@article{14795, abstract = {Metazoan development relies on the formation and remodeling of cell-cell contacts. Dynamic reorganization of adhesion receptors and the actomyosin cell cortex in space and time plays a central role in cell-cell contact formation and maturation. Nevertheless, how this process is mechanistically achieved when new contacts are formed remains unclear. Here, by building a biomimetic assay composed of progenitor cells adhering to supported lipid bilayers functionalized with E-cadherin ectodomains, we show that cortical F-actin flows, driven by the depletion of myosin-2 at the cell contact center, mediate the dynamic reorganization of adhesion receptors and cell cortex at the contact. E-cadherin-dependent downregulation of the small GTPase RhoA at the forming contact leads to both a depletion of myosin-2 and a decrease of F-actin at the contact center. At the contact rim, in contrast, myosin-2 becomes enriched by the retraction of bleb-like protrusions, resulting in a cortical tension gradient from the contact rim to its center. This tension gradient, in turn, triggers centrifugal F-actin flows, leading to further accumulation of F-actin at the contact rim and the progressive redistribution of E-cadherin from the contact center to the rim. Eventually, this combination of actomyosin downregulation and flows at the contact determines the characteristic molecular organization, with E-cadherin and F-actin accumulating at the contact rim, where they are needed to mechanically link the contractile cortices of the adhering cells.}, author = {Arslan, Feyza N and Hannezo, Edouard B and Merrin, Jack and Loose, Martin and Heisenberg, Carl-Philipp J}, issn = {1879-0445}, journal = {Current Biology}, number = {1}, pages = {171--182.e8}, publisher = {Elsevier}, title = {{Adhesion-induced cortical flows pattern E-cadherin-mediated cell contacts}}, doi = {10.1016/j.cub.2023.11.067}, volume = {34}, year = {2024}, } @article{15018, abstract = {The epitaxial growth of a strained Ge layer, which is a promising candidate for the channel material of a hole spin qubit, has been demonstrated on 300 mm Si wafers using commercially available Si0.3Ge0.7 strain relaxed buffer (SRB) layers. The assessment of the layer and the interface qualities for a buried strained Ge layer embedded in Si0.3Ge0.7 layers is reported. The XRD reciprocal space mapping confirmed that the reduction of the growth temperature enables the 2-dimensional growth of the Ge layer fully strained with respect to the Si0.3Ge0.7. Nevertheless, dislocations at the top and/or bottom interface of the Ge layer were observed by means of electron channeling contrast imaging, suggesting the importance of the careful dislocation assessment. The interface abruptness does not depend on the selection of the precursor gases, but it is strongly influenced by the growth temperature which affects the coverage of the surface H-passivation. The mobility of 2.7 × 105 cm2/Vs is promising, while the low percolation density of 3 × 1010 /cm2 measured with a Hall-bar device at 7 K illustrates the high quality of the heterostructure thanks to the high Si0.3Ge0.7 SRB quality.}, author = {Shimura, Yosuke and Godfrin, Clement and Hikavyy, Andriy and Li, Roy and Aguilera Servin, Juan L and Katsaros, Georgios and Favia, Paola and Han, Han and Wan, Danny and de Greve, Kristiaan and Loo, Roger}, issn = {1369-8001}, journal = {Materials Science in Semiconductor Processing}, keywords = {Mechanical Engineering, Mechanics of Materials, Condensed Matter Physics, General Materials Science}, number = {5}, publisher = {Elsevier}, title = {{Compressively strained epitaxial Ge layers for quantum computing applications}}, doi = {10.1016/j.mssp.2024.108231}, volume = {174}, year = {2024}, } @article{15048, abstract = {Embryogenesis results from the coordinated activities of different signaling pathways controlling cell fate specification and morphogenesis. In vertebrate gastrulation, both Nodal and BMP signaling play key roles in germ layer specification and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis is still insufficiently understood. Here, we took a reductionist approach using zebrafish embryonic explants to study the coordination of Nodal and BMP signaling for embryo patterning and morphogenesis. We show that Nodal signaling triggers explant elongation by inducing mesendodermal progenitors but also suppressing BMP signaling activity at the site of mesendoderm induction. Consistent with this, ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm intercalations, key processes during explant elongation. Translating these ex vivo observations to the intact embryo showed that, similar to explants, Nodal signaling suppresses the effect of BMP signaling on cell intercalations in the dorsal domain, thus allowing robust embryonic axis elongation. These findings suggest a dual function of Nodal signaling in embryonic axis elongation by both inducing mesendoderm and suppressing BMP effects in the dorsal portion of the mesendoderm.}, author = {Schauer, Alexandra and Pranjic-Ferscha, Kornelija and Hauschild, Robert and Heisenberg, Carl-Philipp J}, issn = {1477-9129}, journal = {Development}, number = {4}, pages = {1--18}, publisher = {The Company of Biologists}, title = {{Robust axis elongation by Nodal-dependent restriction of BMP signaling}}, doi = {10.1242/dev.202316}, volume = {151}, year = {2024}, } @misc{14926, author = {Hauschild, Robert}, publisher = {ISTA}, title = {{Matlab script for analysis of clone dispersal}}, doi = {10.15479/AT:ISTA:14926}, year = {2024}, } @article{14979, abstract = {Poxviruses are among the largest double-stranded DNA viruses, with members such as variola virus, monkeypox virus and the vaccination strain vaccinia virus (VACV). Knowledge about the structural proteins that form the viral core has remained sparse. While major core proteins have been annotated via indirect experimental evidence, their structures have remained elusive and they could not be assigned to individual core features. Hence, which proteins constitute which layers of the core, such as the palisade layer and the inner core wall, has remained enigmatic. Here we show, using a multi-modal cryo-electron microscopy (cryo-EM) approach in combination with AlphaFold molecular modeling, that trimers formed by the cleavage product of VACV protein A10 are the key component of the palisade layer. This allows us to place previously obtained descriptions of protein interactions within the core wall into perspective and to provide a detailed model of poxvirus core architecture. Importantly, we show that interactions within A10 trimers are likely generalizable over members of orthopox- and parapoxviruses.}, author = {Datler, Julia and Hansen, Jesse and Thader, Andreas and Schlögl, Alois and Bauer, Lukas W and Hodirnau, Victor-Valentin and Schur, Florian KM}, issn = {1545-9985}, journal = {Nature Structural & Molecular Biology}, keywords = {Molecular Biology, Structural Biology}, publisher = {Springer Nature}, title = {{Multi-modal cryo-EM reveals trimers of protein A10 to form the palisade layer in poxvirus cores}}, doi = {10.1038/s41594-023-01201-6}, year = {2024}, }