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פותח על ידי קלירמאש פתרונות בע"מ -
Ectopic expression of MyoD1 in mice causes prenatal lethalities
Year:
1993
Source of publication :
Developmental Dynamics
Authors :
פיירמן, אלכסנדר
;
.
שני, משה
;
.
Volume :
196
Co-Authors:
Faerman, A., Institute of Animal Science, ARO, Volcani Center, Bet Dagan, 50250, Israel
Pearson‐White, S., University of Virginia Medical Center, Charlottesville, Virginia, 22908, United States
Emerson, C., Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania, 19111, United States
Shani, M., Institute of Animal Science, ARO, Volcani Center, Bet Dagan, 50250, Israel
Facilitators :
From page:
165
To page:
173
(
Total pages:
9
)
Abstract:
A variety of differentiated cell types can be converted to skeletal muscle following transfection with the myogenic regulatory gene MyoD1. To determine whether MyoD1 is a dominant muscle regulator in vivo, mouse fertilized eggs were microinjected with a β‐actin/MyoD1 gene. Ectopic expression of MyoD1 during mouse embryogenesis led to embryonic lethalities, the cause of which is not known. Transgenic embryos died before midgestation. The majority of tested embryos between 7.5 and 9.5 days, although retarded compared to control littermates, differentiated normally into tissues representative of all three germ layers. In most transgenic embryos there was no indication of myogenic conversion. The expression of the introduced gene was detected in all ectodermal and mesodermal tissues but was absent in all endodermal cells. Forced expression of MyoD1 was associated with the activation of myogenin and MLC2 (but not myf5 or MRF4) genes in non‐muscle cell types, demonstrating the dominant regulatory function of MyoD1 during development. These results demonstrate that ectopic MyoD1 expression and activation of myogenin and MLC2 have no significant effects in the determination of cell lineages or the developmental fate of differentiated mesodermal and ectodermal cell lineages. © 1993 wiley‐Liss, Inc. Copyright © 1993 Wiley‐Liss, Inc.
Note:
Related Files :
Animal
animal tissue
ectoderm
Embryo and Fetal Development
gene expression
mice
MLC2
regulator gene
עוד תגיות
תוכן קשור
More details
DOI :
10.1002/aja.1001960303
Article number:
0
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
22312
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:50
Scientific Publication
Ectopic expression of MyoD1 in mice causes prenatal lethalities
196
Faerman, A., Institute of Animal Science, ARO, Volcani Center, Bet Dagan, 50250, Israel
Pearson‐White, S., University of Virginia Medical Center, Charlottesville, Virginia, 22908, United States
Emerson, C., Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania, 19111, United States
Shani, M., Institute of Animal Science, ARO, Volcani Center, Bet Dagan, 50250, Israel
Ectopic expression of MyoD1 in mice causes prenatal lethalities
A variety of differentiated cell types can be converted to skeletal muscle following transfection with the myogenic regulatory gene MyoD1. To determine whether MyoD1 is a dominant muscle regulator in vivo, mouse fertilized eggs were microinjected with a β‐actin/MyoD1 gene. Ectopic expression of MyoD1 during mouse embryogenesis led to embryonic lethalities, the cause of which is not known. Transgenic embryos died before midgestation. The majority of tested embryos between 7.5 and 9.5 days, although retarded compared to control littermates, differentiated normally into tissues representative of all three germ layers. In most transgenic embryos there was no indication of myogenic conversion. The expression of the introduced gene was detected in all ectodermal and mesodermal tissues but was absent in all endodermal cells. Forced expression of MyoD1 was associated with the activation of myogenin and MLC2 (but not myf5 or MRF4) genes in non‐muscle cell types, demonstrating the dominant regulatory function of MyoD1 during development. These results demonstrate that ectopic MyoD1 expression and activation of myogenin and MLC2 have no significant effects in the determination of cell lineages or the developmental fate of differentiated mesodermal and ectodermal cell lineages. © 1993 wiley‐Liss, Inc. Copyright © 1993 Wiley‐Liss, Inc.
Scientific Publication
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