A large topographic feature on the surface of the trans-Neptunian object (307261) 2002 MS4_4 measured from stellar occultations

This work aims at constraining the size, shape, and geometric albedo of the dwarf planet candidate 2002 MS4 through the analysis of nine stellar occultation events. Using multichord detection, we also studied the object's topography by analyzing the obtained limb and the residuals between observed chords and the best-fitted ellipse. We predicted and organized the observational campaigns of nine stellar occultations by 2002 MS4 between 2019 and 2022, resulting in two single-chord events, four double-chord detections, and three events with three to up to sixty-one positive chords. Using 13 selected chords from the 8 August 2020 event, we determined the global elliptical limb of 2002 MS4. The best-fitted ellipse, combined with the object's rotational information from the literature, constrains the object's size, shape, and albedo. Additionally, we developed a new method to characterize topography features on the object's limb. The global limb has a semi-major axis of 412 $\pm$ 10 km, a semi-minor axis of 385 $\pm$ 17 km, and the position angle of the minor axis is 121 $^\circ$ $\pm$ 16$^\circ$. From this instantaneous limb, we obtained 2002 MS4's geometric albedo and the projected area-equivalent diameter. Significant deviations from the fitted ellipse in the northernmost limb are detected from multiple sites highlighting three distinct topographic features: one 11 km depth depression followed by a 25$^{+4}_{-5}$ km height elevation next to a crater-like depression with an extension of 322 $\pm$ 39 km and 45.1 $\pm$ 1.5 km deep. Our results present an object that is $\approx$138 km smaller in diameter than derived from thermal data, possibly indicating the presence of a so-far unknown satellite. However, within the error bars, the geometric albedo in the V-band agrees with the results published in the literature, even with the radiometric-derived albedo

Cell type-dependent control of NF-Y activity by TGF-beta

Transforming growth factor beta (TGF-beta) is a pluripotent cytokine that regulates cell growth and differentiation in a cell type-dependent fashion. TGF-beta exerts its effects through the activation of several signaling pathways. One involves membrane proximal events that lead to nuclear translocation of members of the Smad family of transcriptional regulators. TGF-beta can also activate MAPK cascades. Here, we show that TGF-beta induces nuclear translocation of the NF-YA subunit of the transcription factor NF-Y by a process that requires activation of the ERK cascade. This results in increased binding of endogenous NF-Y to chromatin and TGF-beta-dependent transcriptional regulation of the NF-Y target gene cyclin A2. Interestingly, the kinetics of NF-YA relocalization differs between epithelial cells and fibroblasts. NIH3T3 fibroblasts show an elevated basal level of phosphorylated p38 and delayed nuclear accumulation of NF-YA after TGF-beta treatment. In contrast, MDCK cells show low basal p38 activation, higher basal ERK phosphorylation and more rapid localization of NF-YA after induction. Thus, NF-Y activation by TGF-beta1 involves ERK1/2 and potentially an interplay between MAPK pathways, thereby opening the possibility for finely tuned transcriptional regulation

Cell type-dependent control of NF-Y activity by TGF-β

International audienceTransforming growth factor b (TGF-b) is a pluripotent cytokine that regulates cell growth and differentiation in a cell type-dependent fashion. TGF-b exerts its effects through the activation of several signaling pathways. One involves membrane proximal events that lead to nuclear translocation of members of the Smad family of transcriptional regulators. TGF-b can also activate MAPK cascades. Here, we show that TGF-b induces nuclear translocation of the NF-YA subunit of the transcription factor NF-Y by a process that requires activation of the ERK cascade. This results in increased binding of endogenous NF-Y to chromatin and TGF-b-dependent transcriptional regulation of the NF-Y target gene cyclin A2. Interestingly, the kinetics of NF-YA relocalization differs between epithelial cells and fibro-blasts. NIH3T3 fibroblasts show an elevated basal level of phosphorylated p38 and delayed nuclear accumulation of NF-YA after TGF-b treatment. In contrast, MDCK cells show low basal p38 activation, higher basal ERK phosphorylation and more rapid localization of NF-YA after induction. Thus, NF-Y activation by TGF-b1 involves ERK1/2 and potentially an interplay between MAPK pathways, thereby opening the possibility for finely tuned transcriptional regulation

Boosting the sterile insect technique with pyriproxyfen increases tsetse flies Glossina palpalis gambiensis sterilization in controlled conditions

