| Summary |
We have recently discovered that deletion of Ptpn11, which codes for protein tyrosine phosphatase Shp2, blocks Bergmann glia (BG) formation and cerebellar foliation, whereas expressing a constitutively active Mek1 (Map2k1), Mek1DD, reverses the Ptpn11-deficient phenotypes, uncovering a previously unappreciated role of BG in folding of the cerebellar cortex. Relatively little is known regarding to the BG induction. The goal of the study was to determine molecular features of newly generated BG.
To identify transcripts enriched in nascent BG, we performed RNA-seq of microdissected cerebellar tissues from wild type (WT), En1cre/+;Ptpn11F/F (Ptpn11-cKO), and En1cre/+;Ptpn11F/F;R26Mek1DD/+ (Ptpn11-cKO;MEK) embryos at E12.5, E13.5, and E14.5.
As BG are initially formed at E13.5, we reasoned that BG-enriched transcripts should be increased from E12.5 to E14.5, decreased in Ptpn11-cKO cerebella, and restored in Ptpn11-cKO;MEK cerebella. By intersecting differentially expressed (DE) genes based on the above-mentioned assumptions, we wanted to identify genes that are specifically expressed in BG and affected by Ptpn11 deletion.
Conclusions: though RNA-seq and subsequent validation, we have successfully identified genes that enriched in nascent BG in the developing mouse cerebellum.
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