TY - THES AB - We present solutions to several problems originating from geometry and discrete mathematics: existence of equipartitions, maps without Tverberg multiple points, and inscribing quadrilaterals. Equivariant obstruction theory is the natural topological approach to these type of questions. However, for the specific problems we consider it had yielded only partial or no results. We get our results by complementing equivariant obstruction theory with other techniques from topology and geometry. AU - Avvakumov, Sergey ID - 8156 SN - 2663-337X TI - Topological methods in geometry and discrete mathematics ER - TY - JOUR AB - We give the first mathematically rigorous justification of the local density approximation in density functional theory. We provide a quantitative estimate on the difference between the grand-canonical Levy–Lieb energy of a given density (the lowest possible energy of all quantum states having this density) and the integral over the uniform electron gas energy of this density. The error involves gradient terms and justifies the use of the local density approximation in the situation where the density is very flat on sufficiently large regions in space. AU - Lewin, Mathieu AU - Lieb, Elliott H. AU - Seiringer, Robert ID - 14891 IS - 1 JF - Pure and Applied Analysis SN - 2578-5893 TI - The local density approximation in density functional theory VL - 2 ER - TY - JOUR AB - Amyotrophic lateral sclerosis (ALS) leads to a loss of specific motor neuron populations in the spinal cord and cortex. Emerging evidence suggests that interneurons may also be affected, but a detailed characterization of interneuron loss and its potential impacts on motor neuron loss and disease progression is lacking. To examine this issue, the fate of V1 inhibitory neurons during ALS was assessed in the ventral spinal cord using the SODG93A mouse model. The V1 population makes up ∼30% of all ventral inhibitory neurons, ∼50% of direct inhibitory synaptic contacts onto motor neuron cell bodies, and is thought to play a key role in modulating motor output, in part through recurrent and reciprocal inhibitory circuits. We find that approximately half of V1 inhibitory neurons are lost in SODG93A mice at late disease stages, but that this loss is delayed relative to the loss of motor neurons and V2a excitatory neurons. We further identify V1 subpopulations based on transcription factor expression that are differentially susceptible to degeneration in SODG93A mice. At an early disease stage, we show that V1 synaptic contacts with motor neuron cell bodies increase, suggesting an upregulation of inhibition before V1 neurons are lost in substantial numbers. These data support a model in which progressive changes in V1 synaptic contacts early in disease, and in select V1 subpopulations at later stages, represent a compensatory upregulation and then deleterious breakdown of specific interneuron circuits within the spinal cord. AU - Salamatina, Alina AU - Yang, Jerry H AU - Brenner-Morton, Susan AU - Bikoff, Jay B AU - Fang, Linjing AU - Kintner, Christopher R AU - Jessell, Thomas M AU - Sweeney, Lora Beatrice Jaeger ID - 8914 JF - Neuroscience SN - 0306-4522 TI - Differential loss of spinal interneurons in a mouse model of ALS VL - 450 ER - TY - DATA AB - This data collection contains the transport data for figures presented in the supplementary material of "Enhancement of Proximity Induced Superconductivity in Planar Germanium" by K. Aggarwal, et. al. The measurements were done using Labber Software and the data is stored in the hdf5 file format. The files can be opened using either the Labber Log Browser (https://labber.org/overview/) or Labber Python API (http://labber.org/online-doc/api/LogFile.html). AU - Katsaros, Georgios ID - 8834 TI - Enhancement of proximity induced superconductivity in planar Germanium ER - TY - DATA AB - Antibiotics that interfere with translation, when combined, interact in diverse and difficult-to-predict ways. Here, we explain these interactions by "translation bottlenecks": points in the translation cycle where antibiotics block ribosomal progression. To elucidate the underlying mechanisms of drug interactions between translation inhibitors, we generate translation bottlenecks genetically using inducible control of translation factors that regulate well-defined translation cycle steps. These perturbations accurately mimic antibiotic action and drug interactions, supporting that the interplay of different translation bottlenecks causes these interactions. We further show that growth laws, combined with drug uptake and binding kinetics, enable the direct prediction of a large fraction of observed interactions, yet fail to predict suppression. However, varying two translation bottlenecks simultaneously supports that dense traffic of ribosomes and competition for translation factors account for the previously unexplained suppression. These results highlight the importance of "continuous epistasis" in bacterial physiology. AU - Kavcic, Bor ID - 8097 KW - Escherichia coli KW - antibiotic combinations KW - translation KW - growth laws KW - drug interactions KW - bacterial physiology KW - translation inhibitors TI - Analysis scripts and research data for the paper "Mechanisms of drug interactions between translation-inhibiting antibiotics" ER - TY - DATA AB - Here are the research data underlying the publication "Estimating inbreeding and its effects in a long-term study of snapdragons (Antirrhinum majus)". Further information are summed up in the README document. The files for this record have been updated and are now found in the linked DOI https://doi.org/10.15479/AT:ISTA:9192. AU - Arathoon, Louise S ID - 8254 TI - Estimating inbreeding and its effects in a long-term study of snapdragons (Antirrhinum majus) ER - TY - JOUR AB - Semiconductor nanowires have been playing a crucial role in the development of nanoscale devices for the realization of spin qubits, Majorana fermions, single photon