@article{10834,
  abstract     = {Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation and the protrusion of branched actin filament networks. Moreover, Hem1 loss of function in immune cells causes autoimmune diseases in humans. Here, we show that genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis as well as phagocytic cup formation in addition to defects in lamellipodial protrusion and migration. Moreover, Hem1-null macrophages displayed strong defects in cell adhesion despite unaltered podosome formation and concomitant extracellular matrix degradation. Specifically, dynamics of both adhesion and de-adhesion as well as concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly compromised. Accordingly, disruption of WRC function in non-hematopoietic cells coincided with both defects in adhesion turnover and altered FAK and paxillin phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes, but not lamellipodia formation, were partially rescued by small molecule activation of FAK. A full rescue of the phenotype, including lamellipodia formation, required not only the presence of WRCs but also their binding to and activation by Rac. Collectively, our results uncover that WRC impacts on integrin-dependent processes in a FAK-dependent manner, controlling formation and dismantling of adhesions, relevant for properly grabbing onto extracellular surfaces and particles during cell edge expansion, like in migration or phagocytosis.},
  author       = {Stahnke, Stephanie and Döring, Hermann and Kusch, Charly and de Gorter, David J.J. and Dütting, Sebastian and Guledani, Aleks and Pleines, Irina and Schnoor, Michael and Sixt, Michael K and Geffers, Robert and Rohde, Manfred and Müsken, Mathias and Kage, Frieda and Steffen, Anika and Faix, Jan and Nieswandt, Bernhard and Rottner, Klemens and Stradal, Theresia E.B.},
  issn         = {0960-9822},
  journal      = {Current Biology},
  keywords     = {General Agricultural and Biological Sciences, General Biochemistry, Genetics and Molecular Biology},
  number       = {10},
  pages        = {2051--2064.e8},
  publisher    = {Elsevier},
  title        = {{Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion}},
  doi          = {10.1016/j.cub.2021.02.043},
  volume       = {31},
  year         = {2021},
}

@article{11052,
  abstract     = {In order to combat molecular damage, most cellular proteins undergo rapid turnover. We have previously identified large nuclear protein assemblies that can persist for years in post-mitotic tissues and are subject to age-related decline. Here, we report that mitochondria can be long lived in the mouse brain and reveal that specific mitochondrial proteins have half-lives longer than the average proteome. These mitochondrial long-lived proteins (mitoLLPs) are core components of the electron transport chain (ETC) and display increased longevity in respiratory supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site between complexes I and IV, is required for complex IV and supercomplex assembly. Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained for days, effectively uncoupling mitochondrial function from ongoing transcription of its mitoLLPs. Our results suggest that modulating protein longevity within the ETC is critical for mitochondrial proteome maintenance and the robustness of mitochondrial function.},
  author       = {Krishna, Shefali and Arrojo e Drigo, Rafael and Capitanio, Juliana S. and Ramachandra, Ranjan and Ellisman, Mark and HETZER, Martin W},
  issn         = {1534-5807},
  journal      = {Developmental Cell},
  keywords     = {Developmental Biology, Cell Biology, General Biochemistry, Genetics and Molecular Biology, Molecular Biology},
  number       = {21},
  pages        = {P2952--2965.e9},
  publisher    = {Elsevier},
  title        = {{Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain}},
  doi          = {10.1016/j.devcel.2021.10.008},
  volume       = {56},
  year         = {2021},
}

@article{13356,
  abstract     = {Self-assembly of nanoparticles can be mediated by polymers, but has so far led almost exclusively to nanoparticle aggregates that are amorphous. Here, we employed Coulombic interactions to generate a range of composite materials from mixtures of charged nanoparticles and oppositely charged polymers. The assembly behavior of these nanoparticle/polymer composites depends on their order of addition: polymers added to nanoparticles give rise to stable aggregates, but nanoparticles added to polymers disassemble the initially formed aggregates. The amorphous aggregates were transformed into crystalline ones by transiently increasing the ionic strength of the solution. The morphology of the resulting crystals depended on the length of the polymer: short polymer chains mediated the self-assembly of nanoparticles into strongly faceted crystals, whereas long chains led to pseudospherical nanoparticle/polymer assemblies, within which the crystalline order of nanoparticles was retained.},
  author       = {Bian, Tong and Klajn, Rafal},
  issn         = {1749-6632},
  journal      = {Annals of the New York Academy of Sciences},
  keywords     = {History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience},
  number       = {1},
  pages        = {191--201},
  publisher    = {Wiley},
  title        = {{Morphology control in crystalline nanoparticle–polymer aggregates}},
  doi          = {10.1111/nyas.14674},
  volume       = {1505},
  year         = {2021},
}

