Recent publications

Nucleic Acids Res.: co-auth.: I.Xenarios

 Nucleic Acids Res. 2019 Jan 8;47(D1):D596-D600.  doi: 10.1093/nar/gky876.

Updates in Rhea: SPARQLing Biochemical Reaction Data

Free PMC article


Rhea ( is a comprehensive and non-redundant resource of over 11 000 expert-curated biochemical reactions that uses chemical entities from the ChEBI ontology to represent reaction participants. Originally designed as an annotation vocabulary for the UniProt Knowledgebase (UniProtKB), Rhea also provides reaction data for a range of other core knowledgebases and data repositories including ChEBI and MetaboLights. Here we describe recent developments in Rhea, focusing on a new resource description framework representation of Rhea reaction data and an SPARQL endpoint ( that provides access to it. We demonstrate how federated queries that combine the Rhea SPARQL endpoint and other SPARQL endpoints such as that of UniProt can provide improved metabolite annotation and support integrative analyses that link the metabolome through the proteome to the transcriptome and genome. These developments will significantly boost the utility of Rhea as a means to link chemistry and biology for a more holistic understanding of biological systems and their function in health and disease.

PMID: 30272209 PMCID: PMC6324061 DOI: 10.1093/nar/gky876


Mol Ecol.: co-auth.: group Dessimoz

 2020 May 10. doi: 10.1111/mec.15463. [Epub ahead of print]

The phylogenetic range of bacterial and viral pathogens of vertebrates.

Shaw LP1,2Wang AD1,3Dylus D4,5,6Meier M1,7Pogacnik G1Dessimoz C4,5,6,8,9Balloux F1.


Many major human pathogens are multi-host pathogens, able to infect other vertebrate species. Describing the general patterns of host-pathogen associations across pathogen taxa is therefore important to understand risk factors for human disease emergence. However, there is a lack of comprehensive curated databases for this purpose, with most previous efforts focusing on viruses. Here, we report the largest manually compiled host-pathogen association database, covering 2,595 bacteria and viruses infecting 2,656 vertebrate hosts. We also build a tree for host species using nine mitochondrial genes, giving a quantitative measure of the phylogenetic similarity of hosts. We find that the majority of bacteria and viruses are specialists infecting only a single host species, with bacteria having a significantly higher proportion of specialists compared to viruses. Conversely, multi-host viruses have a more restricted host range than multi-host bacteria. We perform multiple analyses of factors associated with pathogen richness per host species and the pathogen traits associated with greater host range and zoonotic potential. We show that factors previously identified as important for zoonotic potential in viruses-such as phylogenetic range, research effort, and being vector-borne-are also predictive in bacteria. We find that the fraction of pathogens shared between two hosts decreases with the phylogenetic distance between them. Our results suggest that host phylogenetic similarity is the primary factor for host-switching in pathogens.


Emerging infectious diseases; Host jumps; Host range; Phylogenetics; Zoonotic diseases

PMID: 32390272



PLoS Genet.: co-auth.: C.Fankhauser

 2020 May 11;16(5):e1008797. doi: 10.1371/journal.pgen.1008797. [Epub ahead of print]

UVR8-mediated inhibition of shade avoidance involves HFR1 stabilization in Arabidopsis.


Sun-loving plants perceive the proximity of potential light-competing neighboring plants as a reduction in the red:far-red ratio (R:FR), which elicits a suite of responses called the “shade avoidance syndrome” (SAS). Changes in R:FR are primarily perceived by phytochrome B (phyB), whereas UV-B perceived by UV RESISTANCE LOCUS 8 (UVR8) elicits opposing responses to provide a counterbalance to SAS, including reduced shade-induced hypocotyl and petiole elongation. Here we show at the genome-wide level that UVR8 broadly suppresses shade-induced gene expression. A subset of this gene regulation is dependent on the UVR8-stabilized atypical bHLH transcription regulator LONG HYPOCOTYL IN FAR-RED 1 (HFR1), which functions in part redundantly with PHYTOCHROME INTERACTING FACTOR 3-LIKE 1 (PIL1). In parallel, UVR8 signaling decreases protein levels of the key positive regulators of SAS, namely the bHLH transcription factors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5, in a COP1-dependent but HFR1-independent manner. We propose that UV-B antagonizes SAS via two mechanisms: degradation of PIF4 and PIF5, and HFR1- and PIL1-mediated inhibition of PIF4 and PIF5 function. This work highlights the importance of typical and atypical bHLH transcription regulators for the integration of light signals from different photoreceptors and provides further mechanistic insight into the crosstalk of UVR8 signaling and SAS.

PMID: 32392219



Call for applications – Subsides « Tremplin », deadline: 06.09.2020

The Equal Opportunities Office is pleased to announce that applications for the “Tremplin” grant in support of young female academics are now open!

 Application deadline: September 6, 2020.

“Tremplin” grants aims to support women planning to pursue an academic career in offering them more opportunities to develop their scientific record (publication, fieldwork, scientific stay abroad, etc.). Candidates can apply for a grant of max. 25’000 CHF in order to be relieved of their administrative or teaching assignments for up to 12 months. From 2019 on, candidates can also apply for a grant in order to get technical support in their research activities (see changes in grant regulation art. 1 and 4).

Women holding non-tenured postdoc positions are eligible, specifically premières-assistantes, maîtres assistantes and assistant professors. Exceptionally, women holding other types of postdoc academic positions and showing evidence of their motivation in pursuing an academic career may also apply, provided their application responds to the grant’s objective to support women in developing their academic career and accessing professorship.

Applicants must hold a contract position at the University of Lausanne. Researchers under contract with the CHUV can also apply provided they are not eligible for CHUV-specific programmes.

For further information regarding application and conditions, please visit our website.

For any question please contact Roxane Roduit by email ( or phone (021 692 20 84).



Mol Nutr Food Res.: co-auth.: F.Preitner

 2020 May 7:e1901141. doi: 10.1002/mnfr.201901141. [Epub ahead of print]

Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.



Intake of fructose-sweetened beverages and chronic stress both increase risk of cardiometabolic diseases. The aim was to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney.


We measured fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics and key metabolic genes expression at the end of feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + chronic stress (CS), 20% liquid high-fructose supplementation (HFr), or HFr+CS. HFr induced hypertriglyceridemia, up-regulated fructose-metabolism and gluconeogenic enzymes, increased IHTG and DNPalm content in IHTG and IRTG, and augmented fDNL at the end of feeding phase. These changes were diminished after the non-feeding phase. CS did not exert such effects, but when combined with HFr, it reduced IHTG and visceral adiposity, enhanced lipogenic gene expression and fDNL, and increased VLDL-DNPalm secretion.


Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of the high-fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase. This article is protected by copyright. All rights reserved.


Chronic stress; high-fructose supplementation; kidney; lipogenesis; liver

PMID: 32379936



Nucleic Acids Res.: auth.: group Dessimoz

 2020 May 6. pii: gkaa308. doi: 10.1093/nar/gkaa308. [Epub ahead of print]

The Quest for Orthologs benchmark service and consensus calls in 2020.


The identification of orthologs-genes in different species which descended from the same gene in their last common ancestor-is a prerequisite for many analyses in comparative genomics and molecular evolution. Numerous algorithms and resources have been conceived to address this problem, but benchmarking and interpreting them is fraught with difficulties (need to compare them on a common input dataset, absence of ground truth, computational cost of calling orthologs). To address this, the Quest for Orthologs consortium maintains a reference set of proteomes and provides a web server for continuous orthology benchmarking ( Furthermore, consensus ortholog calls derived from public benchmark submissions are provided on the Alliance of Genome Resources website, the joint portal of NIH-funded model organism databases.

PMID: 32374845