emitters, nanoprocessors, etc. The monolithic growth of site‐controlled nanowires is a prerequisite toward the next generation of devices that will require addressability and scalability. Here, combining top‐down nanofabrication and bottom‐up self‐assembly, the growth of Ge wires on prepatterned Si (001) substrates with controllable position, distance, length, and structure is reported. This is achieved by a novel growth process that uses a SiGe strain‐relaxation template and can be potentially generalized to other material combinations. Transport measurements show an electrically tunable spin–orbit coupling, with a spin–orbit length similar to that of III–V materials. Also, charge sensing between quantum dots in closely spaced wires is observed, which underlines their potential for the realization of advanced quantum devices. The reported results open a path toward scalable qubit devices using nanowires on silicon. AU - Gao, Fei AU - Wang, Jian-Huan AU - Watzinger, Hannes AU - Hu, Hao AU - Rančić, Marko J. AU - Zhang, Jie-Yin AU - Wang, Ting AU - Yao, Yuan AU - Wang, Gui-Lei AU - Kukucka, Josip AU - Vukušić, Lada AU - Kloeffel, Christoph AU - Loss, Daniel AU - Liu, Feng AU - Katsaros, Georgios AU - Zhang, Jian-Jun ID - 7541 IS - 16 JF - Advanced Materials SN - 0935-9648 TI - Site-controlled uniform Ge/Si hut wires with electrically tunable spin-orbit coupling VL - 32 ER - TY - DATA AB - Phenomenological relations such as Ohm’s or Fourier’s law have a venerable history in physics but are still scarce in biology. This situation restrains predictive theory. Here, we build on bacterial “growth laws,” which capture physiological feedback between translation and cell growth, to construct a minimal biophysical model for the combined action of ribosome-targeting antibiotics. Our model predicts drug interactions like antagonism or synergy solely from responses to individual drugs. We provide analytical results for limiting cases, which agree well with numerical results. We systematically refine the model by including direct physical interactions of different antibiotics on the ribosome. In a limiting case, our model provides a mechanistic underpinning for recent predictions of higher-order interactions that were derived using entropy maximization. We further refine the model to include the effects of antibiotics that mimic starvation and the presence of resistance genes. We describe the impact of a starvation-mimicking antibiotic on drug interactions analytically and verify it experimentally. Our extended model suggests a change in the type of drug interaction that depends on the strength of resistance, which challenges established rescaling paradigms. We experimentally show that the presence of unregulated resistance genes can lead to altered drug interaction, which agrees with the prediction of the model. While minimal, the model is readily adaptable and opens the door to predicting interactions of second and higher-order in a broad range of biological systems. AU - Kavcic, Bor ID - 8930 KW - Escherichia coli KW - antibiotic combinations KW - translation KW - growth laws KW - drug interactions KW - bacterial physiology KW - translation inhibitors TI - Analysis scripts and research data for the paper "Minimal biophysical model of combined antibiotic action" ER - TY - DATA AB - Gene expression levels are influenced by multiple coexisting molecular mechanisms. Some of these interactions, such as those of transcription factors and promoters have been studied extensively. However, predicting phenotypes of gene regulatory networks remains a major challenge. Here, we use a well-defined synthetic gene regulatory network to study how network phenotypes depend on local genetic context, i.e. the genetic neighborhood of a transcription factor and its relative position. We show that one gene regulatory network with fixed topology can display not only quantitatively but also qualitatively different phenotypes, depending solely on the local genetic context of its components. Our results demonstrate that changes in local genetic context can place a single transcriptional unit within two separate regulons without the need for complex regulatory sequences. We propose that relative order of individual transcriptional units, with its potential for combinatorial complexity, plays an important role in shaping phenotypes of gene regulatory networks. AU - Nagy-Staron, Anna A ID - 8951 KW - Gene regulatory networks KW - Gene expression KW - Escherichia coli KW - Synthetic Biology TI - Sequences of gene regulatory network permutations for the article "Local genetic context shapes the function of a gene regulatory network" ER - TY - DATA AB - Organisms cope with change by employing transcriptional regulators. However, when faced with rare environments, the evolution of transcriptional regulators and their promoters may be too slow. We ask whether the intrinsic instability of gene duplication and amplification provides a generic alternative to canonical gene regulation. By real-time monitoring of gene copy number mutations in E. coli, we show that gene duplications and amplifications enable adaptation to fluctuating environments by rapidly generating copy number, and hence expression level, polymorphism. This ‘amplification-mediated gene expression tuning’ occurs on timescales similar to canonical gene regulation and can deal with rapid environmental changes. Mathematical modeling shows that amplifications also tune gene expression in stochastic environments where transcription factor-based schemes are hard to evolve or maintain. The fleeting nature of gene amplifications gives rise to a generic population-level mechanism that relies on genetic heterogeneity to rapidly tune expression of any gene, without leaving any genomic signature. AU - Grah, Rok ID - 7383 KW - Matlab scripts KW - analysis of microfluidics KW - mathematical model TI - Matlab scripts for the Paper: Gene Amplification as a Form of Population-Level Gene Expression regulation ER -