@article{13359,
  abstract     = {Dissipative self-assembly is ubiquitous in nature, where it gives rise to complex structures and functions such as self-healing, homeostasis, and camouflage. These phenomena are enabled by the continuous conversion of energy stored in chemical fuels, such as ATP. Over the past decade, an increasing number of synthetic chemically driven systems have been reported that mimic the features of their natural counterparts. At the same time, it has been shown that dissipative self-assembly can also be fueled by light; these optically fueled systems have been developed in parallel to the chemically fueled ones. In this perspective, we critically compare these two classes of systems. Despite the complementarity and fundamental differences between these two modes of dissipative self-assembly, our analysis reveals that multiple analogies exist between chemically and light-fueled systems. We hope that these considerations will facilitate further development of the field of dissipative self-assembly.},
  author       = {Weißenfels, Maren and Gemen, Julius and Klajn, Rafal},
  issn         = {2451-9294},
  journal      = {Chem},
  keywords     = {Materials Chemistry, Biochemistry (medical), General Chemical Engineering, Environmental Chemistry, Biochemistry, General Chemistry},
  number       = {1},
  pages        = {23--37},
  publisher    = {Elsevier},
  title        = {{Dissipative self-assembly: Fueling with chemicals versus light}},
  doi          = {10.1016/j.chempr.2020.11.025},
  volume       = {7},
  year         = {2021},
}

@article{9387,
  abstract     = {We report the complete analysis of a deterministic model of deleterious mutations and negative selection against them at two haploid loci without recombination. As long as mutation is a weaker force than selection, mutant alleles remain rare at the only stable equilibrium, and otherwise, a variety of dynamics are possible. If the mutation-free genotype is absent, generally the only stable equilibrium is the one that corresponds to fixation of the mutant allele at the locus where it is less deleterious. This result suggests that fixation of a deleterious allele that follows a click of the Muller’s ratchet is governed by natural selection, instead of random drift.},
  author       = {Khudiakova, Kseniia and Neretina, Tatiana Yu. and Kondrashov, Alexey S.},
  issn         = {0022-5193},
  journal      = {Journal of Theoretical Biology},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, Modelling and Simulation, Statistics and Probability, General Immunology and Microbiology, Applied Mathematics, General Agricultural and Biological Sciences, General Medicine},
  publisher    = {Elsevier },
  title        = {{Two linked loci under mutation-selection balance and Muller’s ratchet}},
  doi          = {10.1016/j.jtbi.2021.110729},
  volume       = {524},
  year         = {2021},
}

@article{9429,
  abstract     = {De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3 lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency leads to motor coordination deficits as well as ASD-relevant social and cognitive impairments. However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during a critical developmental window. Here we show that Cul3 is essential to regulate neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice display cortical lamination abnormalities. At the molecular level, we found that Cul3 controls neuronal migration by tightly regulating the amount of Plastin3 (Pls3), a previously unrecognized player of neural migration. Furthermore, we found that Pls3 cell-autonomously regulates cell migration by regulating actin cytoskeleton organization, and its levels are inversely proportional to neural migration speed. Finally, we provide evidence that cellular phenotypes associated with autism-linked gene haploinsufficiency can be rescued by transcriptional activation of the intact allele in vitro, offering a proof of concept for a potential therapeutic approach for ASDs.},
  author       = {Morandell, Jasmin and Schwarz, Lena A and Basilico, Bernadette and Tasciyan, Saren and Dimchev, Georgi A and Nicolas, Armel and Sommer, Christoph M and Kreuzinger, Caroline and Dotter, Christoph and Knaus, Lisa and Dobler, Zoe and Cacci, Emanuele and Schur, Florian KM and Danzl, Johann G and Novarino, Gaia},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Biochemistry, Genetics and Molecular Biology},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development}},
  doi          = {10.1038/s41467-021-23123-x},
  volume       = {12},
  year         = {2021},
}

