The DNMAML1-GFP allele contains a loxP-flanked transcriptional STOP cassette (PGK-Neo-tpolyA), and cDNA containing amino acids 13-74 of the mastermind like 1 (MAML1) gene fused to an enhanced green fluorescent protein (EGFP) and a polyadenylation sequence. MAML1 is a transcriptional co-activator in the Notch signaling pathway and is involved in cell-fate determination. Binding of MAML1 to transcription factor CSL/RBP-J initiates its transformation from a transcriptional repressor to a transcriptional activator. Inhibiting the ability of MAML1 to recruit transcriptional coactivators blocks the transcriptional activation of Notch. This strain expresses a dominant negative (DN) form of MAML1 which consists of amino acids 13-74 which bind the Notch-CSL/RBP-J complex but lacks the MAML1 sequences required to recruit transcriptional coactivators, thereby inhibiting the activation of all four Notch receptors. In the absence of Cre recombinase, reporter gene expression is prevented by the STOP sequence. After removal of the loxP-flanked STOP cassette via Cre-mediated recombination, DNMAML is expressed, Notch signaling is impaired, and EGFP labels all cells where Cre recombinase is expressed. Mice homozygous for the DNMAML1-GFP allele are viable and fertile. When bred to mice containing Tg(Cd4-cre)1Cwi (see Stock No. <a href="https://www.jax.org/strain/022071">022071</a>), T cell development and activation are normal, while IL-4 production is impaired. When challenged with pathogens in vivo, mice that express DNMAML develop an effective Th1 cell response against Leishmania major, but are susceptible to Trichuris Muris infection.&nbsp;

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DNMAML1-GFP has a loxP-flanked transcriptional STOP cassette upstream of a DNMAML1-GFP fusion protein. These mice may be useful for inactivating Notch signaling in specific cells/tissues.

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