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The transcription factor NF-YA is crucial for neural progenitor maintenance during brain development.
Yamanaka, Tomoyuki; Kurosawa, Masaru; Yoshida, Aya; Shimogori, Tomomi; Hiyama, Akiko; Maity, Sankar N; Hattori, Nobutaka; Matsui, Hideaki; Nukina, Nobuyuki.
Afiliación
  • Yamanaka T; Department of Neuroscience of Disease, Brain Research Institute, Niigata University, Niigata, Japan; Laboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto, Japan; Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science,
  • Kurosawa M; Department of Neuroscience for Neurodegenerative Disorders, Juntendo University Graduate School of Medicine, Tokyo, Japan.
  • Yoshida A; Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science, Saitama, Japan.
  • Shimogori T; Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science, Saitama, Japan.
  • Hiyama A; Laboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto, Japan.
  • Maity SN; Department of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
  • Hattori N; Department of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
  • Matsui H; Department of Neuroscience of Disease, Brain Research Institute, Niigata University, Niigata, Japan.
  • Nukina N; Laboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, Kyoto, Japan; Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science, Saitama, Japan; Department of Neuroscience for Neurodegenerative Disorders, Juntendo University Gradu
J Biol Chem ; 300(2): 105629, 2024 Feb.
Article en En | MEDLINE | ID: mdl-38199563
ABSTRACT
In contrast to stage-specific transcription factors, the role of ubiquitous transcription factors in neuronal development remains a matter of scrutiny. Here, we demonstrated that a ubiquitous factor NF-Y is essential for neural progenitor maintenance during brain morphogenesis. Deletion of the NF-YA subunit in neural progenitors by using nestin-cre transgene in mice resulted in significant abnormalities in brain morphology, including a thinner cerebral cortex and loss of striatum during embryogenesis. Detailed analyses revealed a progressive decline in multiple neural progenitors in the cerebral cortex and ganglionic eminences, accompanied by induced apoptotic cell death and reduced cell proliferation. In neural progenitors, the NF-YA short isoform lacking exon 3 is dominant and co-expressed with cell cycle genes. ChIP-seq analysis from the cortex during early corticogenesis revealed preferential binding of NF-Y to the cell cycle genes, some of which were confirmed to be downregulated following NF-YA deletion. Notably, the NF-YA short isoform disappears and is replaced by its long isoform during neuronal differentiation. Forced expression of the NF-YA long isoform in neural progenitors resulted in a significant decline in neuronal count, possibly due to the suppression of cell proliferation. Collectively, we elucidated a critical role of the NF-YA short isoform in maintaining neural progenitors, possibly by regulating cell proliferation and apoptosis. Moreover, we identified an isoform switch in NF-YA within the neuronal lineage in vivo, which may explain the stage-specific role of NF-Y during neuronal development.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Corteza Cerebral / Factor de Unión a CCAAT Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2024 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Corteza Cerebral / Factor de Unión a CCAAT Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2024 Tipo del documento: Article