Molecular clouds towards RCW 49 and Westerlund 2; Evidence for cluster formation triggered by cloud-cloud collision

We have made CO(J=2-1) observations towards the HII region RCW 49 and its ionizing source, the rich stellar cluster Westerlund 2 (hereafter Wd2), with the NANTEN2 sub-mm telescope. These observations have revealed that two molecular clouds in velocity ranges of -11 to +9 km/s and 11 to 21 km/s respectively, show remarkably good spatial correlations with the Spitzer IRAC mid-infrared image of RCW 49, as well a velocity structures indicative of localized expansion around the bright central regions and stellar cluster. This strongly argues that the two clouds are physically associated with RCW 49. We obtain a new kinematic distance estimate to RCW 49 and Wd2 of 5.4^{+ 1.1}_{- 1.4} kpc, based on the mean velocity and velocity spread of the associated gas. We argue that acceleration of the gas by stellar winds from Wd2 is insufficient to explain the entire observed velocity dispersion of the molecular gas, and suggest a scenario in which a collision between the two clouds ~4 Myrs ago may have triggered the formation of the stellar cluster.Comment: A version with higher resolution figures is available from http://www.a.phys.nagoya-u.ac.jp/~naoko/research/apjl2009/fur09_rev_highreso.pd

Year abroad (a dialogue)

This article is the product of an exchange that took place over the course of two months between March and May 2023 and offers reflections on how the year abroad in modern languages has changed as a result of the COVID-19 pandemic. The four contributors each bring a distinct expertise in year abroad provision and represent different language areas and geographical regions of the United Kingdom. The core themes explored in the discussion are the need for flexibility and resilience within degree programmes, the importance of accessibility and inclusion, and the challenges and opportunities of digital developments in a mobilities context. As well as reflecting on the impact of the pandemic on year abroad provision, the contributors also dwell on how the UK’s withdrawal from the European Union has altered the year abroad landscape

Cloning and characterization of mr-s, a novel SAM domain protein, predominantly expressed in retinal photoreceptor cells

BACKGROUND: Sterile alpha motif (SAM) domains are ~70 residues long and have been reported as common protein-protein interaction modules. This domain is found in a large number of proteins, including Polycomb group (PcG) proteins and ETS family transcription factors. In this work, we report the cloning and functional characterization of a novel SAM domain-containing protein, which is predominantly expressed in retinal photoreceptors and the pineal gland and is designated mouse mr-s (major retinal SAM domain protein). RESULTS: mr-s is evolutionarily conserved from zebrafish through human, organisms through which the mechanism of photoreceptor development is also highly conserved. Phylogenetic analysis suggests that the SAM domain of mr-s is most closely related to a mouse polyhomeotic (ph) ortholog, Mph1/Rae28, which is known as an epigenetic molecule involved in chromatin modifications. These findings provide the possibility that mr-s may play a critical role by regulating gene expression in photoreceptor development. mr-s is preferentially expressed in the photoreceptors at postnatal day 3–6 (P3-6), when photoreceptors undergo terminal differentiation, and in the adult pineal gland. Transcription of mr-s is directly regulated by the cone-rod homeodomain protein Crx. Immunoprecipitation assay showed that the mr-s protein self-associates mainly through the SAM domain-containing region as well as ph. The mr-s protein localizes mainly in the nucleus, when mr-s is overexpressed in HEK293T cells. Moreover, in the luciferase assays, we found that mr-s protein fused to GAL4 DNA-binding domain functions as a transcriptional repressor. We revealed that the repression activity of mr-s is not due to a homophilic interaction through its SAM domain but to the C-terminal region. CONCLUSION: We identified a novel gene, mr-s, which is predominantly expressed in retinal photoreceptors and pineal gland. Based on its expression pattern and biochemical analysis, we predict that mr-s may function as a transcriptional repressor in photoreceptor cells and in pinealocytes of the pineal gland

Ceramide structures involved in the recognition of Siglec-7

To analyze the binding specificity of a sialic acid–recognizing lectin, sialic acid-binding Ig-like lectin 7 (SIGLEC7), to disialyl gangliosides (GD3s), here we established GD3-expressing cells by introducing GD3 synthase (GD3S or ST8SIA1) cDNA into a colon cancer cell line, DLD-1, that expresses no ligands for the recombinant protein SIGLEC7-Fc. SIGLEC7-Fc did not recognize newly-expressed GD3 on DLD-1 cells, even though GD3 was highly expressed, as detected by an anti-GD3 antibody. Because milk-derived GD3 could be recognized by this fusion protein when incorporated onto the surface of DLD-1 cells, we compared the ceramides in DLD-1–generated and milk-derived GD3s to identify the SIGLEC7-specific GD3 structures on the cell membrane, revealing that SIGLEC7 recognizes only GD3-containing regular ceramides but not phytoceramides. This was confirmed by knockdown/knockout of the sphingolipid delta(4)-desaturase/C4-monooxygenase (DES2) gene, involved in phytoceramide synthesis, disclosing that DES2 inhibition confers SIGLEC7 binding. Furthermore, knocking out fatty acid 2-hydroxylase also resulted in the emergence of SIGLEC7 binding to the cell surface. To analyze the effects of binding between SIGLEC7 and various GD3 species on natural killer function, we investigated cytotoxicity of peripheral blood mononuclear cells from healthy donors toward GD3S-transfected DLD-1 (DLD-1–GD3S) cells and DLD-1–GD3S cells with modified ceramides. We found that cytotoxicity is suppressed in DLD-1–GD3S cells with dehydroxylated GD3s. These results indicate that the ceramide structures in glycosphingolipids affect SIGLEC7 binding and distribution on the cell surface and influence cell sensitivity to killing by SIGLEC7-expressing effector cells