Deletion of ERK2 Mitogen-Activated Protein Kinase Identifies Its Key Roles in Cortical Neurogenesis and Cognitive Function
Open accessAbstract
The mitogen-activated protein (MAP) kinases ERK1 and ERK2 are critical intracellular signaling intermediates; however, little is known about their isoform-specific functions in vivo. We have examined the role of ERK2 in neural development by conditional inactivation of the murine mapk1/ERK2 gene in neural progenitor cells of the developing cortex. ERK MAP kinase (MAPK) activity in neural progenitor cells is required for neuronal cell fate determination. Loss of ERK2 resulted in a reduction in cortical thickness attributable to impaired proliferation of neural progenitors during the neurogenic period and the generation of fewer neurons. Mutant neural progenitor cells remained in an undifferentiated state until gliogenic stimuli induced their differentiation, resulting in the generation of more astrocytes. The mutant mice displayed profound deficits in associative learning. Importantly, we have identified patients with a 1 Mb microdeletion on chromosome 22q11.2 encompassing the MAPK1/ERK2 gene. These children, who have reduced ERK2 levels, exhibit microcephaly, impaired cognition, and developmental delay. These findings demonstrate an important role for ERK2 in cellular proliferation and differentiation during neural development as well as in cognition and memory formation.
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Induced proliferation by signaling pathways can result in either a thicker or thinner cortex in mouse models depending on the strength of the dysregulation.
“the induced proliferation by the signaling pathways can result in either a thicker or thinner cortex in mice models depending on the strength of the dysregulation.”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [95]
Loss of Erk2 can induce strong G1/S dysregulation causing mouse cells to miss the neurogenesis time window E14.5-E16.5, resulting in fewer neurons, precocious astrogenesis, and potentially microcephaly.
“loss of Erk2 can induce such strong G1/S dysregulation that mice cells miss the time window of neurogenesis (E14.5–E16.5), resulting in fewer neurons, precocious astrogenesis, and potentially microcephaly [95].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [95]
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 [23]
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- Authors
- Samuels, I. S., Karlo, J. C., Faruzzi, A. N., Pickering, K., Herrup, K., Sweatt, J. D., Saitta, S. C., & Landreth, G. E.
- Affiliations
- Case Western Reserve University (US)
- University of Alabama (US)
- Rutgers, The State University of New Jersey (US)
- Rutgers Cancer Institute (US)
- Children's Hospital of Philadelphia (US)
- Case Comprehensive Cancer Center (US)
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-07-02
- Volume
- 28
- Issue
- 27
- Pages
- 6983-6995
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC4364995
- OpenAlex
- W2035079756
- Cited by
- 278
- References
- 53
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 12 · 2023: 12 · 2022: 12 · 2021: 12 · 2020: 13 · 2019: 16 · 2018: 13 · 2017: 20 · 2016: 13 · 2015: 21 · 2014: 13 · 2013: 18 · 2012: 19
- FWCI
- 6.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- National Science Foundation
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health (5p01ns032779-05, NS057098)
- National Heart, Lung, and Blood Institute (K08HL004487, HL04487)
- National Institute of Mental Health (F31MH074241, MH 57014, R01MH057014)
- National Institute of Neurological Disorders and Stroke (NS 057098, NS-13546, R01NS013546, R01NS020591, P30NS057098, NS020591, NS032779)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- ERK2, MAPK signaling, cortical neurogenesis, neural progenitor cells, conditional gene deletion, cortical thickness, astrocyte differentiation, gliogenesis, associative learning, cognitive impairment, microcephaly, developmental delay, memory formation
- MeSH terms
- Animals, Animals, Newborn, Astrocytes, Cell Communication, Cell Differentiation, Cells, Cultured, Cerebral Cortex, Cognition, Learning Disabilities, Neurons, Stem Cells, Gene Expression Regulation, Enzymologic, Mice, Knockout, Gene Expression Regulation, Developmental, Cell Lineage, Mitogen-Activated Protein Kinase 1, MAP Kinase Signaling System, Cell Proliferation, Mice
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