@article{9431,
  abstract     = {Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram averaging, mature capsid-like particles show an IP6-like density in the CA hexamer, coordinated by rings of six lysines and six arginines. Phosphate and IP6 have opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer formation. Subtomogram averaging and classification optimized for analysis of pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast, the CA pentamer forms rigid units organizing the local architecture. These different features of hexamers and pentamers determine the structural mechanism to form CA polyhedrons of variable shape in mature RSV particles.},
  author       = {Obr, Martin and Ricana, Clifton L. and Nikulin, Nadia and Feathers, Jon-Philip R. and Klanschnig, Marco and Thader, Andreas and Johnson, Marc C. and Vogt, Volker M. and Schur, Florian KM and Dick, Robert A.},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, General Physics and Astronomy, General Chemistry},
  number       = {1},
  publisher    = {Nature Research},
  title        = {{Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer}},
  doi          = {10.1038/s41467-021-23506-0},
  volume       = {12},
  year         = {2021},
}

@article{9540,
  abstract     = {The hexameric AAA-ATPase Drg1 is a key factor in eukaryotic ribosome biogenesis and initiates cytoplasmic maturation of the large ribosomal subunit by releasing the shuttling maturation factor Rlp24. Drg1 monomers contain two AAA-domains (D1 and D2) that act in a concerted manner. Rlp24 release is inhibited by the drug diazaborine which blocks ATP hydrolysis in D2. The mode of inhibition was unknown. Here we show the first cryo-EM structure of Drg1 revealing the inhibitory mechanism. Diazaborine forms a covalent bond to the 2′-OH of the nucleotide in D2, explaining its specificity for this site. As a consequence, the D2 domain is locked in a rigid, inactive state, stalling the whole Drg1 hexamer. Resistance mechanisms identified include abolished drug binding and altered positioning of the nucleotide. Our results suggest nucleotide-modifying compounds as potential novel inhibitors for AAA-ATPases.},
  author       = {Prattes, Michael and Grishkovskaya, Irina and Hodirnau, Victor-Valentin and Rössler, Ingrid and Klein, Isabella and Hetzmannseder, Christina and Zisser, Gertrude and Gruber, Christian C. and Gruber, Karl and Haselbach, David and Bergler, Helmut},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, General Physics and Astronomy, General Chemistry},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{Structural basis for inhibition of the AAA-ATPase Drg1 by diazaborine}},
  doi          = {10.1038/s41467-021-23854-x},
  volume       = {12},
  year         = {2021},
}

@article{10163,
  abstract     = {The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a regulatory hub for transcription and RNA processing. Here, we identify PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a CTD reader domain that preferentially binds two phosphorylated Serine-2 marks in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length of genes. PHF3 knock-out or SPOC deletion in human cells results in increased Pol II stalling, reduced elongation rate and an increase in mRNA stability, with marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation. Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation by bridging transcription with mRNA decay.},
  author       = {Appel, Lisa-Marie and Franke, Vedran and Bruno, Melania and Grishkovskaya, Irina and Kasiliauskaite, Aiste and Kaufmann, Tanja and Schoeberl, Ursula E. and Puchinger, Martin G. and Kostrhon, Sebastian and Ebenwaldner, Carmen and Sebesta, Marek and Beltzung, Etienne and Mechtler, Karl and Lin, Gen and Vlasova, Anna and Leeb, Martin and Pavri, Rushad and Stark, Alexander and Akalin, Altuna and Stefl, Richard and Bernecky, Carrie A and Djinovic-Carugo, Kristina and Slade, Dea},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {general physics and astronomy, general biochemistry, genetics and molecular biology, general chemistry},
  number       = {1},
  publisher    = {Springer Nature},
  title        = {{PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC}},
  doi          = {10.1038/s41467-021-26360-2},
  volume       = {12},
  year         = {2021},
}

