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Articles by Andreas Magg
Katholische Morgenfeier 27. September 2026
Die Katholische Morgenfeier vom 27. September 2026 mit Landes-Caritasdirektor Pfarrer Andreas Magg aus München mit dem Thema "Mitarbeiter Gottes".
Conservation of regulatory elements with highly diverged sequences across large evolutionary distances - Nature Genetics
Abstract Developmental gene expression is a remarkably conserved process, yet most cis-regulatory elements (CREs) lack sequence conservation, especially at larger evolutionary distances. Some evidence suggests that CREs at the same genomic position remain functionally conserved independent of sequence conservation. However, the extent of such positional conservation remains unclear.
Temporal misexpression of En1 during limb development causes distinct phenotypes
Abstract The precise spatiotemporal regulation of developmental genes is required for proper organogenesis.
Temporally restricted activities of En1 regulatory elements underlie distinct limb malformations
Abstract The precise spatiotemporal expression of developmental genes is required for proper embryonic development. EN1 plays a key role in dorsal-ventral patterning in mouse limb development from embryonic day (E) 9.5 to E11.5. Previously, we identified the lncRNA locus Maenli which drives En1 expression at E9.5, specifically in the limb. Here we addressed how En1 expression is maintained at later developmental stages when Maenli transcriptional activity is absent.
Non-coding deletions identify Maenli lncRNA as a limb-specific En1 regulator
Abstract Long non-coding RNAs (lncRNAs) can be important components in gene-regulatory networks1, but the exact nature and extent of their involvement in human Mendelian disease is largely unknown. Here we show that genetic ablation of a lncRNA locus on human chromosome 2 causes a severe congenital limb malformation.
Serial genomic inversions induce tissue-specific architectural stripes, gene misexpression and congenital malformations
Abstract Balanced chromosomal rearrangements such as inversions and translocations can cause congenital disease or cancer by inappropriately rewiring promoter–enhancer contacts1,2.
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