Recent publications

Sci Rep.: auth.: W.Wahli

 2018 Jul 27;8(1):11338. doi: 10.1038/s41598-018-29815-7.

Complementary intestinal mucosa and microbiota responses to caloric restriction.


The intestine is key for nutrient absorption and for interactions between the microbiota and its host. Therefore, the intestinal response to caloric restriction (CR) is thought to be more complex than that of any other organ. Submitting mice to 25% CR during 14 days induced a polarization of duodenum mucosa cell gene expression characterised by upregulation, and downregulation of the metabolic and immune/inflammatory pathways, respectively. The HNF, PPAR, STAT, and IRF families of transcription factors, particularly the Pparα and Isgf3 genes, were identified as potentially critical players in these processes. The impact of CR on metabolic genes in intestinal mucosa was mimicked by inhibition of the mTOR pathway. Furthermore, multiple duodenum and faecal metabolites were altered in CR mice. These changes were dependent on microbiota and their magnitude corresponded to microbial density. Further experiments using mice with depleted gut bacteria and CR-specific microbiota transfer showed that the gene expression polarization observed in the mucosa of CR mice is independent of the microbiota and its metabolites. The holistic interdisciplinary approach that we applied allowed us to characterize various regulatory aspects of the host and microbiota response to CR.

PMID: 30054525



Sept 14-15, 2018 Life Sciences PostDoc/Innovation Day 2018, Zurich

Dear postdoctoral fellows and PhD students,

We are pleased to announce and invite you to the Life Sciences PostDoc Day 2018 , which will be held at ETH Zurich main building on the 14th of September. This is an exciting networking and information-based event, offering opportunities for meeting new colleagues and academic resources, learning about their work, initiating exchanges and collaborations that can push your research and career further. This year’s PostDoc Day has been re-invented and expanded to focus on scientific collaboration and transitioning from the postdoctoral period into future careers.

For the first time we are also organizing a second complementary meeting called Life Sciences Innovation Daywhich takes place on the 15th of September at ETH Zurich main building. The Innovation Day brings together leaders from academia and industry to discuss current challenges and develop new concepts for an ecosystem fostering open science and innovation. Innovation Day provides more opportunities for those seeking networks between academia, industry, and clinical medicine.

Together, these two days form the first “Open Innovation in Life Sciences” conference. These back-to-back partner events complement each other and give young researchers unique opportunities to network amongst themselves and take inspiration from leaders in academia and industry. Come explore cross-disciplinary collaborative projects and career paths, and join a sustainable community of like-minded young life scientists!

You can register and submit your abstract by following this link:

Kind regards,

The organizing committee

Monica Ghidinelli (ETHZ), Joyce Kao (NYU/ETHZ), Mateusz Wietecha (ETHZ), Rodrigo Villasenor (UZH), Nino Nikolovski (ETHZ), Evan Williams (ETHZ), Andrea Aloia (ETHZ), Laura De Vargas Roditi (USZ/UZH), Marieke Buffing (ETHZ), Sukalp Muzumdar (ETHZ), Tobias Weiss (USZ/UZH), Servan Grüninger (reatch/UZH/EPFL), Christian Feller (ETHZ)



Welcome to Jonathan!

Hello everyone,

My name is Jonathan Magnenat, I’m 21 years old and live in a small village near Morges.

I come from a bicultural family; half Brazilian and half Swiss. This may explain my two main passions that are traveling and discovering new cultures. I’m a linguaphile.

You may see me in the corridors, as I’m the new admin apprentice at the CIG Direction. I’ll be among you for the next couple of years intending to learn from Julie Papet what involve being commercial and administration employee.

What else can I say?


Well, if I can help you for anything please ask, I’ll be glad to help you.



