Uncategorized Archive

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J Clin Invest.: auth.: group Fajas and Lopez-Mejia

J Clin Invest. 2022 Jul 1;132(13):e162359. doi: 10.1172/JCI162359.

CDK4 is an essential insulin effector in adipocytes

Sylviane LagarrigueIsabel C Lopez-MejiaPierre-Damien DenechaudXavier EscotéJudit Castillo-ArmengolVeronica JimenezCarine ChaveyAlbert GiraltQiuwen LaiLianjun ZhangLaia Martinez-CarreresBrigitte DelacuisineJean-Sébastien AnnicotteEmilie BlanchetSébastien HuréAnna AbellaFrancisco J TinahonesJoan VendrellPierre DubusFatima BoschC Ronald KahnLluis Fajas

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Mobility and fellowships for PhD students and post-doctoral researchers : information session held tomorrow 28.06.2022 at 12:00 in room 315 Amphipôle

The UNIL Research Service is pleased to invite you to an information session, aimed at PhD students and postdoctoral researchers willing to enhance their scientific profile.  This event will be held on June 28th 2022, from 12:00 to 14:00 in Amphipôle building, room 315  

Register here : https://courses.unil.ch/cours/servicerecherche¨

Programme  

12:00 – 12:15: Introduction and presentation of the Research Support Network of the UNIL
Claire Arnold, Grant office UNIL 

12:15 – 12:45: Funding opportunities with Innosuisse, academies, learned societies, NGOs and international programmes + Q&A Session Claire Arnold, Grant office UNIL 

12:45 – 13:15: Marie Skłodowska-Curie Postdoctoral Fellowships (MSC PF) + Q&A Session 
Anne-Emmanuelle de Crousaz, Euresearch UNIL/CHUV 

13:15 – 13:45: Mobility funding scheme Mobi.Doc for PhD students and SNFS « Career » funding schemes + Q&A Session 
Véronique Longchamp, Commission for Research Expertise of UNIL  

Presentations will be in French with slides in English.
The questions & answers will be in both languages.  

For any question: Véronique Longchamp, Responsable FNS Carrières et Mobi.Doc

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Congratulations to Nouria Hernandez on her Lifetime Achievement Award!

We are very proud of Nouria Hernandez who was awarded the FBM Lifetime Achievement Award for her pioneering work on the assembly and mechanisms of the RNA polymerase III complex, and for her outstanding contribution to the UNIL community first as CIG Director and then as Rector of the University.

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Cells.: co-auth.: group B.Thorens

Cells. 2022 May 25;11(11):1737. doi: 10.3390/cells11111737.

Homocysteine Metabolism Pathway Is Involved in the Control of Glucose Homeostasis: A Cystathionine Beta Synthase Deficiency Study in Mouse

Céline Cruciani-Guglielmacci 1Kelly Meneyrol 1Jessica Denom 1Nadim Kassis 1Latif Rachdi 2Fatna Makaci 2Stéphanie Migrenne-Li 1Fabrice Daubigney 1Eleni Georgiadou 3Raphaël G Denis 1 2Ana Rodriguez Sanchez-Archidona 4Jean-Louis Paul 5Bernard Thorens 4Guy A Rutter 3 6 7Christophe Magnan 1Hervé Le Stunff 8Nathalie Janel 1

Abstract

Cystathionine beta synthase (CBS) catalyzes the first step of the transsulfuration pathway from homocysteine to cystathionine, and its deficiency leads to hyperhomocysteinemia (HHcy) in humans and rodents. To date, scarce information is available about the HHcy effect on insulin secretion, and the link between CBS activity and the setting of type 2 diabetes is still unknown. We aimed to decipher the consequences of an inborn defect in CBS on glucose homeostasis in mice. We used a mouse model heterozygous for CBS (CBS+/-) that presented a mild HHcy. Other groups were supplemented with methionine in drinking water to increase the mild to intermediate HHcy, and were submitted to a high-fat diet (HFD). We measured the food intake, body weight gain, body composition, glucose homeostasis, plasma homocysteine level, and CBS activity. We evidenced a defect in the stimulated insulin secretion in CBS+/- mice with mild and intermediate HHcy, while mice with intermediate HHcy under HFD presented an improvement in insulin sensitivity that compensated for the decreased insulin secretion and permitted them to maintain a glucose tolerance similar to the CBS+/+ mice. Islets isolated from CBS+/- mice maintained their ability to respond to the elevated glucose levels, and we showed that a lower parasympathetic tone could, at least in part, be responsible for the insulin secretion defect. Our results emphasize the important role of Hcy metabolic enzymes in insulin secretion and overall glucose homeostasis.

Keywords: autonomic nervous system; hyperhomocysteinemia; insulin secretion; type 2 diabetes.

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Prof. J. van Leeuwen was interviewed for the RTS radio program “CQFD” on May 10, 2022 about CRISPR

Listen to the short program: https://pages.rts.ch/la-1ere/programmes/cqfd/13046064-comment-crispr-le-couteau-suisse-de-la-genetique-ne-cesse-detre-ameliore-10-05-2022.html?mediaShare=1

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Life Sci Alliance.: auth.: group van Leeuwen

Life Sci Alliance. 2022 Jan 11;5(4):e202101153. doi: 10.26508/lsa.202101153. Print 2022 Apr.

Chl1 helicase controls replication fork progression by regulating dNTP pools

Amandine Batté 1Sophie C van der Horst 1Mireille Tittel-Elmer 1 2Su Ming Sun 1Sushma Sharma 3Jolanda van Leeuwen 4Andrei Chabes 3Haico van Attikum 5

Abstract

Eukaryotic cells have evolved a replication stress response that helps to overcome stalled/collapsed replication forks and ensure proper DNA replication. The replication checkpoint protein Mrc1 plays important roles in these processes, although its functional interactions are not fully understood. Here, we show that MRC1 negatively interacts with CHL1, which encodes the helicase protein Chl1, suggesting distinct roles for these factors during the replication stress response. Indeed, whereas Mrc1 is known to facilitate the restart of stalled replication forks, we uncovered that Chl1 controls replication fork rate under replication stress conditions. Chl1 loss leads to increased RNR1 gene expression and dNTP levels at the onset of S phase likely without activating the DNA damage response. This in turn impairs the formation of RPA-coated ssDNA and subsequent checkpoint activation. Thus, the Chl1 helicase affects RPA-dependent checkpoint activation in response to replication fork arrest by ensuring proper intracellular dNTP levels, thereby controlling replication fork progression under replication stress conditions.