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The Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES) has just published a study in the prestigious journal Nature, listing and assessing the different values we place on nature. Nicolas Dendoncker, professor in the Department of Geography and member of the ILEE Institute at UNamur, is one of the co-authors.

Thesis subject Use of BioID within mitochondria: examples with the study of human mitochondrial co-translational import process and with the identification of MPV17 function Summary This thesis was divided into two different parts dedicated to the study of a mitochondrial process and of a mitochondrial protein using a proximity labelling assay called BioID. The first project was dedicated to the study of a poorly characterized process, the mitochondrial co-translational import. In this process, translation is coupled to the translocation of the mitochondrial proteins, alleviating the energy cost typically associated with the post-translational import relying on chaperone systems. However, the mechanisms are still unclear with only few actors identified but none that have been described in mammals yet. We thus profiled endogenously the TOM20 proxisome using BioID. Despite the enrichment of RNA binding proteins in the TOM20 proxisome, we could not demonstrate a role for a selected candidate, LARP4, in the mitochondrial co-translational import process. Nonetheless, additional uses of this BioID cell line were highlighted such as the monitoring of protein entry inside mitochondria and a potential application in the prediction of mitochondrial protein half-life.The second project was dedicated to the study of MPV17, a protein of the inner mitochondrial membrane whose gene is associated with mitochondrial DNA depletion syndrome. However, the exact molecular function of the protein is still unclear. The approach used in this project was to identify the interacting partners of MPV17, using BioID, to get additional clues about the protein function. In this project we demonstrated an interaction of MPV17 with the MICOS complex but the KO of MPV17 didn't impact mitochondria ultrastructure. However, the depletion of MPV17 protein led to increased mitochondria-derived vesicle formation. Therefore, we investigated a potential degradation of the mtDNA as the cause of the mtDNA depletion observed in MPV17 KO cells but, despite a higher mitophagy level in KO cells, the blockade of the lysosomal activity didn't prevent the depletion. Additional in silico analyses suggested a channel activity of MPV17 further supported by its direct interaction with the Cyclophilin D, a protein of the mitochondrial permeability transition pore. Interestingly, MPV17 KO cells also display higher level of mitochondrial calcium which would be related to the degradation of the mtDNA since the blockade of mitochondrial calcium entry prevents the depletion. We thus propose a role of MPV17 as a potential new member of the mitochondrial permeability transition pore whereas in the absence of the protein, the build-up of calcium inside the mitochondria would lead to the observed mtDNA degradation. Jury Prof. Benoît MUYLKENS (UNamur), ChairmanProf. Patsy RENARD (UNamur), Promoter and SecretaryProf. Thierry ARNOULD (UNamur), Co-PromoterProf. Dr. David PLA-MARTIN (Heinrich Heine University Düsseldorf, Germany)Dr. Timothy WAI (Institut Pasteur Paris, France)Prof. David PLA-MARTIN (Heinrich Heine University Düsseldorf, Germany)Dr. Timothy WAI (Institut Pasteur de Paris, France)Prof. Guy LENAERS (Université d'Angers, France)Prof. Sven EYCKERMAN (Universiteit Gent)

In 2023, UNamur opened a fourth CaNDLE call funded through the joint support of the Fonds Jérôme pour le développement durable and the Assemblée des Cercles of UNamur students. Discover one of the 7 selected projects.

In 2023, UNamur opened a fourth CaNDLE call funded through the joint support of the Fonds Jérôme pour le développement durable and the Assemblée des Cercles of UNamur students. Discover one of the 7 selected projects.