CIG Seminars Fall 2018 Program

CIG Seminars Fall 2018

Monday 12:15, Génopode, auditorium A, followed by sandwiches

Download the poster

Monday September 24, 2018
Mark Herman, Duke University, USA
«The role of ChREBP in sugar-induced metabolic disease»
Host: Frédéric Preitner

Monday October 8, 2018
Gregory Jefferis, University of Cambridge, UK
Host: Richard Benton

Monday October 15, 2018
Beverly Davidson, The Children’s Hospital of Philadelphia, USA
«Emerging therapies for neurological diseases»
Host: Vincent Dion

Monday October 22, 2018
Lesley Jones, Cardiff University, UK
«Genetic modifiers in Huntington’s disease»
Host: Vincent Dion

Monday October 29, 2018
Michael S. Levine, Princeton University, USA
«Transcription networks in animal development and evolution»
Host: Maria Cristina Gambetta

Monday November 12, 2018
Katja Lamia, The Scripps Research Institute, USA
«Cryptochromes integrate circadian rhythms with metabolism and genome protection»
Host: David Gatfield

Monday November 19, 2018
Stephan Gruber, DMF, University of Lausanne, CH
«Getting chromosomes organized: The power of DNA looping motors»
Host: Andrzej Stasiak

Monday November 26, 2018
Jody Rosenblatt, University of Utah, USA
«Epithelial cell extrusion and its misregulation in disease»
Host: Fisun Hamaratoglu

Monday December 10, 2018
Matthias Hentze, EMBL Heidelberg, DE
«Hidden treasures of the RNA world: RBPs from moonlighting to riboregulation»
Host: David Gatfield

Monday December 17, 2018
Jean-Yves Masson, Université Laval, Québec, CA
«Charting the roles of Fanconi anemia/breast cancer genes in DNA double-strand break repair and synthetic lethal strategies»
Host: Vincent Dion



Int J Mol Sci.: auth.: W.Wahli

 2018 Jun 27;19(7). pii: E1893. doi: 10.3390/ijms19071893.

Insights into the Role of PPARβ/δ in NAFLD.

Chen J1,2Montagner A3,4Tan NS5,6,7,8Wahli W9,10,11.


Non-alcoholic fatty liver disease (NAFLD) is a major health issue in developed countries. Although usually associated with obesity, NAFLD is also diagnosed in individuals with low body mass index (BMI) values, especially in Asia. NAFLD can progress from steatosis to non-alcoholic steatohepatitis (NASH), which is characterized by liver damage and inflammation, leading to cirrhosis and hepatocellular carcinoma (HCC). NAFLD development can be induced by lipid metabolism alterations; imbalances of pro- and anti-inflammatory molecules; and changes in various other factors, such as gut nutrient-derived signals and adipokines. Obesity-related metabolic disorders may be improved by activation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR)β/δ, which is involved in metabolic processes and other functions. This review is focused on research findings related to PPARβ/δ-mediated regulation of hepatic lipid and glucose metabolism and NAFLD development. It also discusses the potential use of pharmacological PPARβ/δ activation for NAFLD treatment.


NAFLD; NASH; PPARβ/δ; lipid metabolism; liver; steatosis

PMID: 29954129

Am J Physiol Endocrinol Metab.: co-auth.: L.Fajas

 2018 Jun 26. doi: 10.1152/ajpendo.00182.2018. [Epub ahead of print]

β-Klotho deficiency shifts the gut-liver bile acid axis and induces hepatic alterations in mice.


β-Klotho (encoded by Klb) is an obligate co-receptor mediating both fibroblast growth factor (FGF)15 and FGF21 signaling. Klb-/- mice are refractory to metabolic FGF15 and FGF21 action and exhibit derepressed (increased) bile acid (BA) synthesis. Here, we deeply phenotyped male Klb-/- mice on a pure C57BL/6J genetic background fed a chow diet, focusing on metabolic aspects. This aims to better understand the physiological consequences of concomitant FGF15 and FGF21 signaling deficiency, in particular on the gut-liver axis. Klb-/- mice present permanent growth restriction independent of adiposity and energy balance. Klb-/- mice also exhibit few changes in carbohydrate metabolism, combining normal gluco-tolerance, insulin sensitivity and fasting response with increased gluconeogenic capacity and decreased glycogen mobilization. Livers of Klb-/- mice reveal pathologic features, including a pro-inflammatory status and initiation of fibrosis. These defects are associated to a massive shift in BA composition in the enterohepatic system and blood circulation featured by a large excess of microbiota-derived deoxycholic acid (DCA), classically known for its genotoxicity in the gastrointestinal tract. In conclusion, β-Klotho is a gatekeeper of hepatic integrity, through direct action (mediating FGF21 anti-inflammatory signaling) and indirect mechanisms (mediating FGF15 signaling that maintain BA level and composition).


Beta-Klotho; Bile acid; Deoxycholic acid; Fibroblast Growth Factor; inflammation

PMID: 29944388