Thu Feb 22 – Fri Feb 23, 2024 – Lausanne Omics Days 2024

This year, the scope of the Lausanne Genomics Days has broadened since it becomes the Lausanne Omics Days. It is still a 2-days international conference meant to share advances in genomics and their impact on biological research, applied to a wide range of topics(it does involve 5 UNIL departments CIGDBCDBMVDEE, and DMF).

It will take at UNIL / Genopode on February Thursday 22nd and Friday 23rd.

The conference offers 4 sessions:

  • Deep learning in Biology and Medicine (Chair: Prof. Sven Bergmann)
  • Variation in genome structure and organization (Chair: Prof. Sebastian Soyk)
  • Metabolomics – Towards understanding biological interaction (Chair: Prof. Philipp Engel)
  • Single cell and spatial transcriptomics (Chair: Prof. Tanja Schwander)

For detailed program and more information, please visit the event webpage

Registration is FREE of charge. Still, it is mandatory for organization purpose, in particular ensuring that there will not be food wasted (coffee breaks, lunch and apero are offered).

HERE is the direct link for registration

Attendance is worth 0.5 ECTS

Best regards

Julien Marquis, on behalf of the L0D2024 organization team
Head of Lausanne Genomics Technologies Facility (GTF)

Proc Natl Acad Sci U S A, auth.: group Franken

Cortical miR-709 links glutamatergic signaling to NREM sleep EEG slow waves in an activity-dependent manner

Konstantinos Kompotis # 1 2Géraldine M Mang # 1Jeffrey Hubbard 1Sonia Jimenez 1Yann Emmenegger 1Christos Polysopoulos 3Charlotte N Hor 1Leonore Wigger 4Sébastien S Hébert 5 6Valérie Mongrain 7 8 9Paul Franken 1

. 2024 Jan 16;121(3):e2220532121.

 doi: 10.1073/pnas.2220532121. Epub 2024 Jan 11.

Free article


MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression that have been implicated in a plethora of neuronal processes. Nevertheless, their role in regulating brain activity in the context of sleep has so far received little attention. To test their involvement, we deleted mature miRNAs in post-mitotic neurons at two developmental ages, i.e., in early adulthood using conditional Dicer knockout (cKO) mice and in adult mice using an inducible conditional Dicer cKO (icKO) line. In both models, electroencephalographic (EEG) activity was affected and the response to sleep deprivation (SD) altered; while the rapid-eye-movement sleep (REMS) rebound was compromised in both, the increase in EEG delta (1 to 4 Hz) power during non-REMS (NREMS) was smaller in cKO mice and larger in icKO mice compared to controls. We subsequently investigated the effects of SD on the forebrain miRNA transcriptome and found that the expression of 48 miRNAs was affected, and in particular that of the activity-dependent miR-709. In vivo inhibition of miR-709 in the brain increased EEG power during NREMS in the slow-delta (0.75 to 1.75 Hz) range, particularly after periods of prolonged wakefulness. Transcriptome analysis of primary cortical neurons in vitro revealed that miR-709 regulates genes involved in glutamatergic neurotransmission. A subset of these genes was also affected in the cortices of sleep-deprived, miR-709-inhibited mice. Our data implicate miRNAs in the regulation of EEG activity and indicate that miR-709 links neuronal activity during wakefulness to brain synchrony during sleep through the regulation of glutamatergic signaling.

Metabolism, co-auth.: W.Wahli

GDF15 activates AMPK and inhibits gluconeogenesis and fibrosis in the liver by attenuating the TGF-β1/SMAD3 pathway

Javier Jurado-Aguilar 1Emma Barroso 1Maribel Bernard 1Meijian Zhang 1Mona Peyman 1Patricia Rada 2Ángela M Valverde 2Walter Wahli 3Xavier Palomer 1Manuel Vázquez-Carrera 4

. 2024 Jan 3:152:155772.

 doi: 10.1016/j.metabol.2023.155772. Online ahead of print.


Introduction: The levels of the cellular energy sensor AMP-activated protein kinase (AMPK) have been reported to be decreased via unknown mechanisms in the liver of mice deficient in growth differentiation factor 15 (GDF15). This stress response cytokine regulates energy metabolism mainly by reducing food intake through its hindbrain receptor GFRAL.

Genome Med, auth.: group Reymond

Rare copy-number variants as modulators of common disease susceptibility

Chiara Auwerx 1 2 3 4Maarja Jõeloo 5 6Marie C Sadler 7 8 9Nicolò Tesio 10Sven Ojavee 7 8Charlie J Clark 10Reedik Mägi 6Estonian Biobank Research TeamAlexandre Reymond # 11Zoltán Kutalik # 12 13 14

Genome Med. 2024 Jan 8;16(1):5. doi: 10.1186/s13073-023-01265-5.


Background: Copy-number variations (CNVs) have been associated with rare and debilitating genomic disorders (GDs) but their impact on health later in life in the general population remains poorly described.

Diabetologia co-auth.: B.Thorens

GLP-1 metabolite GLP-1(9-36) is a systemic inhibitor of mouse and human pancreatic islet glucagon secretion

Nikhil R Gandasi 1 2Rui Gao 3Lakshmi Kothegala 1Abigail Pearce 4Cristiano Santos 1Samuel Acreman 1 3Davide Basco 5Anna Benrick 1Margarita V Chibalina 3Anne Clark 3Claudia Guida 3Matthew Harris 4Paul R V Johnson 6 7Jakob G Knudsen 8Jinfang Ma 3Caroline Miranda 1 3Makoto Shigeto 3Andrei I Tarasov 3 9Ho Yan Yeung 4Bernard Thorens 5Ingrid W Asterholm 1Quan Zhang 3Reshma Ramracheya 3Graham Ladds 4Patrik Rorsman 10 11 12 13

Affiliations expand


Aims/hypothesis: Diabetes mellitus is associated with impaired insulin secretion, often aggravated by oversecretion of glucagon. Therapeutic interventions should ideally correct both defects. Glucagon-like peptide 1 (GLP-1) has this capability but exactly how it exerts its glucagonostatic effect remains obscure. Following its release GLP-1 is rapidly degraded from GLP-1(7-36) to GLP-1(9-36). We hypothesised that the metabolite GLP-1(9-36) (previously believed to be biologically inactive) exerts a direct inhibitory effect on glucagon secretion and that this mechanism becomes impaired in diabetes.