Impaired Function of PLEKHG2, a Rho-Guanine Nucleotide-Exchange Factor, Disrupts Corticogenesis in Neurodevelopmental Phenotypes Article Swipe
Masashi Nishikawa
,
Hidenori Ito
,
Hidenori Tabata
,
Hiroshi Ueda
,
Koh‐ichi Nagata
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.3390/cells11040696
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.3390/cells11040696
Homozygosity of the p.Arg204Trp variation in the Pleckstrin homology and RhoGEF domain containing G2 (PLEKHG2) gene, which encodes a Rho family-specific guanine nucleotide-exchange factor, is responsible for microcephaly with intellectual disability. However, the role of PLEKHG2 during neurodevelopment remains unknown. In this study, we analyzed mouse Plekhg2 function during cortical development, both in vitro and in vivo. The p.Arg200Trp variant in mouse (Plekhg2-RW), which corresponds to the p.Arg204Trp variant in humans, showed decreased guanine nucleotide-exchange activity for Rac1, Rac3, and Cdc42. Acute knockdown of Plekhg2 using in utero electroporation-mediated gene transfer did not affect the migration of excitatory neurons during corticogenesis. On the other hand, silencing Plekhg2 expression delayed dendritic arbor formation at postnatal day 7 (P7), perhaps because of impaired Rac/Cdc42 and p21-activated kinase 1 signaling pathways. This phenotype was rescued by expressing an RNAi-resistant version of wildtype Plekhg2, but not of Plekhg2-RW. Axon pathfinding was also impaired in vitro and in vivo in Plekhg2-deficient cortical neurons. At P14, knockdown of Plekhg2 was observed to cause defects in dendritic spine morphology formation. Collectively, these results strongly suggest that PLEKHG2 has essential roles in the maturation of axon, dendrites, and spines. Moreover, impairment of PLEKHG2 function is most likely to cause defects in neuronal functions that lead to neurodevelopmental disorders.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.3390/cells11040696
- https://www.mdpi.com/2073-4409/11/4/696/pdf?version=1645102028
- OA Status
- gold
- Cited By
- 8
- References
- 41
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4213154012
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- OpenAlex ID
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https://openalex.org/W4213154012Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.3390/cells11040696Digital Object Identifier
- Title
-
Impaired Function of PLEKHG2, a Rho-Guanine Nucleotide-Exchange Factor, Disrupts Corticogenesis in Neurodevelopmental PhenotypesWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
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2022-02-16Full publication date if available
- Authors
-
Masashi Nishikawa, Hidenori Ito, Hidenori Tabata, Hiroshi Ueda, Koh‐ichi NagataList of authors in order
- Landing page
-
https://doi.org/10.3390/cells11040696Publisher landing page
- PDF URL
-
https://www.mdpi.com/2073-4409/11/4/696/pdf?version=1645102028Direct link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://www.mdpi.com/2073-4409/11/4/696/pdf?version=1645102028Direct OA link when available
- Concepts
-
Guanine nucleotide exchange factor, Corticogenesis, Gene knockdown, CDC42, RHOA, Pleckstrin homology domain, Biology, Phenotype, Axon guidance, Gene silencing, Cell biology, Microcephaly, Genetics, GTPase, Signal transduction, Gene, Axon, Embryonic stem cellTop concepts (fields/topics) attached by OpenAlex
- Cited by
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8Total citation count in OpenAlex
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2025: 2, 2024: 3, 2023: 2, 2022: 1Per-year citation counts (last 5 years)
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41Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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