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HDAC3 But not HDAC2 Mediates Visual Experience-Dependent Radial Glia Proliferation in the Developing Xenopus Tectum

View Article: PubMed Central - PubMed

ABSTRACT

Radial glial cells (RGs) are one of the important progenitor cells that can differentiate into neurons or glia to form functional neural circuits in the developing central nervous system (CNS). Histone deacetylases (HDACs) has been associated with visual activity dependent changes in BrdU-positive progenitor cells in the developing brain. We previously have shown that HDAC1 is involved in the experience-dependent proliferation of RGs. However, it is less clear whether two other members of class I HDACs, HDAC2 and HDAC3, are involved in the regulation of radial glia proliferation. Here, we reported that HDAC2 and HDAC3 expression were developmentally regulated in tectal cells, especially in the ventricular layer of the BLBP-positive RGs. Pharmacological blockade using an inhibitor of class I HDACs, MS-275, decreased the number of BrdU-positive dividing progenitor cells. Specific knockdown of HDAC3 but not HDAC2 decreased the number of BrdU- and BLBP-labeled cells, suggesting that the proliferation of radial glia was selectively mediated by HDAC3. Visual deprivation induced selective augmentation of histone H4 acetylation at lysine 16 in BLBP-positive cells. Furthermore, the visual deprivation-induced increase in BrdU-positive cells was partially blocked by HDAC3 downregulation but not by HDAC2 knockdown at stage 49 tadpoles. These data revealed a specific role of HDAC3 in experience-dependent radial glia proliferation during the development of Xenopus tectum.

No MeSH data available.


Developmental changes in HDAC2 or HDAC3 and colocalization with BLBP in the optic tectum. (A) Representative images showing the colocalization of HDAC2 and BLBP immunostaining at stages 34 (A1, zoom in: A4, A7, A10), 42 (A2, zoom in: A5, A8, A11), and 46 (A3, zoom in: A6, A9, A12) respectively. Arrow heads indicate the BLBP+ RGs processes. Arrows indicate BLBP+ RGs that are HDAC2+. Scale: 100 μm (zoom in: 20 μm). (B) Representative immunofluorescent images showing colocalization of HDAC3 and BLBP staining at stages 34 (B1, zoom in: B4, B7, B10), 42 (B2, zoom in: B5, B8, B11), and 48 (B3, zoom in: B6, B9, B12) respectively. Arrows indicate HDAC3 containing BLBP+ RGs. Scale: 100 μm (zoom in: 20 μm).
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Figure 3: Developmental changes in HDAC2 or HDAC3 and colocalization with BLBP in the optic tectum. (A) Representative images showing the colocalization of HDAC2 and BLBP immunostaining at stages 34 (A1, zoom in: A4, A7, A10), 42 (A2, zoom in: A5, A8, A11), and 46 (A3, zoom in: A6, A9, A12) respectively. Arrow heads indicate the BLBP+ RGs processes. Arrows indicate BLBP+ RGs that are HDAC2+. Scale: 100 μm (zoom in: 20 μm). (B) Representative immunofluorescent images showing colocalization of HDAC3 and BLBP staining at stages 34 (B1, zoom in: B4, B7, B10), 42 (B2, zoom in: B5, B8, B11), and 48 (B3, zoom in: B6, B9, B12) respectively. Arrows indicate HDAC3 containing BLBP+ RGs. Scale: 100 μm (zoom in: 20 μm).

Mentions: Class I HDACs contain four family members (HDAC1, HDAC2, HDAC3 and HDAC8). HDAC1 is developmentally regulated at proliferative glial cells in murine brain (MacDonald and Roskams, 2008) and Xenopus tectum (Guo et al., 2015; Tao et al., 2015). To test whether HDAC2 and HDAC3 expression in RGs were changed with the brain maturation, we immunostained the tectum with the specific antibodies against HDAC2 and HDAC3 (Guo et al., 2015) in cryosections at stages 34, 42 and 48 (Figure 3A). We found that HDAC2 was transiently localized to the mitochondria as HDAC1 (Guo et al., 2015) at stage 34 (Figure 3A7), and mainly confined to the cell nuclei at stage 42 and 48 (Figures 3A8,A9).


