Group Leader

Dr. J. Andrew Pospisilik
Dr. J. Andrew Pospisilik
Group Leader
Phone:+49 761 5108 757

Lab Andrew Pospisilik


Who am I not? – Video abstract: Pospisilik et al. 2016 – Cell 163 (3), 353-364.

We are actually a lot closer to the bugs than we thought, at least epigenetically. Watch the video abstract on the newly discovered regulatory, epigenetic switch, which causes individuals with identical genetic material, such as monozygotic twins, to either be lean or obese.

Pospisilik et al (2016): Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity, Cell 164 (3), 353-364, 28 January 2016.

Selected Publications

Kevin Dalgaard,Kathrin Landgraf, Steffen Heyne, Adelheid Lempradl, John Longinotto, Klaus Gossens, Marius Ruf, Michael Orthofer, Ruslan Strogantsev, Madhan Selvaraj, Tess Tsai-Hsiu Lu, Eduard Casas, Raffaele Teperino, M. Azim Surani, Ilona Zvetkova, Debra Rimmington, Y.C. Loraine Tung, Brian Lam, Rachel Larder, Giles S.H. Yeo, Stephen O’Rahilly, Tanya Vavouri, Emma Whitelaw, Josef M. Penninger, Thomas Jenuwein, Ching-Lung Cheung, Anne C. Ferguson-Smith, Anthony P. Coll, Antje Körner, J. Andrew Pospisilik
Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity
Ost A, Lempradl A, Casas E, Weigert M, Tiko T, Deniz M, Pantano L, Boenisch U, Itskov PM, Stoeckius M, Ruf M, Rajewsky N, Reuter G, Iovino N, Ribeiro C, Alenius M, Heyne S, Vavouri T, Pospisilik JA. (2014)
Paternal diet defines offspring chromatin state and intergenerational obesity.
Jais A, Einwallner E, Sharif O, Gossens K, Lu TT, Soyal SM, Medgyesi D, Neureiter D, Paier-Pourani J, Dalgaard K, Duvigneau JC, Lindroos-Christensen J, Zapf TC, Amann S, Saluzzo S, Jantscher F, Stiedl P, Todoric J, Martins R, Oberkofler H, Müller S, Hauser-Kronberger C, Kenner L, Casanova E, Sutterlüty-Fall H, Bilban M, Miller K, Kozlov AV, Krempler F, Knapp S, Lumeng CN, Patsch W, Wagner O, Pospisilik JA, Esterbauer H. (2014)
Heme oxygenase-1 drives metaflammation and insulin resistance in mouse and man.
Teperino R, Amann S, Bayer M, McGee SL, Loipetzberger A, Connor T, Jaeger C, Kammerer B, Winter L, Wiche G, Dalgaard K, Selvaraj M, Gaster M, Lee-Young RS, Febbraio MA, Knauf C, Cani PD, Aberger F, Penninger JM, Pospisilik JA, Esterbauer H. (2012)
Hedgehog partial agonism drives Warburg-like metabolism in muscle and brown fat.
Haschemi A, Kosma P, Gille L, Evans CR, Burant CF, Starkl P, Knapp B, Haas R, Schmid JA, Jandl C, Amir S, Lubec G, Park J, Esterbauer H, Bilban M, Brizuela L, Pospisilik JA, Otterbein LE, Wagner O. (2012)
The sedoheptulose kinase CARKL directs macrophage polarization through control of glucose metabolism.
Pospisilik JA, Schramek D, Schnidar H, Cronin SJ, Nehme NT, Zhang X, Knauf C, Cani PD, Aumayr K, Todoric J, Bayer M, Haschemi A, Puviindran V, Tar K, Orthofer M, Neely GG, Dietzl G, Manoukian A, Funovics M, Prager G, Wagner O, Ferrandon D, Aberger F, Hui CC, Esterbauer H, Penninger JM. (2010)
Drosophila genome-wide obesity screen reveals hedgehog as a determinant of brown versus white adipose cell fate.

Laboratory J. Andrew Pospisilik

Laboratory J. Andrew Pospisilik

Epigenetic control of complex disease

Current estimates place the prevalence of diabetes and obesity in the range of 300 million to beyond 1 billion by the year 2030. As critical risk factors for heart disease, cancer and stroke, obesity and diabetes currently represent one of the world's chief economic and health care challenges. While studies have established elegant genetic frameworks for our current understanding of these complex disorders, the contribution of a number of critical regulatory layers, in particular epigenetic regulation, remains poorly understood.

Our lab is interested in defining epigenetic regulatory systems that contribute to the susceptibility and development of complex disease. These paradigms are broad and include, among others, post-translational modifications of histones, non-coding RNAs, and modifiers of chromatin stability such as the Polycomb-Trithorax Groups. What is clear at present is that these epigenetic effectors play a critical role in defining set-points for entire functional gene sets; the fundamental outstanding question we are interested in is how these epigenetic cues influence the susceptibility and development of human disease.

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