@dandergassen.bsky.social
Independent Junior Group Leader at TUM - Postdoc in the Rinn & Meissner Lab (Harvard) - PhD in Denise Barlow's lab (CeMM)
This work, led by Lison Lemoine and co-authors @sarahhoelzl.bsky.social, @hasenbeint.bsky.social and Elisabeth Graf @tum.de, has been published today in Scientific Reports: www.nature.com/articles/s41...
November 11, 2025 at 7:00 PM
This work, led by Lison Lemoine and co-authors @sarahhoelzl.bsky.social, @hasenbeint.bsky.social and Elisabeth Graf @tum.de, has been published today in Scientific Reports: www.nature.com/articles/s41...
Cracking the code of the non-coding genome via allele-specific genomics?
Can we link non-coding elements—like lncRNAs and enhancers—to their protein-coding target genes, and in doing so, connect overlapping non-coding disease variants to their protein-coding counterparts?
Can we link non-coding elements—like lncRNAs and enhancers—to their protein-coding target genes, and in doing so, connect overlapping non-coding disease variants to their protein-coding counterparts?
October 24, 2025 at 2:44 AM
Cracking the code of the non-coding genome via allele-specific genomics?
Can we link non-coding elements—like lncRNAs and enhancers—to their protein-coding target genes, and in doing so, connect overlapping non-coding disease variants to their protein-coding counterparts?
Can we link non-coding elements—like lncRNAs and enhancers—to their protein-coding target genes, and in doing so, connect overlapping non-coding disease variants to their protein-coding counterparts?
We are so happy to be on the cover @sarahhoelzl.bsky.social 🎉 The cover depicts the Three Fates, who manipulate the threads of life and death. The Fates are shown as three older women, unraveling the threads of the inactive X chromosome during aging. www.nature.com/nataging/vol...
June 18, 2025 at 5:20 PM
We are so happy to be on the cover @sarahhoelzl.bsky.social 🎉 The cover depicts the Three Fates, who manipulate the threads of life and death. The Fates are shown as three older women, unraveling the threads of the inactive X chromosome during aging. www.nature.com/nataging/vol...
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
May 2, 2025 at 7:57 PM
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
May 2, 2025 at 7:57 PM
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
May 2, 2025 at 7:57 PM
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
May 2, 2025 at 7:57 PM
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
May 2, 2025 at 7:57 PM
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
May 2, 2025 at 7:46 PM
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
May 2, 2025 at 7:46 PM
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
May 2, 2025 at 7:46 PM
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
May 2, 2025 at 7:46 PM
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
May 2, 2025 at 7:46 PM
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
May 2, 2025 at 7:17 PM
In addition, allele-specific single-cell analysis revealed that age-specific escape manifests within distinct cell types, further providing evidence that age-related epigenetic changes promote gene escape.
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
May 2, 2025 at 7:17 PM
An intriguing example is Reps2, where a specific isoform escapes in an age-dependent manner. While the long isoform of Reps2 is expressed from the Xa, the promoter of the short isoform shows age-dependent biallelic activity, leading to Xi-specific expression of the short isoform.
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
May 2, 2025 at 7:17 PM
Consistently, chromatin accessibility was increased during aging and enriched across multiple megabases at chromosome ends, affecting regulatory elements of escapees.
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
May 2, 2025 at 7:17 PM
We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions.
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
May 2, 2025 at 7:17 PM
Here, we used allele-specific multi-omics approaches to generate a comprehensive catalog of genes that escape X chromosome inactivation across major mouse organs throughout development and aging.
12/ Integrating the GWAS catalog, we found that 30.59% of disease variants overlapping informative lncRNAs were linked to their protein-coding gene targets, allowing us to establish a direct link between a non-coding variant and its protein-coding target.
March 6, 2025 at 11:40 AM
12/ Integrating the GWAS catalog, we found that 30.59% of disease variants overlapping informative lncRNAs were linked to their protein-coding gene targets, allowing us to establish a direct link between a non-coding variant and its protein-coding target.
11/ By benchmarking our predictions against eQTL data, we achieved a 77.47% validation rate. Moreover, we identified high-confidence ncRNA linkages based on the over-representation of target genes and mechanisms across many individuals.
March 6, 2025 at 11:40 AM
11/ By benchmarking our predictions against eQTL data, we achieved a 77.47% validation rate. Moreover, we identified high-confidence ncRNA linkages based on the over-representation of target genes and mechanisms across many individuals.
10/ First validation for our approach was provided by the lncRNA MEG3, known for maternal-mediated DLK1 repression, where we correctly identified 79.46% of 564 individual linkages as repressive.
March 6, 2025 at 11:40 AM
10/ First validation for our approach was provided by the lncRNA MEG3, known for maternal-mediated DLK1 repression, where we correctly identified 79.46% of 564 individual linkages as repressive.
9/ Now let's go to Human! Given the outbred nature of humans, each individual enables the discovery of novel lncRNA to target predictions. Applying our strategy to nearly 1,000 individuals of the GTEx database, we uncovered 2,291 ncRNA-mRNA ASE events and associated mechanisms.
March 6, 2025 at 11:40 AM
9/ Now let's go to Human! Given the outbred nature of humans, each individual enables the discovery of novel lncRNA to target predictions. Applying our strategy to nearly 1,000 individuals of the GTEx database, we uncovered 2,291 ncRNA-mRNA ASE events and associated mechanisms.
8/ Explore our mouse lncRNA target and mechanism predictions directly in the IGV browser for the heart: tinyurl.com/25rzvrhv, or for all major mouse organs, with green indicating enhancing links and red indicating repressive links: tinyurl.com/yruzdr4f
March 6, 2025 at 11:40 AM
8/ Explore our mouse lncRNA target and mechanism predictions directly in the IGV browser for the heart: tinyurl.com/25rzvrhv, or for all major mouse organs, with green indicating enhancing links and red indicating repressive links: tinyurl.com/yruzdr4f
7/ Here is a novel non-imprinted example of a repressive linkage shown by the Allelome.LINK output as a red arc. The allele-specific mapping below validates the maternal expression of the lncRNA (Gm35993) and the nearby paternally expressed putative target (Acmsd).
March 6, 2025 at 11:40 AM
7/ Here is a novel non-imprinted example of a repressive linkage shown by the Allelome.LINK output as a red arc. The allele-specific mapping below validates the maternal expression of the lncRNA (Gm35993) and the nearby paternally expressed putative target (Acmsd).
5/ A repressive interaction occurs when the lncRNA and nearby protein-coding genes show opposite allele-specific expression biases, while an enhancing interaction occurs when both show allelic expression bias toward the same allele. See Xist!
March 6, 2025 at 11:40 AM
5/ A repressive interaction occurs when the lncRNA and nearby protein-coding genes show opposite allele-specific expression biases, while an enhancing interaction occurs when both show allelic expression bias toward the same allele. See Xist!