Gene expression profiles of presenilin deficient DP thymocytes
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ABSTRACT: Notch1 signaling is an important regulator of cell fate in early stages of T cell development. Because Notch receptors can function redundantly, we sought an approach for inhibiting all endogenous Notch signaling in thymocytes. Upon ligand engagement, Notch receptors undergo two successive proteolytic cleavages, the second involving a Presenilin (PS) containing complex with -secretase activity that releases a small intracellular fragment of Notch. This activated form of Notch (NotchIC) translocates from the membrane to the nucleus, where it acts as a transcription factor, inducing the expression of multiple target genes . Since Presenilins are required for the activation of all four mammalian forms of Notch, we generated mice with deletions of both Presenilin1 and Presenilin2 genes, the only genes encoding Presenilin in the mouse genome. To target Notch inactivation specifically to developing T cells, we introduced Cd4-Cre to mediate Presenilin gene deletion in a tissue- and stage-specific manner. Direct target genes of Notch signaling are largely unknown, and are likely to be cell lineage and stage specific. Therefore in order to identify potential Notch target genes , we compared RNA of thymocytes at the CD4+CD8+ stage of development from H-2b transgenic 5CC7 TCR/ RAG2-deficient / Presenilin1flox/flox /PS2-/- mice, with and without Cd4-Cre. Keywords: presenilin, thymocytes, mouse
ORGANISM(S): Mus musculus
PROVIDER: GSE6590 | GEO | 2007/09/14
SECONDARY ACCESSION(S): PRJNA98901
REPOSITORIES: GEO
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