Cep55 regulation of PI3K/Akt signaling is required for neocortical development and ciliogenesis Article Swipe
Behnam Rashidieh
,
Belal Shohayeb
,
Amanda L. Bain
,
Patrick R.J. Fortuna
,
Debottam Sinha
,
Andrew Burgess
,
Richard Mills
,
Rachael C. Adams
,
J. Alejandro Lopez
,
Peter Blumbergs
,
John Finnie
,
Murugan Kalimutho
,
Michael Piper
,
James E. Hudson
,
Dominic C.H. Ng
,
Kum Kum Khanna
·
YOU?
·
· 2021
· Open Access
·
YOU?
·
· 2021
· Open Access
·
Homozygous nonsense mutations in CEP55 are associated with several congenital malformations that lead to perinatal lethality suggesting that it plays a critical role in regulation of embryonic development. CEP55 has previously been studied as a crucial regulator of cytokinesis, predominantly in transformed cells, and its dysregulation is linked to carcinogenesis. However, its molecular functions during embryonic development in mammals require further investigation. We have generated a Cep55 knockout (Cep55-/-) mouse model which demonstrated preweaning lethality associated with a wide range of neural defects. Focusing our analysis on the neocortex, we show that Cep55-/- embryos exhibited depleted neural stem/progenitor cells in the ventricular zone as a result of significantly increased cellular apoptosis. Mechanistically, we demonstrated that Cep55-loss downregulates the pGsk3β/β-Catenin/Myc axis in an Akt-dependent manner. The elevated apoptosis of neural stem/progenitors was recapitulated using Cep55-deficient human cerebral organoids and we could rescue the phenotype by inhibiting active Gsk3β. Additionally, we show that Cep55-loss leads to a significant reduction of ciliated cells, highlighting a novel role in regulating ciliogenesis. Collectively, our findings demonstrate a critical role of Cep55 during brain development and provide mechanistic insights that may have important implications for genetic syndromes associated with Cep55-loss. Author summary Despite extensive investigation on the roles of CEP55 in tumorigenesis, its physiological role during development has remained largely uncharacterized. Recently, homozygous CEP55 mutations have been linked to two lethal fetal syndromes, MKS-like Syndrome and MARCH, demonstrating the importance of CEP55 in embryogenesis and neural development. These syndromes exhibit multiple severe clinical manifestations that lead to perinatal lethality. However, the exact molecular mechanism underlying complex Cep55-deficient developmental phenotypes remain elusive. To address this question, we have generated a Cep55-/- (KO) mouse model and to bridge the gap between the mouse model and human disease, we have used brain organoids generated from pluripotent stem cells as a promising approach to investigate the mechanism of Cep55-associated neurodevelopment phenotype. Our detailed mechanistic studies suggest that Cep55 regulates neural development through the Akt-downstream effector, Gsk3β, and its mediators β-Catenin and Myc, which are known regulators of neural proliferation and differentiation. Additionally, we discovered a critical role for Cep55 in regulating cilia formation. Together, these results illustrate an important role of Cep55 in regulating neurogenesis and ciliogenesis via regulation of the Akt pathway.
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- Type
- article
- Language
- en
- Landing Page
- https://doaj.org/article/ca113dc23d2f42909600bf1b070bc7e6
- OA Status
- green
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4286949289
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4286949289Canonical identifier for this work in OpenAlex
- Title
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Cep55 regulation of PI3K/Akt signaling is required for neocortical development and ciliogenesisWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2021Year of publication
- Publication date
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2021-10-01Full publication date if available
- Authors
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Behnam Rashidieh, Belal Shohayeb, Amanda L. Bain, Patrick R.J. Fortuna, Debottam Sinha, Andrew Burgess, Richard Mills, Rachael C. Adams, J. Alejandro Lopez, Peter Blumbergs, John Finnie, Murugan Kalimutho, Michael Piper, James E. Hudson, Dominic C.H. Ng, Kum Kum KhannaList of authors in order