Summary: Impact of the UPR pathway on the establishment of the UVB-induced senescent phenotype Skin aging, influenced by a combination of intrinsic and extrinsic factors, leads to damage capable of altering skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. In particular, these elements lead to an accumulation of senescent cells capable of contributing to the development of age-related pathologies such as skin cancers. Indeed, senescence is accompanied by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched with pro-inflammatory cytokines, growth factors and extracellular matrix remodeling enzymes, altering the characteristics of tissues as they age. Nevertheless, the precise mechanisms leading to the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify molecular mechanisms underlying the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that could contribute to skin aging. In vitro, we confirmed that repeated UVB exposures induce premature senescence in NHDFs and that this state is associated with activation of the three branches of the UPR (Unfolded Protein Response) pathway responsible for maintaining homeostasis of the endoplasmic reticulum (ER), the primary secretory compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements linked to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we showed that the ATF6α branch plays a central role in the occurrence of biomarkers of the UVB-induced senescent phenotype. Indeed, ATF6α invalidation not only protects against UVB-induced morphological changes, but reduces the percentage of SA-βgalactosidase (SA-βgal)-positive cells, prevents persistent DNA damage, and alters the expression of major factors of the senescence-associated secretory phenotype (SASP). As SASP exerts, among other things, a pro-tumoral action, we sought to assess whether the conditioned medium (CM) of UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma-derived cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects.To highlight a potential role for ATF6α in another biological process, we exploited our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteases) regulated by ATF6α and whose impact on the tissue environment was known. Next, we treated a reconstructed human epidermis (RHE) model with MC derived from NHDFs exposed to UVB or not, and invalidated or not for ATF6α. Surprisingly, we observed that MC from UVB-exposed NHDFs increased RHE thickness and basal keratinocyte proliferation, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, since IL-8 blockade by neutralizing antibodies prevents excessive keratinocyte proliferation. In conclusion, we report the role of ATF6α in UVB-induced senescence as well as its impact on the preservation of skin homeostasis under stress conditions notably through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets controlling the effects of skin aging.Abstract: Impact of the UPR pathway on the establishment of the senescent phenotype induced by UVBSkin aging, influenced by a combination of intrinsic and extrinsic factors, can result in damage that has the potential to alter skin functions. Among extrinsic factors, ultraviolet (UV) radiation is responsible for skin photoaging. These factors notably contribute to the accumulation of senescent cells which in turn can contribute to the development of age-related pathologies, including skin cancers. Indeed, senescence is characterized by profound morphological and molecular changes within the cell. This includes a modification of its secretome, which becomes enriched in pro-inflammatory cytokines, growth factors, and matrix-remodeling enzymes, altering tissue characteristics during aging. However, the exact mechanisms driving the senescent phenotype induced by UVB remain largely unknown. In this context, the main objective of this work was to identify the underlying molecular mechanisms responsible for the establishment of UVB-induced senescence in normal human dermal fibroblasts (NHDFs), mechanisms that may play a role in skin aging. In vitro, we confirmed that repeated exposures to UVB induce premature senescence of NHDFs and that this state is associated with the activation of the three branches of the Unfolded Protein Response (UPR), which are responsible for maintaining endoplasmic reticulum (ER) homeostasis, the primary cellular secretion compartment. These observations were supported by transcriptomic analysis, revealing regulatory elements related to major senescence pathways and ER functions in UVB-exposed NHDFs. Subsequently, we demonstrated that the ATF6α branch plays a central role in the development of the UVB-induced senescent phenotype. Indeed, the silencing of ATF6α not only protects against morphological changes induced by UVB, but also reduces the percentage of senescence-associated β-galactosidase (SA-βgal) positive cells, prevents the persistence of DNA damage, and alters the expression of major factors associated with the senescence-associated secretory phenotype (SASP).The SASP, exerting a pro-tumoral action, led us to assess whether the conditioned medium (CM) from UVB-exposed fibroblasts invalidated for ATF6α could impact the migration and invasion potential of melanoma cells. However, we did not observe any ATF6α-dependent pro-migratory or pro-invasive effects. To highlight a potential role of ATF6α in another biological process, we further analyzed our transcriptomic and secretomic analyses and identified a possible effect of ATF6α on the paracrine control of the skin environment. To explore this, we focused on SASP factors (cytokines and metalloproteinases) regulated by ATF6α and whose impact on tissue environment was known. Subsequently, we treated a reconstructed human epidermis (RHE) model with CM from NHDFs exposed or not to UVB and invalidated or not for ATF6α. Surprisingly, we observed that the CM from UVB-exposed NHDFs increased the thickness of the RHE as well as the proliferation of basal keratinocytes, via an ATF6α-dependent mechanism. Finally, we identified IL8 as a major paracrine factor involved in this process, as blocking IL-8 with neutralizing antibodies prevented excessive proliferation of keratinocytes. In conclusion, we report the role of ATF6α in UVB-induced senescence and its impact on the preservation of skin homeostasis under stress conditions, particularly through the regulation of the expression of SASP components. This suggests that ATF6α and its effectors could be promising targets for controlling the effects of skin aging. Jury Prof. Yves POUMAY (Department of Medicine, UNamur), chairmanProf. Florence CHAINIAUX (Department of Biology, UNamur), promoter and secretaryProf. Olivier PLUQUET (Canther, University of Lille), co-promoterProf. Isabelle PETROPULOS (Adaptation Biologique et Vieillissement, Sorbonne Université)Prof. Jérôme LAMARTINE (Laboratoire de Biologie Tissulaire et d'Ingénierie thérapeutique, Université Claude Bernard Lyon 1)Prof. Fabienne FOUFELLE (Maladies métaboliques, diabète et comorbidités, Sorbonne Université)

EMBO Courses and Workshops are selected for their excellent scientific quality and timelines, provision of good networking activities for all participants and speaker gender diversity (at least 40% of speakers must be from the underrepresented gender). Organisers are encouraged to implement measures to make the meeting environmentally more sustainable.Upon registration - More info and registration on the EMBO website.