International audienceTsetse flies (Diptera: Glossinidae) are the main vectors of animal and human trypanosomoses in Africa. The Sterile Insect Technique (SIT) has proven effective in controlling tsetse flies when applied to isolated populations but necessitates the production of large numbers of sterile males. A new approach, called boosted SIT, combining SIT with the contamination of wild females by sterile males coated with biocides has been proposed for large-scale control of vector populations. The aim of the study was to evaluate this new approach using pyriproxyfen on the riverine species Glossina palpalis gambiensis (Vanderplank, 1949) in the laboratory. The contamination dose and persistence of pyriproxyfen on sterile males, the impact of pyriproxyfen on male survival, and the dynamics of pyriproxyfen transfer from a sterile male to a female during mating, as well as the impact of pyriproxyfen on pupal production and adult emergence, were evaluated in the laboratory. For this purpose, a method of treatment by impregnating sterile males with a powder containing 40% pyriproxyfen has been developed. The results showed that the pyriproxyfen has no impact on the survival of sterile males. pyriproxyfen persisted on sterile males for up to 10 days at a dose of 100 ng per fly. In addition, the horizontal transfer of pyriproxyfen from a treated sterile male to a female during mating could be measured with an average of 50 ng of pyriproxyfen transferred. After contacts without mating, the average quantity transferred was more than 10 ng. Finally, the pyriproxyfen powder was very effective on G. p. gambiensis leading to 0% emergence of the pupae produced by contaminated females. These promising results must be confirmed in the field. A large-scale assessment of this boosted pyriproxyfen-based SIT approach will be carried out against tsetse flies in Senegal (West Africa). On the African continent, tsetse flies (Diptera: Glossinidae) are the main vectors of the parasites responsible for Human African Trypanosomosis (HAT), or sleeping sickness, and Animal African Trypanosomosis (AAT), also called Nagana 1. These diseases caused by Trypanosomatidae belong to the group of neglected tropical diseases (NTDs), occurring in developing areas 2. Sub-Saharan African countries suffer from a significant impact of NTDs on public health and economic development 3. Glossina palpalis gambiensis (Vanderplank, 1949) is one of the main vectors of the HAT parasite in West Africa and is responsible for the persistence of many residual outbreaks of this disease in forest and savannah areas 4. There is still no vaccine against HAT and curative treatments are difficult to access for the most exposed and vulnerable populations 5. Glossina palpalis gambiensis is also involved in the transmission of AAT, which affects livestock and reduces animal production thus limiting the availability of food resources 6,7. Despite the millions of doses of trypanocides administered, nearly 3 million cattle die each year in Africa from AAT. Annual direct and indirect agricultural losses attributed to this disease are estimated a

Boosting the sterile insect technique with pyriproxyfen increases tsetse flies Glossina palpalis gambiensis sterilization in controlled conditions

FWN – Publicaties zonder aanstelling Universiteit LeidenEnvironmental Biolog

Tissue-specific and SRSF1-dependent splicing of fibronectin, a matrix protein that controls host cell invasion.

Cell invasion targets specific tissues in physiological placental implantation and pathological metastasis, which raises questions about how this process is controlled. We compare dermis and endometrium capacities to support trophoblast invasion, using matching sets of human primary fibroblasts in a coculture assay with human placental explants. Substituting endometrium, the natural trophoblast target, with dermis dramatically reduces trophoblast interstitial invasion. Our data reveal that endometrium expresses a higher rate of the fibronectin (FN) extra type III domain A+ (EDA+) splicing isoform, which displays stronger matrix incorporation capacity. We demonstrate that the high FN content of the endometrium matrix, and not specifically the EDA domain, supports trophoblast invasion by showing that forced incorporation of plasma FN (EDA-) promotes efficient trophoblast invasion. We further show that the serine/arginine-rich protein serine/arginine-rich splicing factor 1 (SRSF1) is more highly expressed in endometrium and, using RNA interference, that it is involved in the higher EDA exon inclusion rate in endometrium. Our data therefore show a mechanism by which tissues can be distinguished, for their capacity to support invasion, by their different rates of EDA inclusion, linked to their SRSF1 protein levels. In the broader context of cancer pathology, the results suggest that SRSF1 might play a central role not only in the tumor cells, but also in the surrounding stroma