Journal
CELL REPORTS
Volume 12, Issue 6, Pages 913-921Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.07.011
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Funding
- Cole foundation
- Association pour la Recherche contre le Cancer
- Fonds de la recherche en sante du Quebec
- Canadian Institutes of Health Research [MOP-119327]
- Canadian Cancer Society Research Institute
- UK Medical Research Council
- Canadian network of Centres of Excellence in Commercialization and Research
- Canada Foundation for Innovation
- FRQ
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ERK1 and ERK2 are the effector kinases of the ERK1/2 MAP-kinase signaling pathway, which plays a central role in transducing signals controlling cell proliferation, differentiation, and survival. Deregulated activity of the ERK1/2 pathway is linked to a group of developmental syndromes and contributes to the pathogenesis of various human diseases. One fundamental question that remains unaddressed is whether ERK1 and ERK2 have evolved unique physiological functions or whether they are used redundantly to reach a threshold of global ERK activity. Here, we show that the extent of development of the mouse placenta and embryo bearing different combinations of Erk1 and Erk2 alleles is strictly correlated with total ERK1/2 activity. We further demonstrate that transgenic expression of ERK1 fully rescues the embryonic and placental developmental defects associated with the loss of ERK2. We conclude that ERK1 and ERK2 exert redundant functions in mouse development.
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