On Thursday May 30, for our last Chill&Sciences of the season, Candy Sonvaux and Alexis Coyette, mathematics researchers, invite you to discover the mathematics where the movements of the planets and the spread of viruses intertwine until they impact our society.Chill&Science: enriching encountersWith nearly 20 years' experience of scientific cafés, the Confluent des Savoirs has set up a new concept of scientific encounters. The Chill&Sciences are a unique opportunity for the public to come and discuss and ask questions of experts on research topics related to current affairs and citizen issues.Come and enjoy the unique, relaxed atmosphere of Quai22. Researchers and experts from the seven faculties of the University of Namur will present their research and discuss with you over a drink (or two, but never without exaggeration).In practiceThe meetings are open to everyone aged 16 and over. Evenings are limited to around 20 people to ensure a relaxed atmosphere and to facilitate discussions. Meetings take place if a minimum of 10 people are registered. Except in exceptional circumstances, meetings take place every 2 months at the University of Namur's cultural space, Quai22, located at n°22 Rue du Séminaire.Tarif Participation in a Chill&Sciences costs 5€. A discounted annual pass is available. Please note: preferential rate for students (discount code: PromoCDS).The booking fee includes a drink* (soft or beer), a snack (chips and cookies) and management fees linked to the organization Unless cancelled by us, bookings are non-refundable. (*additional drinks will be available upon electronic payment.)

Title of the dissertation: Ion implantation in Low-E coatings Low-emissivity (Low-E) coating technology revolutionizes glass applications for windows, offering high optical transparency while reducing heat transfer. They consist of a silver-based thin film deposited on a glass panel by physical vapor deposition. However, these coatings are fragile and must be placed inside a double-glazing cavity where an inert gas resides. Otherwise, they can be easily degraded by bad atmospheric conditions.The thesis approach is to combine low-E technology with a post-treatment of ion implantation. The research question driving this thesis is: how does ion implantation enhance the durability of low-E coatings containing silver?The experiments conducted during the thesis show that implantation indeed increases the coating resistance while having a small impact on its color. However, the treatment degrades the thermal insulation properties. Hence, a series of hypotheses are formulated based on the literature to explain and control this behavior.A deeper investigation shows that implantation impacts the silver nanostructure. First by dewetting the film which allows reorganization into larger crystallites, second by forcing silver mixing at its interface through ballistic ejections. These two phenomena increase the toughness of the silver interface by interlocking effects. However, dewetting has also been linked to thermal insulation properties degradation. Nonetheless, it was shown that using light gas implantation limits the destructive effect (dewetting) while still inducing good durability (due to interface mixing).. Jury Prof. Julien COLAUX (UNamur), presidentProf. Stéphane LUCAS (UNamur), promoter and secretaryDr Amory JACQUES (Service Public de Wallonie)Dr Philippe ROQUINY (AGC Glass Europe)Prof. Rony SNYDERS (University of Mons)

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The morning will be marked by a lecture by Julien Berthaud, a specialist in the social integration of students, who will share his insights on how this integration becomes a genuine vector for success.Then, scientific papers and experience sharing will enrich our knowledge and spark constructive debate. Lunch will be an opportunity to discover innovative student projects, highlighted in an inspiring exhibition.The afternoon promises to be just as stimulating with a round table moderated by Sabine Henry, where experts will discuss service learning, educational entrepreneurship and spirituality. This dynamic dialogue will be followed by a closing activity: the fresco of engagement, a collective brainstorming session that will lay the foundations for an innovative educational game.Join us for this day of exchange and reflection, and help shape the future of education where student engagement and knowledge vivacity will be the cornerstones of a new educational paradigm.

On the program for all The start of the 2024-2025 academic year will take place on September 16, 2024.09:30 | Welcome ceremony at the Vauban amphitheater (Bd Frère Orban - 5000 Namur).11:00 | Back-to-school celebration at Saint-Aubain Cathedral (Place Saint-Aubain - 5000 Namur) then welcome students by the Cercles. Read more Les infos des paragraphes suivants concernent l'année académique 2024-2025 - elles seront mises à jour prochainement ! Home of the Faculty of Science Tuesday, September 17 at S01from 8:30 am to 9:30 am: for B1 Bio-VTfrom 10 am to 11 am: for B1 Math / Physics / Chemistry / Geology / Geography Home by department Tuesday, September 17After the Faculty welcome, you will be allocated according to your department: DepartmentSchedule and roomMathematics11h at S09Physics14h at S05Chemistry11h15 at Hall CH01Geography and Geology1pm in the Academic Science Room (5th floor of the Faculty Building)BiologyPrimo-arrivals : 9:30 am at the Cour MédecineBisseurs bloc 1, Blocs 2 and 3: 10:30 am at Pool 42Veterinary medicine9:30 am at S01: first-time arrivals only. Discover the full program.Click on this link to get all the information about your academic start at UNamur. You need your login (eid) and the associated mdp to access it.

Courses, exercise sessions, practical laboratory work, field days and internships... everything is done to ensure excellent mastery of concepts and the development of practical skills.