Deletion of ERK1 and ERK2 in the CNS Causes Cortical Abnormalities and Neonatal Lethality:Erk1 Deficiency Enhances the Impairment of Neurogenesis in Erk2-Deficient Mice
Open accessAbstract
Intracellular signaling through extracellular signal-regulated kinase (ERK) is important in regulating cellular functions in a variety of tissues including the CNS. Although ERK1 and ERK2 have a very similar substrate profile and amino acid sequences, there are strikingly different phenotypes between Erk1- and Erk2-deficient mice. Thus, the question arose as to whether these two proteins are functional homologs that compensate for each other, or whether they have distinct functions. Here, we generated double knock-out mice deficient for Erk2 in the CNS, with ubiquitous homozygous deletion of Erk1, and compared the phenotypes of these mice with those of monogenic Erk2-deficient mice. Although we did obtain double knock-out newborn pups, they survived for not >1 d. These pups appeared normal just after parturition. However, they had no milk in their stomachs even 6–7 h after birth. Intracerebral hemorrhages with varying location and severity were observed. The ventricular zones and corpus callosum of the double knock-out pups did not develop adequately. Neuronal size and nuclear morphology in some brain regions were markedly aberrant in the double knock-out pups compared with controls, while deficiency in Erk2 only caused a mild phenotype. These results suggest that total ERK1/2 activity governs cellular behaviors to ensure proper brain development.
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Genetic abrogation of Erk2 causes significant developmental changes.
“Consistent with this hypothesis, previous reports have indicated significant developmental changes by genetic abrogation of Erk2222324, but not in Erk1 KO mice25.”
From Transient blockade of ERK phosphorylation in the critical period causes autistic phenotypes as an adult in mice (2015) · cites this paper as [22]
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- Authors
- Satoh, Y., Kobayashi, Y., Takeuchi, A., Pagès, G., Pouysségur, J., & Kazama, T.
- Affiliations
- Kyoto University (JP)
- National Defense Medical College Hospital (JP)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-01-19
- Volume
- 31
- Issue
- 3
- Pages
- 1149-1155
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6632941
- OpenAlex
- W2158698293
- Cited by
- 66
- References
- 19
- Citations by year
- 2024: 4 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 1 · 2018: 7 · 2017: 3 · 2016: 7 · 2015: 11 · 2014: 3 · 2013: 4 · 2012: 9
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- ERK1, ERK2, extracellular signal-regulated kinase, double knockout mice, neurogenesis, cortical development, neonatal lethality, intracerebral hemorrhage, corpus callosum, ventricular zone, neuronal morphology, compensatory function, brain development
- MeSH terms
- Animals, Cell Count, Cerebral Cortex, Corpus Callosum, Genes, Lethal, Blotting, Western, Apoptosis, Mice, Knockout, Mitogen-Activated Protein Kinase 1, In Situ Nick-End Labeling, Mitogen-Activated Protein Kinase 3, Cell Proliferation, Mice, Neurogenesis, Agenesis of Corpus Callosum
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