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https://doaj.org/article/ca113dc23d2f42909600bf1b070bc7e6Publisher landing page
- Open access
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
- OA URL
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https://doaj.org/article/ca113dc23d2f42909600bf1b070bc7e6Direct OA link when available
- Concepts
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Ciliogenesis, PI3K/AKT/mTOR pathway, Protein kinase B, Cell biology, Signal transduction, Neuroscience, Biology, Chemistry, CiliumTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.mouse | 69, 275, 284 |
| abstract_inverted_index.novel | 162 |
| abstract_inverted_index.plays | 19 |
| abstract_inverted_index.range | 79 |
| abstract_inverted_index.roles | 201 |
| abstract_inverted_index.these | 354 |
| abstract_inverted_index.using | 132 |
| abstract_inverted_index.which | 71, 332 |
| abstract_inverted_index.Author | 194 |
| abstract_inverted_index.MARCH, | 230 |
| abstract_inverted_index.active | 145 |
| abstract_inverted_index.bridge | 279 |
| abstract_inverted_index.cells, | 42, 159 |
| abstract_inverted_index.during | 54, 176, 209 |
| abstract_inverted_index.lethal | 224 |
| abstract_inverted_index.linked | 47, 221 |
| abstract_inverted_index.neural | 81, 96, 128, 239, 319, 337 |
| abstract_inverted_index.remain | 263 |
| abstract_inverted_index.rescue | 140 |
| abstract_inverted_index.result | 105 |
| abstract_inverted_index.severe | 245 |
| abstract_inverted_index.Despite | 196 |
| abstract_inverted_index.Gsk3β, | 325 |
| abstract_inverted_index.Gsk3β. | 146 |
| abstract_inverted_index.address | 266 |
| abstract_inverted_index.between | 282 |
| abstract_inverted_index.complex | 259 |
| abstract_inverted_index.crucial | 35 |
| abstract_inverted_index.embryos | 93 |
| abstract_inverted_index.exhibit | 243 |
| abstract_inverted_index.further | 60 |
| abstract_inverted_index.genetic | 189 |
| abstract_inverted_index.largely | 213 |
| abstract_inverted_index.mammals | 58 |
| abstract_inverted_index.manner. | 123 |
| abstract_inverted_index.provide | 180 |
| abstract_inverted_index.require | 59 |
| abstract_inverted_index.results | 355 |
| abstract_inverted_index.several | 8 |
| abstract_inverted_index.studied | 32 |
| abstract_inverted_index.studies | 314 |
| abstract_inverted_index.suggest | 315 |
| abstract_inverted_index.summary | 195 |
| abstract_inverted_index.through | 321 |
| abstract_inverted_index.Cep55-/- | 92, 273 |
| abstract_inverted_index.Focusing | 83 |
| abstract_inverted_index.However, | 50, 253 |
| abstract_inverted_index.MKS-like | 227 |
| abstract_inverted_index.Syndrome | 228 |
| abstract_inverted_index.analysis | 85 |
| abstract_inverted_index.approach | 302 |
| abstract_inverted_index.cellular | 109 |
| abstract_inverted_index.cerebral | 135 |
| abstract_inverted_index.ciliated | 158 |
| abstract_inverted_index.clinical | 246 |
| abstract_inverted_index.critical | 21, 172, 345 |
| abstract_inverted_index.defects. | 82 |
| abstract_inverted_index.depleted | 95 |
| abstract_inverted_index.detailed | 312 |
| abstract_inverted_index.disease, | 288 |
| abstract_inverted_index.elevated | 125 |
| abstract_inverted_index.elusive. | 264 |
| abstract_inverted_index.findings | 169 |
| abstract_inverted_index.insights | 182 |
| abstract_inverted_index.knockout | 67 |
| abstract_inverted_index.multiple | 244 |
| abstract_inverted_index.nonsense | 1 |
| abstract_inverted_index.pathway. | 372 |
| abstract_inverted_index.remained | 212 |
| abstract_inverted_index.Recently, | 215 |
| abstract_inverted_index.Together, | 353 |
| abstract_inverted_index.apoptosis | 126 |
| abstract_inverted_index.effector, | 324 |
| abstract_inverted_index.embryonic | 26, 55 |
| abstract_inverted_index.exhibited | 94 |
| abstract_inverted_index.extensive | 197 |
| abstract_inverted_index.functions | 53 |
| abstract_inverted_index.generated | 64, 271, 294 |
| abstract_inverted_index.important | 186, 358 |
| abstract_inverted_index.increased | 108 |
