Zebrafish PEX1 Is Required for the Generation of GABAergic Neuron in p3 Domain
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Maintenance of neural progenitors requires Notch signaling in vertebrate development. Previous study has shown that Jagged2-mediated Notch signaling maintains proliferating neural progenitors in the ventral spinal cord. However, components for Jagged-mediated signaling remain poorly defined during late neurogenesis. Here we performed yeasttwo hybrid screening by using the intracellular domain (ICD) of zebrafish Jagged2, and investigated a possible role of PEX1 as a component of Notch signaling for the cell-fate decision and the differentiation of neural precursors in p3 domain. Western blotting showed that zebrafish PEX1 might interacts with the ICD of zebrafish Jagged2 physically. PEX1 morpholino-injected embryos showed the increased number of GABAergic KA” neurons as well as the ectopic expression of secondary motor neurons in the p3 domain. The increased number of KA” neurons was also observed in the zebrafish embryos with PEX1 mutation induced by CRISPR/Cas9. These phenotypes resemble with that of Jagged2 morphant. Our observations imply that a critical role of PEX1 in the cell-fate decision of proliferating neural precursors in the p3 domain during the continuing growth and development of the vertebrate nervous system.
Abstract
Maintenance of neural progenitors requires Notch signaling in vertebrate development. Previous study has shown that Jagged2-mediated Notch signaling maintains proliferating neural progenitors in the ventral spinal cord. However, components for Jagged-mediated signaling remain poorly defined during late neurogenesis. Here we performed yeasttwo hybrid screening by using the intracellular domain (ICD) of zebrafish Jagged2, and investigated a possible role of PEX1 as a component of Notch signaling for the cell-fate decision and the differentiation of neural precursors in p3 domain. Western blotting showed that zebrafish PEX1 might interacts with the ICD of zebrafish Jagged2 physically. PEX1 morpholino-injected embryos showed the increased number of GABAergic KA” neurons as well as the ectopic expression of secondary motor neurons in the p3 domain. The increased number of KA” neurons was also observed in the zebrafish embryos with PEX1 mutation induced by CRISPR/Cas9. These phenotypes resemble with that of Jagged2 morphant. Our observations imply that a critical role of PEX1 in the cell-fate decision of proliferating neural precursors in the p3 domain during the continuing growth and development of the vertebrate nervous system.
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