  
S Canterini ◽  
A Bevilacqua ◽  
M G Narducci ◽  
...  

1974 ◽  
Vol 71 (4) ◽  
pp. 1056-1060 ◽  
Author(s):  
E. K. Barbehenn ◽  
R. G. Wales ◽  
O. H. Lowry
Keyword(s):  

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  

1995 ◽  
Vol 108 (12) ◽  
pp. 3677-3684 ◽  
Author(s):  
G. Zhou ◽  
S. Garofalo ◽  
K. Mukhopadhyay ◽  
V. Lefebvre ◽  
C.N. Smith ◽  
...  

Type II collagen is a major chondrocyte-specific component of the cartilage extracellular matrix and it represents a typical differentiation marker of mature chondrocytes. In order to delineate cis-acting elements of the mouse pro alpha 1(II) collagen gene that control chondrocyte-specific expression in intact mouse embryos, we generated transgenic mice harboring chimeric constructions in which varying lengths of the promoter and intron 1 sequences were linked to a beta-galactosidase reporter gene. A construction containing a 3,000 bp promoter and a 3,020 bp intron 1 fragment directed high levels of beta-galactosidase expression specifically to chondrocytes. Expression of the transgene coincided with the temporal expression of the endogenous gene at all stages of embryonic development. Successive deletions of intron 1 delineated a 182 bp fragment which targeted beta-galactosidase expression to chondrocytes with the same specificity as the larger intron 1 fragment. Transgenic mice harboring a 309 bp Col2a1 promoter lacking intron 1 tester sequences showed no beta-galactosidase expression in chondrocytes. Reduction of the 182 bp fragment to a 73 bp subfragment surrounding a decamer sequence previously reported to be involved in chondrocyte specificity, resulted in loss of transgene expression in chondrocytes. When the Col2a1 promoter was replaced with a minimal beta-globin promoter, the 182 bp intron 1 sequence was still able to target expression of the transgene to chondrocytes. We conclude that a 182 bp intron 1 DNA segment of the mouse Col2a1 gene contains the necessary information to confer high-level, temporally correct, chondrocyte expression on a reporter gene in intact mouse embryos and that Col2a1 promoter sequences are dispensable for chondrocyte expression.


Development ◽  
1978 ◽  
Vol 48 (1) ◽  
pp. 37-51
Author(s):  
S. J. Kelly ◽  
J. G. Mulnard ◽  
C. F. Graham

Cell division was observed in intact and dissociated mouse embryos between the 2-cell stage and the blastocyst in embryos developing in culture. Division to the 4-cell stage was usually asynchronous. The first cell to divide to the 4-cell stage produced descendants which tended to divide ahead of those cells produced by its slow partner at all subsequent stages of development up to the blastocyte stage. The descendants of the first cell to divide to the 4-cell stage did not subsequently have short cell cycles. The first cell or last cell to divide from the 4-cell stage was labelled with tritiated thymidine. The embryo was reassembled, and it was found that the first pair of cells to reach the 8-cell stage contributed disproportionately more descendants to the ICM when compared with the last cell to divide to the 8-cell stage.


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