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Fig. 6 | Acta Neuropathologica Communications

Fig. 6

From: The transcriptional coactivator and histone acetyltransferase CBP regulates neural precursor cell development and migration

Fig. 6

The migration deficit observed in hGFAP-cre::CBPFl/Fl mice is mediated by an IGF1-deficiency in the olfactory bulb. a13 The intrinsic migration potential of SVZ derived neuroblasts is independent of CBP function, shown through the culture of SVZ explants in the extracellular matrix Matrigel. b The number of single cells was measured around explants of the SVZ cultured in Matrigel. A piece of OB from the wild type induces an exit of neuroblasts from their migratory chains and thereby an increase in single cells. The mutant OB is unable to induce this effect. The same effect can be observed with medium conditioned with tissue from the OB of wild type or mutant mice. c1 RNA Sequencing (Seq.) of SVZ explants, which were stimulated with medium conditioned from the OB of control or hGFAP-cre::CBPFl/Fl. In total, 106 genes are statistically different between control and mutant with a log2-fold change ≥0.25 and an FDR < 0.1. Genes with high log2-fold changes are annotated. c2 RNA Seq. reveals a difference in IGF signaling between control and mutant. Clustering of RNA Seq. data by the GO-term “0005520 insulin-like growth factor binding” reveals clustering according to the genotype. (d) IGF1 is able to rescue the effect of the CBP deletion on the exit of neuroblasts from chain migration. The addition of recombinant IGF1 to medium conditioned by the OB of control mice has no effect on the number of single cells. In contrast, the number of single cells in the presence of medium conditioned by a CBP deficient OB tissue supplemented with IGF1 is comparable to the number of single cells from wild type medium. Scale bar: 1 mm; *p < 0.05, **p < 0.01

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