Ferdinand von Meyenn


Last Name

von Meyenn

First Name

Ferdinand

ORCID

0000-0001-9920-3075

Organisational unit

09658 - von Meyenn, Ferdinand / von Meyenn, Ferdinand

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Publications 1 - 10 of 62
  • A comprehensive approach for genome-wide efficiency profiling of DNA modifying enzymes
    Item type: Journal Article
    Kyriakopoulos, Charalampos; Nordström, Karl; Kramer, Paula Linh; et al. (2022)
    Cell Reports Methods
    A precise understanding of DNA methylation dynamics is of great importance for a variety of biological processes including cellular reprogramming and differentiation. To date, complex integration of multiple and distinct genome-wide datasets is required to realize this task. We present GwEEP (genome-wide epigenetic efficiency profiling) a versatile approach to infer dynamic efficiencies of DNA modifying enzymes. GwEEP relies on genome-wide hairpin datasets, which are translated by a hidden Markov model into quantitative enzyme efficiencies with reported confidence around the estimates. GwEEP predicts de novo and maintenance methylation efficiencies of Dnmts and furthermore the hydroxylation efficiency of Tets. Its design also allows capturing further oxidation processes given available data. We show that GwEEP predicts accurately the epigenetic changes of ESCs following a Serum-to-2i shift and applied to Tet TKO cells confirms the hypothesized mutual interference between Dnmts and Tets.
  • Adipocyte p53 coordinates the response to intermittent fasting by regulating adipose tissue immune cell landscape
    Item type: Journal Article
    Reinisch, Isabel; Michenthaler, Helene; Sulaj, Alba; et al. (2024)
    Nature Communications
    In obesity, sustained adipose tissue (AT) inflammation constitutes a cellular memory that limits the effectiveness of weight loss interventions. Yet, the impact of fasting regimens on the regulation of AT immune infiltration is still elusive. Here we show that intermittent fasting (IF) exacerbates the lipid-associated macrophage (LAM) inflammatory phenotype of visceral AT in obese mice. Importantly, this increase in LAM abundance is strongly p53 dependent and partly mediated by p53-driven adipocyte apoptosis. Adipocyte-specific deletion of p53 prevents LAM accumulation during IF, increases the catabolic state of adipocytes, and enhances systemic metabolic flexibility and insulin sensitivity. Finally, in cohorts of obese/diabetic patients, we describe a p53 polymorphism that links to efficacy of a fasting-mimicking diet and that the expression of p53 and TREM2 in AT negatively correlates with maintaining weight loss after bariatric surgery. Overall, our results demonstrate that p53 signalling in adipocytes dictates LAM accumulation in AT under IF and modulates fasting effectiveness in mice and humans.
  • Basic Science and Pathogenesis
    Item type: Other Conference Item
    Sona, Chandan; Yeh, Yu-Te; Ghosh, Adhideb; et al. (2024)
    Alzheimer's & Dementia: The Journal of the Alzheimer's Association
  • Investigations into early and late insulin signaling mechanism
    Item type: Doctoral Thesis
    von Meyenn, Ferdinand (2011)
  • ATAC-clock: An aging clock based on chromatin accessibility
    Item type: Journal Article
    Morandini, Francesco; Rechsteiner, Cheyenne; Perez, Kevin; et al. (2024)
    GeroScience
    The establishment of aging clocks highlighted the strong link between changes in DNA methylation and aging. Yet, it is not known if other epigenetic features could be used to predict age accurately. Furthermore, previous studies have observed a lack of effect of age-related changes in DNA methylation on gene expression, putting the interpretability of DNA methylation-based aging clocks into question. In this study, we explore the use of chromatin accessibility to construct aging clocks. We collected blood from 159 human donors and generated chromatin accessibility, transcriptomic, and cell composition data. We investigated how chromatin accessibility changes during aging and constructed a novel aging clock with a median absolute error of 5.27 years. The changes in chromatin accessibility used by the clock were strongly related to transcriptomic alterations, aiding clock interpretation. We additionally show that our chromatin accessibility clock performs significantly better than a transcriptomic clock trained on matched samples. In conclusion, we demonstrate that the clock relies on cell-intrinsic chromatin accessibility alterations rather than changes in cell composition. Further, we present a new approach to construct epigenetic aging clocks based on chromatin accessibility, which bear a direct link to age-related transcriptional alterations, but which allow for more accurate age predictions than transcriptomic clocks.
  • Adipose tissue retains an epigenetic memory of obesity after weight loss
    Item type: Journal Article
    Hinte, Laura; Castellano Castillo, Daniel; Ghosh, Adhideb; et al. (2024)
    Nature
    Reducing body weight to improve metabolic health and related comorbidities is a primary goal in treating obesity1,2. However, maintaining weight loss is a considerable challenge, especially as the body seems to retain an obesogenic memory that defends against body weight changes3,4. Overcoming this barrier for long-term treatment success is difficult because the molecular mechanisms underpinning this phenomenon remain largely unknown. Here, by using single-nucleus RNA sequencing, we show that both human and mouse adipose tissues retain cellular transcriptional changes after appreciable weight loss. Furthermore, we find persistent obesity-induced alterations in the epigenome of mouse adipocytes that negatively affect their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain, and the epigenetic memory can explain future transcriptional deregulation in adipocytes in response to further high-fat diet feeding. In summary, our findings indicate the existence of an obesogenic memory, largely on the basis of stable epigenetic changes, in mouse adipocytes and probably other cell types. These changes seem to prime cells for pathological responses in an obesogenic environment, contributing to the problematic ‘yo-yo’ effect often seen with dieting. Targeting these changes in the future could improve long-term weight management and health outcomes.
  • Microalgae as more sustainable and affordable micronutrient-rich sources for humans
    Item type: Other Conference Item
    Gao, Fengzheng; Zimmermann, Michael; von Meyenn, Ferdinand; et al. (2024)
  • Microalgae in human nutrition and health: using microalgae for iron-deficiency anaemia treatment
    Item type: Other Conference Item
    Gao, Fengzheng; Zimmermann, Michael; von Meyenn, Ferdinand; et al. (2023)
  • Cold-induced epigenetic programming of the sperm enhances brown adipose tissue activity in the offspring
    Item type: Journal Article
    Sun, Wenfei; Dong, Hua; Becker, Anton S.; et al. (2018)
    Nature Medicine
  • Bioaccessibility, bioavailability, and bioactivity assessment of microalgae-derived products for human nutrition and health
    Item type: Other Conference Item
    Gao, Fengzheng; Zimmermann, Michael; von Meyenn, Ferdinand; et al. (2024)
Publications 1 - 10 of 62