@article{10301,
  abstract     = {De novo protein synthesis is required for synapse modifications underlying stable memory encoding. Yet neurons are highly compartmentalized cells and how protein synthesis can be regulated at the synapse level is unknown. Here, we characterize neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR activation and restricts the mTOR-dependent translation of specific activity-regulated mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent protein synthesis, and facilitates the consolidation of associative and spatial memories in mice. The memory enhancement becomes evident with light or spaced training, can be achieved by selectively deleting GluN3A from excitatory neurons during adulthood, and does not compromise other aspects of cognition such as memory flexibility or extinction. Our findings provide mechanistic insight into synaptic translational control and reveal a potentially selective target for cognitive enhancement.},
  author       = {Conde-Dusman, María J and Dey, Partha N and Elía-Zudaire, Óscar and Garcia Rabaneda, Luis E and García-Lira, Carmen and Grand, Teddy and Briz, Victor and Velasco, Eric R and Andero Galí, Raül and Niñerola, Sergio and Barco, Angel and Paoletti, Pierre and Wesseling, John F and Gardoni, Fabrizio and Tavalin, Steven J and Perez-Otaño, Isabel},
  issn         = {2050-084X},
  journal      = {eLife},
  keywords     = {general immunology and microbiology, general biochemistry, genetics and molecular biology, general medicine, general neuroscience},
  publisher    = {eLife Sciences Publications},
  title        = {{Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly}},
  doi          = {10.7554/elife.71575},
  volume       = {10},
  year         = {2021},
}

@article{10310,
  abstract     = {A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI) from Thermosynechococcus elongatus was reported as the first atomic model of PSI almost 20 years ago. However, the monomeric PSI structure has not yet been reported despite long-standing interest in its structure and extensive spectroscopic characterization of the loss of red chlorophylls upon monomerization. Here, we describe the structure of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the trimer structure gave detailed insights into monomerization-induced changes in both the central trimerization domain and the peripheral regions of the complex. Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization of red chlorophylls and that lipids of the surrounding membrane present a major source of thermal energy for uphill excitation energy transfer from red chlorophylls to P700.},
  author       = {Çoruh, Mehmet Orkun and Frank, Anna and Tanaka, Hideaki and Kawamoto, Akihiro and El-Mohsnawy, Eithar and Kato, Takayuki and Namba, Keiichi and Gerle, Christoph and Nowaczyk, Marc M. and Kurisu, Genji},
  issn         = {2399-3642},
  journal      = {Communications Biology},
  keywords     = {general agricultural and biological Sciences, general biochemistry, genetics and molecular biology, medicine (miscellaneous)},
  number       = {1},
  publisher    = {Springer },
  title        = {{Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster}},
  doi          = {10.1038/s42003-021-01808-9},
  volume       = {4},
  year         = {2021},
}

@article{10406,
  abstract     = {Multicellular organisms develop complex shapes from much simpler, single-celled zygotes through a process commonly called morphogenesis. Morphogenesis involves an interplay between several factors, ranging from the gene regulatory networks determining cell fate and differentiation to the mechanical processes underlying cell and tissue shape changes. Thus, the study of morphogenesis has historically been based on multidisciplinary approaches at the interface of biology with physics and mathematics. Recent technological advances have further improved our ability to study morphogenesis by bridging the gap between the genetic and biophysical factors through the development of new tools for visualizing, analyzing, and perturbing these factors and their biochemical intermediaries. Here, we review how a combination of genetic, microscopic, biophysical, and biochemical approaches has aided our attempts to understand morphogenesis and discuss potential approaches that may be beneficial to such an inquiry in the future.},
  author       = {Mishra, Nikhil and Heisenberg, Carl-Philipp J},
  issn         = {1545-2948},
  journal      = {Annual Review of Genetics},
  keywords     = {morphogenesis, forward genetics, high-resolution microscopy, biophysics, biochemistry, patterning},
  pages        = {209--233},
  publisher    = {Annual Reviews},
  title        = {{Dissecting organismal morphogenesis by bridging genetics and biophysics}},
  doi          = {10.1146/annurev-genet-071819-103748},
  volume       = {55},
  year         = {2021},
}

