The Symmetry of Neural Stem Cell and Progenitor Divisions in the Vertebrate Brain

Gimeno, Gloria Casas; Paridaen, Judith T.M.L.

doi:10.3389/fcell.2022.885269

Cited by 20 publications

(18 citation statements)

References 136 publications

(220 reference statements)

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“…4), suggesting that EGFR signaling controls exit from cell cycle arrest in quiescent HBCs. However, this observation does not inform whether HB‐EGF‐activated HBCs only undergo amplification of the stem cell pool through symmetric/self‐renewing divisions or also differentiation by dividing asymmetrically [123]. HB‐EGF stimulation increases the number of ascl1 ‐positive GBCs (Fig.…”

Section: Discussionmentioning

confidence: 99%

HB‐EGF promotes progenitor cell proliferation and sensory neuron regeneration in the zebrafish olfactory epithelium

Sireci,

Kocagöz,

Alkiraz

et al. 2023

The FEBS Journal

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Maintenance and regeneration of the zebrafish olfactory epithelium (OE) are supported by two distinct progenitor cell populations that occupy spatially discrete stem cell niches and respond to different tissue conditions. Globose basal cells (GBCs) reside at the inner and peripheral margins of the sensory OE and are constitutively active to replace sporadically dying olfactory sensory neurons (OSNs). In contrast, horizontal basal cells (HBCs) are uniformly distributed across the sensory tissue and are selectively activated by acute injury conditions. Here we show that expression of the heparin‐binding epidermal growth factor‐like growth factor (HB‐EGF) is strongly and transiently upregulated in response to OE injury and signals through the EGF receptor (EGFR), which is expressed by HBCs. Exogenous stimulation of the OE with recombinant HB‐EGF promotes HBC expansion and OSN neurogenesis in a pattern that resembles the tissue response to injury. In contrast, pharmacological inhibition of HB‐EGF membrane shedding, HB‐EGF availability, and EGFR signaling strongly attenuate or delay injury‐induced HBC activity and OSN restoration without affecting maintenance neurogenesis by GBCs. Thus, HB‐EGF/EGFR signaling appears to be a critical component of the signaling network that controls HBC activity and, consequently, repair neurogenesis in the zebrafish OE.

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Section: Discussionmentioning

confidence: 99%

HB‐EGF promotes progenitor cell proliferation and sensory neuron regeneration in the zebrafish olfactory epithelium

Sireci,

Kocagöz,

Alkiraz

et al. 2023

The FEBS Journal

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“…The length of cell cycle and the mitotic progression and division orientation of NPCs are tightly regulated for early neurogenesis 39–41 . We assessed mitotic cell populations with their division angle based on the N‐Cadherin‐positive apical membrane in hTM organoids.…”

Section: Resultsmentioning

confidence: 99%

MeCP2 dysfunction prevents proper BMP signaling and neural progenitor expansion in brain organoid

Hong

Yoon

Park

et al. 2023

Ann Clin Transl Neurol

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Objectives Sporadic mutations in MeCP2 are a hallmark of Rett syndrome (RTT). Many RTT brain organoid models have exhibited pathogenic phenotypes such as decreased spine density and small size of soma with altered electrophysiological signals. However, previous models are mainly focused on the phenotypes observed in the late phase and rarely provide clues for the defect of neural progenitors which generate different types of neurons and glial cells. Methods We newly established the RTT brain organoid model derived from MeCP2‐truncated iPS cells which were genetically engineered by CRISPR/Cas9 technology. By immunofluorescence imaging, we studied the development of NPC pool and its fate specification into glutamatergic neurons or astrocytes in RTT organoids. By total RNA sequencing, we investigated which signaling pathways were altered during the early brain development in RTT organoids. Results Dysfunction of MeCP2 caused the defect of neural rosette formation in the early phase of cortical development. In total transcriptome analysis, BMP pathway‐related genes are highly associated with MeCP2 depletion. Moreover, levels of pSMAD1/5 and BMP target genes are excessively increased, and treatment of BMP inhibitors partially rescues the cell cycle progression of neural progenitors. Subsequently, MeCP2 dysfunction reduced the glutamatergic neurogenesis and induced overproduction of astrocytes. Nevertheless, early inhibition of BMP pathway rescued VGLUT1 expression and suppressed astrocyte maturation. Interpretation Our results demonstrate that MeCP2 is required for the expansion of neural progenitor cells by modulating BMP pathway at early stages of development, and this influence persists during neurogenesis and gliogenesis at later stages of brain organoid development.

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“…Exogenous stimulation of the OE with HB-EGF promotes strong HBC proliferation ( Figure 4 ), suggesting that EGFR signaling controls exit from cell cycle arrest in quiescent HBCs. However, this observation does not inform whether HB-EGF-activated HBCs only undergo amplification of the stem cell pool through symmetric/self-renewing divisions or also differentiation by dividing asymmetrically ( Casas Gimeno and Paridaen, 2022 ). HB-EGF stimulation increases the number of ascl1 -positive GBCs ( Figure 5G ) and OSN neurogenesis ( Figure 4D ), thus, at least some of the newly generated cells have the potential to differentiate and to enter the neurogenic lineage.…”

Section: Discussionmentioning

confidence: 99%

HB-EGF Promotes Horizontal Basal Cell Proliferation and Olfactory Sensory Neuron Regeneration in the Zebrafish Olfactory Epithelium

Sireci

Kocagöz

Alkiraz

et al. 2022

Preprint

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Maintenance and regeneration of the zebrafish olfactory epithelium (OE) are supported by distinct progenitor cell populations that occupy discrete stem cell niches and respond to different tissue conditions. Globose basal cells (GBCs) reside at the inner and peripheral margins of the sensory OE and are constitutively active to replace sporadically dying olfactory sensory neurons (OSNs). In contrast, horizontal basal cells (HBCs) are more uniformly distributed across the tissue, including basal layers of the sensory region, and are selectively activated by acute injury conditions that affect the morphological integrity of the OE. Here we show that expression of the heparin-binding epidermal growth factor-like growth factor (HB-EGF) is strongly and transiently upregulated in response to OE injury and signals through the EGF receptor (EGFR), which is expressed by HBCs. Exogenous stimulation of the OE with recombinant HB-EGF promotes HBC expansion and OSN neurogenesis within the sensory OE, resembling the tissue response to injury. In contrast, pharmacological inhibition of HB-EGF shedding, HB-EGF availability, and EGFR signaling strongly attenuate or delay injury-induced HBC activity and OSN restoration without affecting maintenance neurogenesis by GBCs. Thus, HB-EGF/EGFR signaling appears to be a critical component of a complex signaling network that controls HBC activity and, consequently, repair neurogenesis in the zebrafish OE.

show abstract

The Symmetry of Neural Stem Cell and Progenitor Divisions in the Vertebrate Brain

Cited by 20 publications

References 136 publications

HB‐EGF promotes progenitor cell proliferation and sensory neuron regeneration in the zebrafish olfactory epithelium

HB‐EGF promotes progenitor cell proliferation and sensory neuron regeneration in the zebrafish olfactory epithelium

MeCP2 dysfunction prevents proper BMP signaling and neural progenitor expansion in brain organoid

HB-EGF Promotes Horizontal Basal Cell Proliferation and Olfactory Sensory Neuron Regeneration in the Zebrafish Olfactory Epithelium

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