摘要

Background: Promyelocytic leukemia zinc finger (Plzf), a transcriptional regulator involved in a lot of important biological processes during development, has been implied to maintain neural stem cells and inhibit their differentiation into neurons. However, the effects of Plzf on brain structures and functions are still not clarified. Results: We showed that Plzf expression was detected as early as embryonic day (E) 9.5 in Pax6 + cells in the mouse brain, and was completely disappeared in telencephalon before the initiation of cortical neurogenesis. Loss of Plzf resulted in a smaller cerebral cortex with a decrease in the number of Tbr1 + deep layer neurons due to a decrease of mitotic cell number in the ventricular zone of forebrain at early developmental stage. Microarray, qRT-PCR, and flow cytometry analysis identified dysregulation of Mash1 proneural gene expression. We also observed an impairment of recognition memory in Plzf-deficient mice. Conclusions: Plzf is expressed at early stages of brain development and involved in the formation of deep layer cortical neurons. Loss of Plzf results in dysregulation of Mash1, microcephaly with reduced numbers of early-born neurons, and impairment of recognition memory.
原文英語
文章編號30
期刊Journal of Biomedical Science
26
發行號1
DOIs
出版狀態已發佈 - 四月 26 2019

指紋

Zinc Fingers
Neurons
Zinc
Leukemia
Brain
Biological Phenomena
Telencephalon
Microcephaly
Neural Stem Cells
Data storage equipment
Neurogenesis
Prosencephalon
Flow cytometry
Cerebral Cortex
Microarrays
Stem cells
Gene expression
Flow Cytometry
Cell Count
Gene Expression

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Pharmacology (medical)

引用此文

Promyelocytic leukemia zinc finger is involved in the formation of deep layer cortical neurons. / Lin, Hsin Chuan; Ching, Yung Hao; Huang, Chi Chen; Pao, Ping Chieh; Lee, Yi Hua; Chang, Wen Chang; Kao, Tzu Jen; Lee, Yi Chao.

於: Journal of Biomedical Science, 卷 26, 編號 1, 30, 26.04.2019.

研究成果: 雜誌貢獻文章

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abstract = "Background: Promyelocytic leukemia zinc finger (Plzf), a transcriptional regulator involved in a lot of important biological processes during development, has been implied to maintain neural stem cells and inhibit their differentiation into neurons. However, the effects of Plzf on brain structures and functions are still not clarified. Results: We showed that Plzf expression was detected as early as embryonic day (E) 9.5 in Pax6 + cells in the mouse brain, and was completely disappeared in telencephalon before the initiation of cortical neurogenesis. Loss of Plzf resulted in a smaller cerebral cortex with a decrease in the number of Tbr1 + deep layer neurons due to a decrease of mitotic cell number in the ventricular zone of forebrain at early developmental stage. Microarray, qRT-PCR, and flow cytometry analysis identified dysregulation of Mash1 proneural gene expression. We also observed an impairment of recognition memory in Plzf-deficient mice. Conclusions: Plzf is expressed at early stages of brain development and involved in the formation of deep layer cortical neurons. Loss of Plzf results in dysregulation of Mash1, microcephaly with reduced numbers of early-born neurons, and impairment of recognition memory.",
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author = "Lin, {Hsin Chuan} and Ching, {Yung Hao} and Huang, {Chi Chen} and Pao, {Ping Chieh} and Lee, {Yi Hua} and Chang, {Wen Chang} and Kao, {Tzu Jen} and Lee, {Yi Chao}",
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AU - Lin, Hsin Chuan

AU - Ching, Yung Hao

AU - Huang, Chi Chen

AU - Pao, Ping Chieh

AU - Lee, Yi Hua

AU - Chang, Wen Chang

AU - Kao, Tzu Jen

AU - Lee, Yi Chao

PY - 2019/4/26

Y1 - 2019/4/26

N2 - Background: Promyelocytic leukemia zinc finger (Plzf), a transcriptional regulator involved in a lot of important biological processes during development, has been implied to maintain neural stem cells and inhibit their differentiation into neurons. However, the effects of Plzf on brain structures and functions are still not clarified. Results: We showed that Plzf expression was detected as early as embryonic day (E) 9.5 in Pax6 + cells in the mouse brain, and was completely disappeared in telencephalon before the initiation of cortical neurogenesis. Loss of Plzf resulted in a smaller cerebral cortex with a decrease in the number of Tbr1 + deep layer neurons due to a decrease of mitotic cell number in the ventricular zone of forebrain at early developmental stage. Microarray, qRT-PCR, and flow cytometry analysis identified dysregulation of Mash1 proneural gene expression. We also observed an impairment of recognition memory in Plzf-deficient mice. Conclusions: Plzf is expressed at early stages of brain development and involved in the formation of deep layer cortical neurons. Loss of Plzf results in dysregulation of Mash1, microcephaly with reduced numbers of early-born neurons, and impairment of recognition memory.

AB - Background: Promyelocytic leukemia zinc finger (Plzf), a transcriptional regulator involved in a lot of important biological processes during development, has been implied to maintain neural stem cells and inhibit their differentiation into neurons. However, the effects of Plzf on brain structures and functions are still not clarified. Results: We showed that Plzf expression was detected as early as embryonic day (E) 9.5 in Pax6 + cells in the mouse brain, and was completely disappeared in telencephalon before the initiation of cortical neurogenesis. Loss of Plzf resulted in a smaller cerebral cortex with a decrease in the number of Tbr1 + deep layer neurons due to a decrease of mitotic cell number in the ventricular zone of forebrain at early developmental stage. Microarray, qRT-PCR, and flow cytometry analysis identified dysregulation of Mash1 proneural gene expression. We also observed an impairment of recognition memory in Plzf-deficient mice. Conclusions: Plzf is expressed at early stages of brain development and involved in the formation of deep layer cortical neurons. Loss of Plzf results in dysregulation of Mash1, microcephaly with reduced numbers of early-born neurons, and impairment of recognition memory.

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