Aey69, a micropthalmic mouse mutant was found to result from a mutation in H3.2 coding genes, Hist2h3c1. Using a combination of different immunohistochemical markers, a timeline of microphthalmic pathology was charted, with particular focus on lens and retinal pathological changes. In addition, using CRISPR/CAS9 a transgenic mouse line expressing the fusion protein H3.2-GFP was established and characterized. Analysis of incorporation sites of H3.2 in transgenic embryos, illustrated a novel role of H3.2 in ocular development.
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Aey69, a micropthalmic mouse mutant was found to result from a mutation in H3.2 coding genes, Hist2h3c1. Using a combination of different immunohistochemical markers, a timeline of microphthalmic pathology was charted, with particular focus on lens and retinal pathological changes. In addition, using CRISPR/CAS9 a transgenic mouse line expressing the fusion protein H3.2-GFP was established and characterized. Analysis of incorporation sites of H3.2 in transgenic embryos, illustrated a novel role...
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Translated abstract:
Die dominante Mausmutante Aey69 ist durch eine Mikrophthalmie charakterisiert, die durch eine c.358A->C Mutation (Ile120Leu) im Hist2h3c1 Gen verursacht wird, das für ein Histon H3.2 kodiert. Die Mutation führt in der Embryonalentwicklung zum Abbau des Linsenbläschens und zur Hyperproliferation der Retina. Es wurde eine transgene Mauslinie etabliert, die für ein H3.2-GFP-Fusionsprotein kodiert. Die CHiP-Seq-Analyse deutet darauf hin, dass der Ephrin-Signalweg durch das Histon H3.2 betroffen ist.