Her4-Positive Population in the Tectum Opticum Is Proliferating Neural Precursors in the Adult Zebrafish Brain

Jung, Seung-Hyun; Kim, Hyung-Seok; Ryu, Jae-Ho; Gwak, Jung-Woo; Bae, Young-Ki; Kim, Cheol-Hee; Yeo, Sang-Yeob

doi:10.1007/s10059-012-0091-5

Cited by 15 publications

(14 citation statements)

References 13 publications

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“…S1A-J′). Moreover, the direct target of the notch intracellular domain (NICD), her4.1, which labels proliferating neural precursors (Jung et al, 2012;Takke et al, 1999), was also activated in mecp2 morphants (supplementary material Fig. S1K-L′), suggesting that there is elevated Notch overall signaling in mecp2 morphants, which is consistent with a recent report on MeCP2 function in regulating adult neurogenesis through the Notch signaling pathway in mice (Li et al, 2014).…”

Section: Mecp2 Fine-tunes Her2 Expression To Regulate Neural Cell Difsupporting

confidence: 88%

Mecp2 regulates neural cell differentiation by suppressing the Id1 to Her2 axis in zebrafish

Gao

et al. 2015

Journal of Cell Science

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Rett syndrome (RTT) is a progressive neurological disorder caused by mutations in the X-linked protein methyl-CpG-binding protein 2 (MeCP2). The endogenous function of MeCP2 during neural differentiation is still unclear. Here, we report that mecp2 is required for brain development in zebrafish. Mecp2 was broadly expressed initially in embryos and enriched later in the brain. Either morpholino knockdown or genetic depletion of mecp2 inhibited neuronal differentiation, whereas its overexpression promoted neuronal differentiation, suggesting an essential role of mecp2 in directing neural precursors into differentiated neurons. Mechanistically, her2 (the zebrafish ortholog of mammalian Hes5) was upregulated in mecp2 morphants in an Id1-dependent manner. Moreover, knockdown of either her2 or id1 fully rescued neuronal differentiation in mecp2 morphants. These results suggest that Mecp2 plays an important role in neural cell development by suppressing the Id1-Her2 axis, and provide new evidence that embryonic neural defects contribute to the later motor and cognitive dysfunctions in RTT.

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Section: Mecp2 Fine-tunes Her2 Expression To Regulate Neural Cell Difsupporting

confidence: 88%

Mecp2 regulates neural cell differentiation by suppressing the Id1 to Her2 axis in zebrafish

Gao

et al. 2015

Journal of Cell Science

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“…We also examined the function of Notch signaling on RG proliferation and differentiation into neuron after the stab injury. Her4 and her6, a target of Notch signaling, and a type of beta helix loop helix (bHLH) transcriptional factor are expressed in the deep layer of the PGZ in the adult optic tectum (Chapouton et al, 2011;Jung et al, 2012). Notch signaling and her4 and her6 are involved in other types of tissue regeneration, such as fin, and retina (Conner, Ackerman, Lahne, Hobgood, & Hyde, 2014;Grotek, Wehner, & Weidinger, 2013;Kishimoto et al, 2012;Munch, Gonzalez-Rajal, & de la Pompa, 2013;Zhao et al, 2014).…”

Section: Notch Inhibition Enhanced Rg Proliferation Following Stab mentioning

confidence: 99%

Involvement of sonic hedgehog and notch signaling in regenerative neurogenesis in adult zebrafish optic tectum after stab injury

Ueda

Shimizu

et al. 2018

J of Comparative Neurology

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Unlike humans and other mammals, adult zebrafish have the superior capability to recover from central nervous system (CNS) injury. We previously found that proliferation of radial glia (RG) is induced in response to stab injury in optic tectum and that new neurons are generated from RG after stab injury. However, molecular mechanisms which regulate proliferation and differentiation of RG are not well known. In the present study, we investigated Shh and Notch signaling as potential mechanisms regulating regeneration in the optic tectum of adult zebrafish. We used Shh reporter fish and confirmed that canonical Shh signaling is activated specifically in RG after stab injury. Moreover, we have shown that Shh signaling promotes RG proliferation and suppresses their differentiation into neurons after stab injury. In contrast, Notch signaling was down-regulated after stab injury, indicated by the decrease in the expression level of her4 and her6, a target gene of Notch signaling. We also found that inhibition of Notch signaling after stab injury induced more proliferative RG, but that inhibition of Notch signaling inhibited generation of newborn neurons from RG after stab injury. These results suggest that high level of Notch signaling keeps RG quiescent and that appropriate level of Notch signaling is required for generation of newborn neurons from RG. Under physiological condition, activation of Shh signaling or inhibition of Notch signaling also induced RG proliferation. In adult optic tectum of zebrafish, canonical Shh signaling and Notch signaling play important roles in proliferation and differentiation of RG in physiological and regenerative conditions.

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“…The zebrafish and their embryos were handled (Jung et al, 2012) and staged according to a standard protocol (Kimmel et al, 1995). Mini Tol2 col10a1:mGFP constructs were injected together with transposase mRNA at the 1-cell stage of zebrafish embryos, as previously described.…”

Section: Zebrafish Care and Transgenesismentioning

confidence: 99%

Establishment of a Bone-Specific col10a1:GFP Transgenic Zebrafish

Kim

Lee

Jung

et al. 2013

Molecules and Cells

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During skeletal development, both osteogenic and chondrogenic programs are initiated from multipotent mesenchymal cells, requiring a number of signaling molecules, transcription factors, and downstream effectors to orchestrate the sophisticated process. Col10a1, an important downstream effector gene, has been identified as a marker for maturing chondrocytes in higher vertebrates, such as mammals and birds. In zebrafish, this gene has been shown to be expressed in both osteoblasts and chondrocytes, but no study has reported its role in osteoblast development. To initially delineate the osteogenic program from chondrogenic lineage development, we used the zebrafish col10a1 promoter to establish a transgenic zebrafish expressing a GFP reporter specifically in osteoblast-specific bone structures that do not involve cartilaginous programs. A construct harboring a ~2.2-kb promoter region was found to be sufficient to drive the reporter gene in osteoblast-specific bone structures within the endogenous col10a1 expression domain, confirming that separable cis-acting elements exist for distinct cell type-specific expression of col10a1 during zebrafish skeletal development. The ~2.2-kb col10a1:GFP transgenic zebrafish marking only bone structures derived from osteoblasts will undoubtedly be an invaluable tool for identifying and characterizing molecular events driving osteoblast development in zebrafish, which may further provide a differential mechanism where col10a1 is involved in the development of chondrocytes undergoing maturation in other vertebrate systems.

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Her4-Positive Population in the Tectum Opticum Is Proliferating Neural Precursors in the Adult Zebrafish Brain

Cited by 15 publications

References 13 publications

Mecp2 regulates neural cell differentiation by suppressing the Id1 to Her2 axis in zebrafish

Mecp2 regulates neural cell differentiation by suppressing the Id1 to Her2 axis in zebrafish

Involvement of sonic hedgehog and notch signaling in regenerative neurogenesis in adult zebrafish optic tectum after stab injury

Establishment of a Bone-Specific col10a1:GFP Transgenic Zebrafish

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