@article{12585,
  abstract     = {Glaciers in High Mountain Asia generate meltwater that supports the water needs of 250 million people, but current knowledge of annual accumulation and ablation is limited to sparse field measurements biased in location and glacier size. Here, we present altitudinally-resolved specific mass balances (surface, internal, and basal combined) for 5527 glaciers in High Mountain Asia for 2000–2016, derived by correcting observed glacier thinning patterns for mass redistribution due to ice flow. We find that 41% of glaciers accumulated mass over less than 20% of their area, and only 60% ± 10% of regional annual ablation was compensated by accumulation. Even without 21st century warming, 21% ± 1% of ice volume will be lost by 2100 due to current climatic-geometric imbalance, representing a reduction in glacier ablation into rivers of 28% ± 1%. The ablation of glaciers in the Himalayas and Tien Shan was mostly unsustainable and ice volume in these regions will reduce by at least 30% by 2100. The most important and vulnerable glacier-fed river basins (Amu Darya, Indus, Syr Darya, Tarim Interior) were supplied with >50% sustainable glacier ablation but will see long-term reductions in ice mass and glacier meltwater supply regardless of the Karakoram Anomaly.},
  author       = {Miles, Evan and McCarthy, Michael and Dehecq, Amaury and Kneib, Marin and Fugger, Stefan and Pellicciotti, Francesca},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Physics and Astronomy, General Biochemistry, Genetics and Molecular Biology, General Chemistry, Multidisciplinary},
  publisher    = {Springer Nature},
  title        = {{Health and sustainability of glaciers in High Mountain Asia}},
  doi          = {10.1038/s41467-021-23073-4},
  volume       = {12},
  year         = {2021},
}

@article{9778,
  abstract     = {The hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit. Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this synaptic connection. It is widely believed that mossy fiber PTP is an entirely presynaptic phenomenon, implying that PTP induction is input-specific, and requires neither activity of multiple inputs nor stimulation of postsynaptic neurons. To directly test cooperativity and associativity, we made paired recordings between single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain slices. By stimulating non-overlapping mossy fiber inputs converging onto single CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly, mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only minimal PTP after combined pre- and postsynaptic high-frequency stimulation with intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels, group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire of synaptic computations, implementing a brake on mossy fiber detonation and a “smart teacher” function of hippocampal mossy fiber synapses.},
  author       = {Vandael, David H and Okamoto, Yuji and Jonas, Peter M},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {general physics and astronomy, general biochemistry, genetics and molecular biology, general chemistry},
  number       = {1},
  publisher    = {Springer},
  title        = {{Transsynaptic modulation of presynaptic short-term plasticity in hippocampal mossy fiber synapses}},
  doi          = {10.1038/s41467-021-23153-5},
  volume       = {12},
  year         = {2021},
}

@article{11055,
  abstract     = {Vascular dysfunctions are a common feature of multiple age-related diseases. However, modeling healthy and pathological aging of the human vasculature represents an unresolved experimental challenge. Here, we generated induced vascular endothelial cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial junction stability, as vascular aging markers. A functional assay performed on PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which plays a key role in both vascular calcification and endothelial barrier damage observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered the functionality of the vascular barrier in vitro, hence representing a potential future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These results show that iVECs and iSMCs retain disease-related signatures, allowing modeling of vascular aging and HGPS in vitro.},
  author       = {Bersini, Simone and Schulte, Roberta and Huang, Ling and Tsai, Hannah and HETZER, Martin W},
  issn         = {2050-084X},
  journal      = {eLife},
  keywords     = {General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine, General Neuroscience},
  publisher    = {eLife Sciences Publications},
  title        = {{Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome}},
  doi          = {10.7554/elife.54383},
  volume       = {9},
  year         = {2020},
}