HDAC3 But not HDAC2 Mediates Visual Experience-Dependent Radial Glia Proliferation in the Developing Xenopus Tectum
Developmental changes in HDAC2 or HDAC3 and colocalization with BLBP in the optic tectum. (A) Representative images showing the colocalization of HDAC2 and BLBP immunostaining at stages 34 (A1, zoom in: A4, A7, A10), 42 (A2, zoom in: A5, A8, A11), and 46 (A3, zoom in: A6, A9, A12) respectively. Arrow heads indicate the BLBP+ RGs processes. Arrows indicate BLBP+ RGs that are HDAC2+. Scale: 100 μm (zoom in: 20 μm). (B) Representative immunofluorescent images showing colocalization of HDAC3 and BLBP staining at stages 34 (B1, zoom in: B4, B7, B10), 42 (B2, zoom in: B5, B8, B11), and 48 (B3, zoom in: B6, B9, B12) respectively. Arrows indicate HDAC3 containing BLBP+ RGs. Scale: 100 μm (zoom in: 20 μm).
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Figure 3: Developmental changes in HDAC2 or HDAC3 and colocalization with BLBP in the optic tectum. (A) Representative images showing the colocalization of HDAC2 and BLBP immunostaining at stages 34 (A1, zoom in: A4, A7, A10), 42 (A2, zoom in: A5, A8, A11), and 46 (A3, zoom in: A6, A9, A12) respectively. Arrow heads indicate the BLBP+ RGs processes. Arrows indicate BLBP+ RGs that are HDAC2+. Scale: 100 μm (zoom in: 20 μm). (B) Representative immunofluorescent images showing colocalization of HDAC3 and BLBP staining at stages 34 (B1, zoom in: B4, B7, B10), 42 (B2, zoom in: B5, B8, B11), and 48 (B3, zoom in: B6, B9, B12) respectively. Arrows indicate HDAC3 containing BLBP+ RGs. Scale: 100 μm (zoom in: 20 μm).
Mentions: Class I HDACs contain four family members (HDAC1, HDAC2, HDAC3 and HDAC8). HDAC1 is developmentally regulated at proliferative glial cells in murine brain (MacDonald and Roskams, 2008) and Xenopus tectum (Guo et al., 2015; Tao et al., 2015). To test whether HDAC2 and HDAC3 expression in RGs were changed with the brain maturation, we immunostained the tectum with the specific antibodies against HDAC2 and HDAC3 (Guo et al., 2015) in cryosections at stages 34, 42 and 48 (Figure 3A). We found that HDAC2 was transiently localized to the mitochondria as HDAC1 (Guo et al., 2015) at stage 34 (Figure 3A7), and mainly confined to the cell nuclei at stage 42 and 48 (Figures 3A8,A9).

View Article: PubMed Central - PubMed

ABSTRACT

Radial glial cells (RGs) are one of the important progenitor cells that can differentiate into neurons or glia to form functional neural circuits in the developing central nervous system (CNS). Histone deacetylases (HDACs) has been associated with visual activity dependent changes in BrdU-positive progenitor cells in the developing brain. We previously have shown that HDAC1 is involved in the experience-dependent proliferation of RGs. However, it is less clear whether two other members of class I HDACs, HDAC2 and HDAC3, are involved in the regulation of radial glia proliferation. Here, we reported that HDAC2 and HDAC3 expression were developmentally regulated in tectal cells, especially in the ventricular layer of the BLBP-positive RGs. Pharmacological blockade using an inhibitor of class I HDACs, MS-275, decreased the number of BrdU-positive dividing progenitor cells. Specific knockdown of HDAC3 but not HDAC2 decreased the number of BrdU- and BLBP-labeled cells, suggesting that the proliferation of radial glia was selectively mediated by HDAC3. Visual deprivation induced selective augmentation of histone H4 acetylation at lysine 16 in BLBP-positive cells. Furthermore, the visual deprivation-induced increase in BrdU-positive cells was partially blocked by HDAC3 downregulation but not by HDAC2 knockdown at stage 49 tadpoles. These data revealed a specific role of HDAC3 in experience-dependent radial glia proliferation during the development of Xenopus tectum.

No MeSH data available.