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ATRX is required for maintenance of the neuroprogenitor cell pool in the embryonic mouse brain.

Ritchie K, Watson LA, Davidson B, Jiang Y, Bérubé NG - Biol Open (2014)

Bottom Line: We observed increased cell cycle exit during early-mid neurogenesis, and a depletion of apical progenitors by late neurogenesis in the Atrx- neocortex, explaining the disproportionate layering.Premature differentiation was associated with an increased generation of outer radial glia (oRG) and TBR2-expressing basal progenitors, as well as increased generation of early-born post-mitotic projection neurons.Atrx deletion also reduced the fidelity of mitotic spindle orientation in apical progenitors, where mutant cells were often oriented at non-parallel angles of division relative to the ventricular surface.

View Article: PubMed Central - PubMed

Affiliation: Departments of Paediatrics and Biochemistry, Children's Health Research Institute, University of Western Ontario, Victoria Research Laboratories, 800 Commissioners Road East, London, ON N6C 2V5, Canada.

No MeSH data available.


Related in: MedlinePlus

The apical progenitor pool becomes progressively depleted by late neurogenesis in the Atrx-deficient cortex.(A) SOX2 and TBR2 immunostaining in E13.5 control and Atrx- cortex. Scale bar: 100 µm. (B) Quantification of SOX2+ and TBR2+ cells as a percentage of DAPI+ cells in E13.5 control and Atrx- cortex (n = 3). (C) SOX2 and TBR2 immunostaining in E16.5 control and Atrx- cortex. Scale bar: 100 µm. (D) Quantification of SOX2+ (both within the VZ and beyond the VZ) and TBR2+ cells as a percentage of total DAPI+ cells in E16.5 control and Atrx- cortex (n = 3). Data expressed as mean ± S.E.M. *P<0.05.
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f02: The apical progenitor pool becomes progressively depleted by late neurogenesis in the Atrx-deficient cortex.(A) SOX2 and TBR2 immunostaining in E13.5 control and Atrx- cortex. Scale bar: 100 µm. (B) Quantification of SOX2+ and TBR2+ cells as a percentage of DAPI+ cells in E13.5 control and Atrx- cortex (n = 3). (C) SOX2 and TBR2 immunostaining in E16.5 control and Atrx- cortex. Scale bar: 100 µm. (D) Quantification of SOX2+ (both within the VZ and beyond the VZ) and TBR2+ cells as a percentage of total DAPI+ cells in E16.5 control and Atrx- cortex (n = 3). Data expressed as mean ± S.E.M. *P<0.05.

Mentions: Altered postnatal cortical layering could result from precocious differentiation early in neurogenesis, resulting in depletion of the progenitor pool and a failure to generate the correct number of late-born neurons. To determine if the cortical layer abnormalities in the Atrx- cortex were due to increased differentiation of apical progenitor cells, we analyzed the progenitor pool composition, cell cycle exit, and generation of post-mitotic neurons in control and Atrx- cortical cryosections at different developmental time points during the neurogenic period (Figs 2, 3).


ATRX is required for maintenance of the neuroprogenitor cell pool in the embryonic mouse brain.

Ritchie K, Watson LA, Davidson B, Jiang Y, Bérubé NG - Biol Open (2014)

The apical progenitor pool becomes progressively depleted by late neurogenesis in the Atrx-deficient cortex.(A) SOX2 and TBR2 immunostaining in E13.5 control and Atrx- cortex. Scale bar: 100 µm. (B) Quantification of SOX2+ and TBR2+ cells as a percentage of DAPI+ cells in E13.5 control and Atrx- cortex (n = 3). (C) SOX2 and TBR2 immunostaining in E16.5 control and Atrx- cortex. Scale bar: 100 µm. (D) Quantification of SOX2+ (both within the VZ and beyond the VZ) and TBR2+ cells as a percentage of total DAPI+ cells in E16.5 control and Atrx- cortex (n = 3). Data expressed as mean ± S.E.M. *P<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4265753&req=5

f02: The apical progenitor pool becomes progressively depleted by late neurogenesis in the Atrx-deficient cortex.(A) SOX2 and TBR2 immunostaining in E13.5 control and Atrx- cortex. Scale bar: 100 µm. (B) Quantification of SOX2+ and TBR2+ cells as a percentage of DAPI+ cells in E13.5 control and Atrx- cortex (n = 3). (C) SOX2 and TBR2 immunostaining in E16.5 control and Atrx- cortex. Scale bar: 100 µm. (D) Quantification of SOX2+ (both within the VZ and beyond the VZ) and TBR2+ cells as a percentage of total DAPI+ cells in E16.5 control and Atrx- cortex (n = 3). Data expressed as mean ± S.E.M. *P<0.05.
Mentions: Altered postnatal cortical layering could result from precocious differentiation early in neurogenesis, resulting in depletion of the progenitor pool and a failure to generate the correct number of late-born neurons. To determine if the cortical layer abnormalities in the Atrx- cortex were due to increased differentiation of apical progenitor cells, we analyzed the progenitor pool composition, cell cycle exit, and generation of post-mitotic neurons in control and Atrx- cortical cryosections at different developmental time points during the neurogenic period (Figs 2, 3).

Bottom Line: We observed increased cell cycle exit during early-mid neurogenesis, and a depletion of apical progenitors by late neurogenesis in the Atrx- neocortex, explaining the disproportionate layering.Premature differentiation was associated with an increased generation of outer radial glia (oRG) and TBR2-expressing basal progenitors, as well as increased generation of early-born post-mitotic projection neurons.Atrx deletion also reduced the fidelity of mitotic spindle orientation in apical progenitors, where mutant cells were often oriented at non-parallel angles of division relative to the ventricular surface.

View Article: PubMed Central - PubMed

Affiliation: Departments of Paediatrics and Biochemistry, Children's Health Research Institute, University of Western Ontario, Victoria Research Laboratories, 800 Commissioners Road East, London, ON N6C 2V5, Canada.

No MeSH data available.


Related in: MedlinePlus