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| Status |
Public on Oct 14, 2008 |
| Title |
The role of Insulinoma associated 1 protein in the development of the mammalian neocortex |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
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| Summary |
Basal (intermediate) progenitors are the major source of neurons in the mammalian cerebral cortex. The molecular machinery governing basal progenitor biogenesis is unknown. Here we show that the zinc finger transcription factor Insm1 (insulinoma-associated 1) is expressed specifically in progenitors undergoing neurogenic divisions and has a key role in basal progenitor formation. Mouse embryos lacking Insm1 contained half the number of basal progenitors and showed a marked reduction in cortical plate radial thickness. Forced premature expression of Insm1 in neuroepithelial cells resulted in their mitosis occurring at the basal (rather than apical) side of the ventricular zone and induced expression of the basal progenitor marker Tbr2. Remarkably, these cells remained negative for Tis21, a marker of neurogenic progenitors, and did not generate neurons but underwent self-amplification. Our data imply that Insm1 is involved in the generation and expansion of basal progenitors, a hallmark of cerebral cortex evolution.
Keywords: knock out, genetic modification,
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| Overall design |
Dorsal telencephalon from four Insm1 knock out, six heterozygous , and eight wild type mouse embryos (E13.5) were isolated and genome wide gene expression was monitored in order to find target genes of Insm1.
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| Citation(s) |
18940587 |
| Submission date |
Jul 30, 2008 |
| Last update date |
Mar 06, 2018 |
| Contact name |
Thomas Giger |
| E-mail(s) |
giger@eva.mpg.de
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| Organization name |
Max-Planck-Institute of Evolutionary Anthropology
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| Department |
Evolutionary Genetics
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| Street address |
Deutscher Platz 6
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| City |
Leipzig |
| ZIP/Postal code |
04106 |
| Country |
Germany |
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| Platforms (1) |
| GPL6096 |
[MoEx-1_0-st] Affymetrix Mouse Exon 1.0 ST Array [transcript (gene) version] |
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| Samples (18)
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| Relations |
| BioProject |
PRJNA113587 |
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