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Holoprosencephaly phenotypes in LRP2 deficient mouse models are strongly modified by genetic background

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spite of sequence divergence. We are currently identifying functional transcription factor binding sites in endodermal enhancers in both species to identify conserved upstream regulators shared between Phallusia and Ciona. Taken… Click to show full abstract

spite of sequence divergence. We are currently identifying functional transcription factor binding sites in endodermal enhancers in both species to identify conserved upstream regulators shared between Phallusia and Ciona. Taken together our results suggest that extensive transcription factor binding site turn over, without radical change in GRNs architecture, may explain the qualitative conservation of gene expression patterns between highly divergent ascidian genomes.

Keywords: mouse models; lrp2 deficient; deficient mouse; holoprosencephaly phenotypes; models strongly; phenotypes lrp2

Journal Title: Mechanisms of Development
Year Published: 2017

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