DOI . ORG {
}
We began analyzing https://www.jneurosci.org/content/30/9/3489, but it redirected us to https://www.jneurosci.org/content/30/9/3489. The analysis below is for the second page.
Title[redir]:
Essential Roles of Notch Signaling in Maintenance of Neural Stem Cells in Developing and Adult Brains | Journal of Neuroscience
Description:
Activation of Notch signaling induces the expression of transcriptional repressor genes such as Hes1 , leading to repression of proneural gene expression and maintenance of neural stem/progenitor cells. However, a requirement for Notch signaling in the telencephalon was not clear, because in Hes1;Hes3;Hes5 triple-mutant mice, neural stem/progenitor cells are depleted in most regions of the developing CNS, but not in the telencephalon. Here, we investigated a role for Notch signaling in the telencephalon by generating tamoxifen-inducible conditional knock-out mice that lack Rbpj , an intracellular signal mediator of all Notch receptors. When Rbpj was deleted in the embryonic brain, almost all telencephalic neural stem/progenitor cells prematurely differentiated into neurons and were depleted. When Rbpj was deleted in the adult brain, all neural stem cells differentiated into transit-amplifying cells and neurons. As a result, neurogenesis increased transiently, but 3 months later all neural stem cells were depleted and neurogenesis was totally lost. These results indicated an absolute requirement of Notch signaling for the maintenance of neural stem cells and a proper control of neurogenesis in both embryonic and adult brains.
Title[redir]:
Essential Roles of Notch Signaling in Maintenance of Neural Stem Cells in Developing and Adult Brains | Journal of Neuroscience
Description:
Activation of Notch signaling induces the expression of transcriptional repressor genes such as Hes1 , leading to repression of proneural gene expression and maintenance of neural stem/progenitor cells. However, a requirement for Notch signaling in the telencephalon was not clear, because in Hes1;Hes3;Hes5 triple-mutant mice, neural stem/progenitor cells are depleted in most regions of the developing CNS, but not in the telencephalon. Here, we investigated a role for Notch signaling in the telencephalon by generating tamoxifen-inducible conditional knock-out mice that lack Rbpj , an intracellular signal mediator of all Notch receptors. When Rbpj was deleted in the embryonic brain, almost all telencephalic neural stem/progenitor cells prematurely differentiated into neurons and were depleted. When Rbpj was deleted in the adult brain, all neural stem cells differentiated into transit-amplifying cells and neurons. As a result, neurogenesis increased transiently, but 3 months later all neural stem cells were depleted and neurogenesis was totally lost. These results indicated an absolute requirement of Notch signaling for the maintenance of neural stem cells and a proper control of neurogenesis in both embryonic and adult brains.
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Keywords {🔍}
cells, neural, stem, mice, notch, signaling, adult, fig, scholar, supplemental, hes, cell, brain, embryonic, brdu, rbpj, neurogenesis, openurlcrossrefpubmedgoogle, type, dividing, neurons, number, maintenance, expression, transitamplifying, lateral, rbpjmutant, telencephalon, tamoxifen, material, wwwjneurosciorg, svz, control, slowly, controls, full, results, development, openurlabstractfree, textgoogle, developing, brains, regions, knockout, increased, inactivation, absence, stemprogenitor, radial, glial,
Topics {✒️}
rosa26-loxp-stop-loxp-cfp mice basic helix-loop-helix factors cytosine-β-d-arabinofuranoside infusion cytosine-β-d-arabinofuranoside development/plasticity/repair essential roles nes-creert2 double-transgenic mice neural stem/progenitor cells displayed cre-mediated recombination transit-amplifying cells respond mouse anti-βiii-tubulin tamoxifen-inducible nestin-creert2 mice numerous label-retaining cells transit-amplifying cells proliferated brdu+ transit-amplifying cells brdu pulse-labeling experiments brdu-incorporated dividing progenitors mash1+ transit-amplifying cells ires-nlslacz expression cassette crossing rbpj-floxed mice x-gal stain buffer lacz-expressing cell types generating hes5-nlslacz mice generated rbpj-conditional knock numerous dcx-positive neurons cre-mediated recombination neural progenitor cells intermediate neural progenitors brdu-incorporated cells increased dividing progenitor cells rbpj-dependent cell proliferation hes5-nlslacz targeting vector main content log mount x-gal staining neural stem cells hes5 triple-mutant mice long-term brdu administration brdu-incorporating cells wild-type rbpj allele rbpj-conditional mutant mice cre recombination efficiency drug-resistant cells hey1-mutant mice suggest nicd-rbpj complex induces slowly dividing cells rbpj-dependent notch signaling long g1 phase rbpj-conditional mutant embryos transit-amplifying cells issue journal arac-treated rbpj-mutant
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