| abstract_inverted_index.lethality | 15, 74 |
| abstract_inverted_index.mechanism | 257, 306 |
| abstract_inverted_index.mediators | 328 |
| abstract_inverted_index.molecular | 52, 256 |
| abstract_inverted_index.mutations | 2, 218 |
| abstract_inverted_index.organoids | 136, 293 |
| abstract_inverted_index.perinatal | 14, 251 |
| abstract_inverted_index.phenotype | 142 |
| abstract_inverted_index.promising | 301 |
| abstract_inverted_index.question, | 268 |
| abstract_inverted_index.reduction | 156 |
| abstract_inverted_index.regulates | 318 |
| abstract_inverted_index.regulator | 36 |
| abstract_inverted_index.syndromes | 190, 242 |
| abstract_inverted_index.(Cep55-/-) | 68 |
| abstract_inverted_index.Cep55-loss | 115, 151 |
| abstract_inverted_index.Homozygous | 0 |
| abstract_inverted_index.apoptosis. | 110 |
| abstract_inverted_index.associated | 6, 75, 191 |
| abstract_inverted_index.congenital | 9 |
| abstract_inverted_index.discovered | 343 |
| abstract_inverted_index.formation. | 352 |
| abstract_inverted_index.homozygous | 216 |
| abstract_inverted_index.illustrate | 356 |
| abstract_inverted_index.importance | 233 |
| abstract_inverted_index.inhibiting | 144 |
| abstract_inverted_index.lethality. | 252 |
| abstract_inverted_index.neocortex, | 88 |
| abstract_inverted_index.phenotype. | 310 |
| abstract_inverted_index.phenotypes | 262 |
| abstract_inverted_index.previously | 30 |
| abstract_inverted_index.preweaning | 73 |
| abstract_inverted_index.regulating | 165, 350, 363 |
| abstract_inverted_index.regulation | 24, 368 |
| abstract_inverted_index.regulators | 335 |
| abstract_inverted_index.suggesting | 16 |
| abstract_inverted_index.syndromes, | 226 |
| abstract_inverted_index.underlying | 258 |
| abstract_inverted_index.β-Catenin | 329 |
| abstract_inverted_index.Cep55-loss. | 193 |
| abstract_inverted_index.demonstrate | 170 |
| abstract_inverted_index.development | 56, 178, 210, 320 |
| abstract_inverted_index.investigate | 304 |
| abstract_inverted_index.mechanistic | 181, 313 |
| abstract_inverted_index.pluripotent | 296 |
| abstract_inverted_index.significant | 155 |
| abstract_inverted_index.transformed | 41 |
| abstract_inverted_index.ventricular | 101 |
| abstract_inverted_index.ciliogenesis | 366 |
| abstract_inverted_index.cytokinesis, | 38 |
| abstract_inverted_index.demonstrated | 72, 113 |
| abstract_inverted_index.development. | 27, 240 |
| abstract_inverted_index.highlighting | 160 |
| abstract_inverted_index.implications | 187 |
| abstract_inverted_index.neurogenesis | 364 |
| abstract_inverted_index.Additionally, | 147, 341 |
| abstract_inverted_index.Akt-dependent | 122 |
| abstract_inverted_index.Collectively, | 167 |
| abstract_inverted_index.ciliogenesis. | 166 |
| abstract_inverted_index.demonstrating | 231 |
| abstract_inverted_index.developmental | 261 |
| abstract_inverted_index.downregulates | 116 |
| abstract_inverted_index.dysregulation | 45 |
| abstract_inverted_index.embryogenesis | 237 |
| abstract_inverted_index.investigation | 198 |
| abstract_inverted_index.malformations | 10 |
| abstract_inverted_index.physiological | 207 |
| abstract_inverted_index.predominantly | 39 |
| abstract_inverted_index.proliferation | 338 |
| abstract_inverted_index.recapitulated | 131 |
| abstract_inverted_index.significantly | 107 |
| abstract_inverted_index.Akt-downstream | 323 |
| abstract_inverted_index.investigation. | 61 |
| abstract_inverted_index.manifestations | 247 |
| abstract_inverted_index.tumorigenesis, | 205 |
| abstract_inverted_index.Cep55-deficient | 133, 260 |
| abstract_inverted_index.carcinogenesis. | 49 |
| abstract_inverted_index.stem/progenitor | 97 |
| abstract_inverted_index.Cep55-associated | 308 |
| abstract_inverted_index.Mechanistically, | 111 |
| abstract_inverted_index.differentiation. | 340 |
| abstract_inverted_index.neurodevelopment | 309 |
| abstract_inverted_index.stem/progenitors | 129 |
| abstract_inverted_index.uncharacterized. | 214 |
| abstract_inverted_index.pGsk3β/β-Catenin/Myc | 118 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 16 |
| citation_normalized_percentile.value | 0.51727078 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |