Recent publications

Sept 11, 2017 J. Herman BMI Extraordinary seminar EPFL

BMI SEMINAR James Herman 11.9.17











Laboratory of Behavioral Genetics
SV 2805, Station 19
CH- 1015 Lausanne

PH: +41 21 693 17 62


Conférence et table ronde “genre et recherche”, Géopolis, Sept 13, 2017

Genre et recherche: « Integrating gender in science »


Prof. Alison Woodward, Research Professor at the Free University of Brussels (VUB) and Co-Director of RHEA, the Center for Gender Studies and Diversity Research.


Table ronde :

Dr Carole Clair Willi, Physician (CHUV & UNIL)

– Prof. Farinaz Fassa, Sociologist (UNIL & NCCR LIVES)

Prof. em. René Levy, Sociologist (UNIL)

– Damien Michelet, Coordinator PlaGe (UNIL)


Programme et inscription

Poster of the event: Genre-Recherche-Woodward_Sept2017



InnoPACTT: a financial support to create your start‐up Automn CALL 2017, deadline Sept. 27, 2017

InnoPACTT: a financial support to create your start‐up Automn CALL 2017

You are a UNIL‐CHUV scientist and would like to create a start‐up and need a financial support to start?

Apply for a one‐year InnoTREK grant to launch your UNIL‐ CHUV spin‐off! PACTT, Technology Transfer Office of UNIL‐CHUV, is calling for start‐up projects for the InnoTREK grant, part of InnoPACTT, a financial fund to accelerate innovation and UNIL‐CHUV spin‐off creation. With this InnoTREK support, PACTT wants to encourage researchers with innovative ideas to jump into the entrepreneurship adventure.

Deadline for application: September 27th , 2017

For more information please contact us on:
Phone:   021.314.39.84


Postdoc position available at the University of Zurich, Switzerland

Postdoc position in the analysis of long non-coding transcriptome in cardiac regeneration
University of Zurich, Switzerland
 The research group of Raffaella Santoro offers a postdoc position in the field of epigenetic and lncRNA in cardiac regeneration on a collaborative SINERGIA project, “Regenerative strategies for heart disease via targeting the long noncoding transcriptome”, funded by the Swiss National Science Foundation.
Please send applications (including a letter of motivation, CV and contact details of two professional references) as a single PDF to Dr. Raffaella Santoro (
Outstanding candidates will be contacted for interview within two weeks after their application.
Starting date: 1st October 2017


PDF version: Postdoc position June 2017


Open Biol.: co-auth.: V.Kapuria (group Herr)

Open Biol. 2017 Jun;7(6). pii: 170078. doi: 10.1098/rsob.170078.

Recognition of a glycosylation substrate by the O-GlcNAc transferase TPR repeats.


O-linked N-acetylglucosamine (O-GlcNAc) is an essential and dynamic post-translational modification found on hundreds of nucleocytoplasmic proteins in metazoa. Although a single enzyme, O-GlcNAc transferase (OGT), generates the entire cytosolic O-GlcNAc proteome, it is not understood how it recognizes its protein substrates, targeting only a fraction of serines/threonines in the metazoan proteome for glycosylation. We describe a trapped complex of human OGT with the C-terminal domain of TAB1, a key innate immunity-signalling O-GlcNAc protein, revealing extensive interactions with the tetratricopeptide repeats of OGT. Confirmed by mutagenesis, this interaction suggests that glycosylation substrate specificity is achieved by recognition of a degenerate sequon in the active site combined with an extended conformation C-terminal of the O-GlcNAc target site.


O-GlcNAc; O-GlcNAc transferase; glycosylation; signalling; substrate recognition

PMID: 28659383




G3 (Bethesda).: co-auth.: GTF

G3 (Bethesda). 2017 Aug 7;7(8):2413-2426. doi: 10.1534/g3.117.042887.

Comparative Genomics of Two Sequential Candida glabrata Clinical Isolates.


Candida glabrata is an important fungal pathogen which develops rapid antifungal resistance in treated patients. It is known that azole treatments lead to antifungal resistance in this fungal species and that multidrug efflux transporters are involved in this process. Specific mutations in the transcriptional regulator PDR1 result in upregulation of the transporters. In addition, we showed that the PDR1 mutations can contribute to enhance virulence in animal models. In this study, we were interested to compare genomes of two specific C. glabrata-related isolates, one of which was azole susceptible (DSY562) while the other was azole resistant (DSY565). DSY565 contained a PDR1 mutation (L280F) and was isolated after a time-lapse of 50 d of azole therapy. We expected that genome comparisons between both isolates could reveal additional mutations reflecting host adaptation or even additional resistance mechanisms. The PacBio technology used here yielded 14 major contigs (sizes 0.18-1.6 Mb) and mitochondrial genomes from both DSY562 and DSY565 isolates that were highly similar to each other. Comparisons of the clinical genomes with the published CBS138 genome indicated important genome rearrangements, but not between the clinical strains. Among the unique features, several retrotransposons were identified in the genomes of the investigated clinical isolates. DSY562 and DSY565 each contained a large set of adhesin-like genes (101 and 107, respectively), which exceed by far the number of reported adhesins (63) in the CBS138 genome. Comparison between DSY562 and DSY565 yielded 17 nonsynonymous SNPs (among which the was the expected PDR1 mutation) as well as small size indels in coding regions (11) but mainly in adhesin-like genes. The genomes contained a DNA mismatch repair allele of MSH2 known to be involved in the so-called hyper-mutator phenotype of this yeast species and the number of accumulated mutations between both clinical isolates is consistent with the presence of a MSH2 defect. In conclusion, this study is the first to compare genomes of C. glabrata sequential clinical isolates using the PacBio technology as an approach. The genomes of these isolates taken in the same patient at two different time points exhibited limited variations, even if submitted to the host pressure.


Genome Report; adhesins; drug resistance; fungal pathogens; genome comparisons

PMID: 28663342