@article{11056,
  abstract     = {Aging of the circulatory system correlates with the pathogenesis of a large spectrum of diseases. However, it is largely unknown which factors drive the age-dependent or pathological decline of the vasculature and how vascular defects relate to tissue aging. The goal of the study is to design a multianalytical approach to identify how the cellular microenvironment (i.e., fibroblasts) and serum from healthy donors of different ages or Alzheimer disease (AD) patients can modulate the functionality of organ-specific vascular endothelial cells (VECs). Long-living human microvascular networks embedding VECs and fibroblasts from skin biopsies are generated. RNA-seq, secretome analyses, and microfluidic assays demonstrate that fibroblasts from young donors restore the functionality of aged endothelial cells, an effect also achieved by serum from young donors. New biomarkers of vascular aging are validated in human biopsies and it is shown that young serum induces angiopoietin-like-4, which can restore compromised vascular barriers. This strategy is then employed to characterize transcriptional/functional changes induced on the blood–brain barrier by AD serum, demonstrating the importance of PTP4A3 in the regulation of permeability. Features of vascular degeneration during aging and AD are recapitulated, and a tool to identify novel biomarkers that can be exploited to develop future therapeutics modulating vascular function is established.},
  author       = {Bersini, Simone and Arrojo e Drigo, Rafael and Huang, Ling and Shokhirev, Maxim N. and HETZER, Martin W},
  issn         = {2366-7478},
  journal      = {Advanced Biosystems},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, Biomedical Engineering, Biomaterials},
  number       = {5},
  publisher    = {Wiley},
  title        = {{Transcriptional and functional changes of the human microvasculature during physiological aging and Alzheimer disease}},
  doi          = {10.1002/adbi.202000044},
  volume       = {4},
  year         = {2020},
}

@article{11058,
  abstract     = {Nucleoporin 93 (Nup93) expression inversely correlates with the survival of triple-negative breast cancer patients. However, our knowledge of Nup93 function in breast cancer besides its role as structural component of the nuclear pore complex is not understood. Combination of functional assays and genetic analyses suggested that chromatin interaction of Nup93 partially modulates the expression of genes associated with actin cytoskeleton remodeling and epithelial to mesenchymal transition, resulting in impaired invasion of triple-negative, claudin-low breast cancer cells. Nup93 depletion induced stress fiber formation associated with reduced cell migration/proliferation and impaired expression of mesenchymal-like genes. Silencing LIMCH1, a gene responsible for actin cytoskeleton remodeling and up-regulated upon Nup93 depletion, partially restored the invasive phenotype of cancer cells. Loss of Nup93 led to significant defects in tumor establishment/propagation in vivo, whereas patient samples revealed that high Nup93 and low LIMCH1 expression correlate with late tumor stage. Our approach identified Nup93 as contributor of triple-negative, claudin-low breast cancer cell invasion and paves the way to study the role of nuclear envelope proteins during breast cancer tumorigenesis.},
  author       = {Bersini, Simone and Lytle, Nikki K and Schulte, Roberta and Huang, Ling and Wahl, Geoffrey M and HETZER, Martin W},
  issn         = {2575-1077},
  journal      = {Life Science Alliance},
  keywords     = {Health, Toxicology and Mutagenesis, Plant Science, Biochemistry, Genetics and Molecular Biology (miscellaneous), Ecology},
  number       = {1},
  publisher    = {Life Science Alliance},
  title        = {{Nup93 regulates breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling}},
  doi          = {10.26508/lsa.201900623},
  volume       = {3},
  year         = {2020},
}

@article{8402,
  abstract     = {Background: The mitochondrial pyruvate carrier (MPC) plays a central role in energy metabolism by transporting pyruvate across the inner mitochondrial membrane. Its heterodimeric composition and homology to SWEET and semiSWEET transporters set the MPC apart from the canonical mitochondrial carrier family (named MCF or SLC25). The import of the canonical carriers is mediated by the carrier translocase of the inner membrane (TIM22) pathway and is dependent on their structure, which features an even number of transmembrane segments and both termini in the intermembrane space. The import pathway of MPC proteins has not been elucidated. The odd number of transmembrane segments and positioning of the N-terminus in the matrix argues against an import via the TIM22 carrier pathway but favors an import via the flexible presequence pathway.
Results: Here, we systematically analyzed the import pathways of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible presequence pathway, yeast MPC proteins with an odd number of transmembrane segments and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic motifs that are also required for the interaction with canonical carrier proteins.
Conclusions: The carrier pathway can import paired and non-paired transmembrane helices and translocate N-termini to either side of the mitochondrial inner membrane, revealing an unexpected versatility of the mitochondrial import pathway for non-cleavable inner membrane proteins.},
  author       = {Rampelt, Heike and Sucec, Iva and Bersch, Beate and Horten, Patrick and Perschil, Inge and Martinou, Jean-Claude and van der Laan, Martin and Wiedemann, Nils and Schanda, Paul and Pfanner, Nikolaus},
  issn         = {1741-7007},
  journal      = {BMC Biology},
  keywords     = {Biotechnology, Plant Science, General Biochemistry, Genetics and Molecular Biology, Developmental Biology, Cell Biology, Physiology, Ecology, Evolution, Behavior and Systematics, Structural Biology, General Agricultural and Biological Sciences},
  publisher    = {Springer Nature},
  title        = {{The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments}},
  doi          = {10.1186/s12915-019-0733-6},
  volume       = {18},
  year         = {2020},
}

