Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex

Narayanan, Ramanathan; Pham, Linh; Kerimoğlu, Cemil; Watanabe, Takashi; Hernandez, Ricardo Castro; Sokpor, Godwin; Ulmke, Pauline Antonie; Kiszka, Kamila A.; Tonchev, Anton B.; Rosenbusch, Joachim; Seong, Rho Hyun; Teichmann, Ulrike; Frahm, Jens; Fischer, André; Bonn, Stefan; Stoykova, Anastassia; Staiger, Jochen F.; Tuoc, Tran

doi:10.1016/j.isci.2018.05.014

Cited by 36 publications

(61 citation statements)

References 62 publications

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“…Shh activation in the mouse via the Gpr161 conditional KO also induced heterotopias that are accompanied with “bRG-like” cell amplification (Shimada et al, 2019). Furthermore, Pax6 loss of function in the small eye mouse mutant also displays basally located progenitors that carry RG characteristics, which is consistent with the results obtained in the Pax6 conditional mutants (Götz et al, 1998; Narayanan et al, 2018). Other mutations have also been shown to be associated with the presence of ectopically located progenitors (reviewed by Bizzotto and Francis, 2015) such as Arl13b and Marcks mouse mutants, potentially showing subtle differences from bRG-like cells.…”

Section: Brgs and Pathologysupporting

confidence: 89%

“…This suggests that epigenetic markers, regulated partly by the BAF complex, play a crucial role during several processes of cortical development (Narayanan et al, 2015; Nguyen et al, 2016). In a follow-up study, a Baf155 conditional KO (obtained by crossing Baf155 fl/fl with Emx1-Cre mice) led to an overall decrease of Tbr2+ cells, but also among the remaining Tbr2+ cells, the presence of ectopic IPs in the IZ (Narayanan et al, 2018). The total proportion of Pax6+ cells was not affected, yet ectopic Pax6+/pVim+ cells that resembled bRG-like cells were observed in the IZ, suggesting a delamination of aRGs or bRG-like cell generation.…”

Section: Molecular Mechanisms Associated With the Generation And Amplmentioning

confidence: 99%

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Genes and Mechanisms Involved in the Generation and Amplification of Basal Radial Glial Cells

Penisson

Ladewig

Belvindrah

et al. 2019

Front. Cell. Neurosci.

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The development of the cerebral cortex relies on different types of progenitor cell. Among them, the recently described basal radial glial cell (bRG) is suggested to be of critical importance for the development of the brain in gyrencephalic species. These cells are highly numerous in primate and ferret brains, compared to lissencephalic species such as the mouse in which they are few in number. Their somata are located in basal subventricular zones in gyrencephalic brains and they generally possess a basal process extending to the pial surface. They sometimes also have an apical process directed toward the ventricular surface, similar to apical radial glial cells (aRGs) from which they are derived, and whose somata are found more apically in the ventricular zone. bRGs share similarities with aRGs in terms of gene expression ( SOX2 , PAX6 , and NESTIN ), whilst also expressing a range of more specific genes (such as HOPX ). In primate brains, bRGs can divide multiple times, self-renewing and/or generating intermediate progenitors and neurons. They display a highly specific cytokinesis behavior termed mitotic somal translocation. We focus here on recently identified molecular mechanisms associated with the generation and amplification of bRGs, including bRG-like cells in the rodent. These include signaling pathways such as the FGF-MAPK cascade, SHH, PTEN/AKT, PDGF pathways, and proteins such as INSM, GPSM2, ASPM, TRNP1, ARHGAP11B, PAX6, and HIF1α. A number of these proteins were identified through transcriptome comparisons in human aRGs vs. bRGs, and validated by modifying their activities or expression levels in the mouse. This latter experiment often revealed enhanced bRG-like cell production, even in some cases generating folds (gyri) on the surface of the mouse cortex. We compare the features of the identified cells and methods used to characterize them in each model. These important data converge to indicate pathways essential for the production and expansion of bRGs, which may help us understand cortical development in health and disease.

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Section: Brgs and Pathologysupporting

confidence: 89%

Section: Molecular Mechanisms Associated With the Generation And Amplmentioning

confidence: 99%

Genes and Mechanisms Involved in the Generation and Amplification of Basal Radial Glial Cells

Penisson

Ladewig

Belvindrah

et al. 2019

Front. Cell. Neurosci.

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“…Recently, a role for adhesion junction belt downregulation at the VZ surface during basal progenitor delamination (Tavano et al, 2018) was shown to be facilitated by Plekha7, a paralog of Plekhg6, which also exhibits differential isoform expression. Furthermore, non-cell autonomous basal progenitor expansion was also recently reported upon knockdown of the chromatin remodeling factor BAF155 (Narayanan et al, 2018). Thus, although the exact underlying mechanism resulting in basal progenitor expansion after PLEKHG6_4 overexpression has yet to be fully elucidated, a wider role for this family of proteins and the non-cell autonomous features associated with such events in cortical neurogenesis may be emerging.…”

Section: Plekhg6 Influences Vz Integritymentioning

confidence: 95%

A Primate-Specific Isoform of PLEKHG6 Regulates Neurogenesis and Neuronal Migration

et al. 2018

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“…We hence focused on bRG-like cell production at mid-corticogenesis in Lis1 HET mouse mutants. bRG producing mechanisms have been associated with either alterations of mitosis spindle orientation leading to more oblique and vertical divisions (Kalebic et al, 2018; Liu et al, 2017; Wang et al, 2016; Wong et al, 2015), and/or to detachment from the apical surface via decreased cell adhesion (Ju et al, 2016; Martínez-Martínez et al, 2016; Narayanan et al, 2018; Tavano et al, 2018; Taverna et al, 2014). Many of the genes that were described to increase bRG-like cell generation induce more oblique divisions (Penisson et al, 2019), and mitotic spindle orientation is a well-described mechanism that may contribute to the fine tuning of aRG daughter cell fate (LaMonica et al, 2013; Taverna et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Lis1 mutation prevents basal radial glia-like cell production in the mouse

Penisson

Hirotsune

Francis

et al. 2020

Preprint

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Human cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Progenitor cells include apical radial glia, intermediate progenitors and basal (or outer) radial glia (bRGs or oRGs). bRGs are few in number in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 (coding for a RAB-GAP protein) at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 expression in wild-type (WT) brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, using the same approach, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Indeed, we observe disruption of the ventricular zone (VZ) in the mutant. Lis1 depletion altered adhesion proteins and mitotic spindle orientations at the ventricular surface and increased the proportion of abventricular mitoses. Progenitor outcome could not be further altered by TBC1D3. We conclude that perturbation of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis.

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Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex

Cited by 36 publications

References 62 publications

Genes and Mechanisms Involved in the Generation and Amplification of Basal Radial Glial Cells

Genes and Mechanisms Involved in the Generation and Amplification of Basal Radial Glial Cells

A Primate-Specific Isoform of PLEKHG6 Regulates Neurogenesis and Neuronal Migration

Lis1 mutation prevents basal radial glia-like cell production in the mouse

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