@article{8529,
  abstract     = {Practical quantum networks require low-loss and noise-resilient optical interconnects as well as non-Gaussian resources for entanglement distillation and distributed quantum computation. The latter could be provided by superconducting circuits but existing solutions to interface the microwave and optical domains lack either scalability or efficiency, and in most cases the conversion noise is not known. In this work we utilize the unique opportunities of silicon photonics, cavity optomechanics and superconducting circuits to demonstrate a fully integrated, coherent transducer interfacing the microwave X and the telecom S bands with a total (internal) bidirectional transduction efficiency of 1.2% (135%) at millikelvin temperatures. The coupling relies solely on the radiation pressure interaction mediated by the femtometer-scale motion of two silicon nanobeams reaching a <jats:italic>V</jats:italic><jats:sub><jats:italic>π</jats:italic></jats:sub> as low as 16 μV for sub-nanowatt pump powers. Without the associated optomechanical gain, we achieve a total (internal) pure conversion efficiency of up to 0.019% (1.6%), relevant for future noise-free operation on this qubit-compatible platform.},
  author       = {Arnold, Georg M and Wulf, Matthias and Barzanjeh, Shabir and Redchenko, Elena and Rueda Sanchez, Alfredo R and Hease, William J and Hassani, Farid and Fink, Johannes M},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, General Physics and Astronomy, General Chemistry},
  publisher    = {Springer Nature},
  title        = {{Converting microwave and telecom photons with a silicon photonic nanomechanical interface}},
  doi          = {10.1038/s41467-020-18269-z},
  volume       = {11},
  year         = {2020},
}

@article{8568,
  abstract     = {Aqueous iodine based electrochemical energy storage is considered a potential candidate to improve sustainability and performance of current battery and supercapacitor technology. It harnesses the redox activity of iodide, iodine, and polyiodide species in the confined geometry of nanoporous carbon electrodes. However, current descriptions of the electrochemical reaction mechanism to interconvert these species are elusive. Here we show that electrochemical oxidation of iodide in nanoporous carbons forms persistent solid iodine deposits. Confinement slows down dissolution into triiodide and pentaiodide, responsible for otherwise significant self-discharge via shuttling. The main tools for these insights are in situ Raman spectroscopy and in situ small and wide-angle X-ray scattering (in situ SAXS/WAXS). In situ Raman confirms the reversible formation of triiodide and pentaiodide. In situ SAXS/WAXS indicates remarkable amounts of solid iodine deposited in the carbon nanopores. Combined with stochastic modeling, in situ SAXS allows quantifying the solid iodine volume fraction and visualizing the iodine structure on 3D lattice models at the sub-nanometer scale. Based on the derived mechanism, we demonstrate strategies for improved iodine pore filling capacity and prevention of self-discharge, applicable to hybrid supercapacitors and batteries.},
  author       = {Prehal, Christian and Fitzek, Harald and Kothleitner, Gerald and Presser, Volker and Gollas, Bernhard and Freunberger, Stefan Alexander and Abbas, Qamar},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Biochemistry, Genetics and Molecular Biology, General Physics and Astronomy, General Chemistry},
  publisher    = {Springer Nature},
  title        = {{Persistent and reversible solid iodine electrodeposition in nanoporous carbons}},
  doi          = {10.1038/s41467-020-18610-6},
  volume       = {11},
  year         = {2020},
}