@article{10547, abstract = {We establish global-in-time existence results for thermodynamically consistent reaction-(cross-)diffusion systems coupled to an equation describing heat transfer. Our main interest is to model species-dependent diffusivities, while at the same time ensuring thermodynamic consistency. A key difficulty of the non-isothermal case lies in the intrinsic presence of cross-diffusion type phenomena like the Soret and the Dufour effect: due to the temperature/energy dependence of the thermodynamic equilibria, a nonvanishing temperature gradient may drive a concentration flux even in a situation with constant concentrations; likewise, a nonvanishing concentration gradient may drive a heat flux even in a case of spatially constant temperature. We use time discretisation and regularisation techniques and derive a priori estimates based on a suitable entropy and the associated entropy production. Renormalised solutions are used in cases where non-integrable diffusion fluxes or reaction terms appear.}, author = {Fischer, Julian L and Hopf, Katharina and Kniely, Michael and Mielke, Alexander}, issn = {0036-1410}, journal = {SIAM Journal on Mathematical Analysis}, keywords = {Energy-Reaction-Diffusion Systems, Cross Diffusion, Global-In-Time Existence of Weak/Renormalised Solutions, Entropy Method, Onsager System, Soret/Dufour Effect}, number = {1}, pages = {220--267}, publisher = {Society for Industrial and Applied Mathematics}, title = {{Global existence analysis of energy-reaction-diffusion systems}}, doi = {10.1137/20M1387237}, volume = {54}, year = {2022}, } @article{10548, abstract = {Consider a linear elliptic partial differential equation in divergence form with a random coefficient field. The solution operator displays fluctuations around its expectation. The recently developed pathwise theory of fluctuations in stochastic homogenization reduces the characterization of these fluctuations to those of the so-called standard homogenization commutator. In this contribution, we investigate the scaling limit of this key quantity: starting from a Gaussian-like coefficient field with possibly strong correlations, we establish the convergence of the rescaled commutator to a fractional Gaussian field, depending on the decay of correlations of the coefficient field, and we investigate the (non)degeneracy of the limit. This extends to general dimension $d\ge1$ previous results so far limited to dimension $d=1$, and to the continuum setting with strong correlations recent results in the discrete iid case.}, author = {Duerinckx, Mitia and Fischer, Julian L and Gloria, Antoine}, issn = {1050-5164}, journal = {Annals of applied probability}, number = {2}, pages = {1179--1209}, publisher = {Institute of Mathematical Statistics}, title = {{Scaling limit of the homogenization commutator for Gaussian coefficient fields}}, doi = {10.1214/21-AAP1705}, volume = {32}, year = {2022}, } @misc{17057, abstract = {Martin Loose studied chemistry at the University of Heidelberg, Germany. He then joined Petra Schwille's group at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, where he obtained his PhD degree in 2010 for work on self-organization and pattern formation in the bacterial Min protein system. He then moved to Tim Mitchison's lab at Harvard Medical School, Boston, USA for his postdoc, funded by Human Frontier Science Program (HSFP) and European Molecular Biology Organization (EMBO) long-term fellowships; there, he discovered that the bacterial cell division proteins FtsA and FtsZ self-organize into dynamic cytoskeletal patterns. Martin established his independent research group at the Institute of Science and Technology (IST) Austria in 2015, supported by an European Research Council (ERC) starting grant and HFSP Young Investigator Grant. His lab studies the self-organization of bacterial cell division and small GTPase networks.}, author = {Loose, Martin}, booktitle = {Journal of Cell Science}, issn = {1477-9137}, number = {2}, publisher = {The Company of Biologists}, title = {{Cell scientist to watch – Martin Loose}}, doi = {10.1242/jcs.259715}, volume = {135}, year = {2022}, } @article{17058, abstract = {We compare the Manin-type conjecture for Campana points recently formulated by Pieropan, Smeets, Tanimoto and Várilly-Alvarado with an alternative prediction of Browning and Van Valckenborgh in the special case of the orbifold (P1,D), where D=1/2[0]+1/2[1]+1/2[∞]. We find that the two predicted leading constants do not agree, and we discuss whether thin sets could explain this discrepancy. Motivated by this, we provide a counterexample to the Manin-type conjecture for Campana points, by considering orbifolds corresponding to squareful values of binary quadratic forms.}, author = {Shute, Alec L}, issn = {1730-6264}, journal = {Acta Arithmetica}, number = {4}, pages = {317--346}, publisher = {Institute of Mathematics}, title = {{On the leading constant in the Manin-type conjecture for Campana points}}, doi = {10.4064/aa210430-1-7}, volume = {204}, year = {2022}, } @inproceedings{17059, abstract = {The recent focus on the efficiency of deep neural networks (DNNs) has led to significant work on model compression approaches, of which weight pruning is one of the most popular. At the same time, there is rapidly-growing computational support for efficiently executing the unstructured-sparse models obtained via pruning. Yet, most existing pruning methods minimize just the number of remaining weights, i.e. the size of the model, rather than optimizing for inference time. We address this gap by introducing SPDY, a new compression method which automatically determines layer-wise sparsity targets achieving a desired inference speedup on a given system, while minimizing accuracy loss. SPDY is the composition of two new techniques. The first is an efficient and general dynamic programming algorithm for solving constrained layer-wise compression problems, given a set of layer-wise error scores. The second technique is a local search procedure for automatically determining such scores in an accurate and robust manner. Experiments across popular vision and language models show that SPDY guarantees speedups while recovering higher accuracy relative to existing strategies, both for one-shot and gradual pruning scenarios, and is compatible with most existing pruning approaches. We also extend our approach to the recently-proposed task of pruning with very little data, where we achieve the best known accuracy recovery when pruning to the GPU-supported 2:4 sparsity pattern.}, author = {Frantar, Elias and Alistarh, Dan-Adrian}, booktitle = {39th International Conference on Machine Learning}, location = {Baltimore, MD, United States}, pages = {6726--6743}, publisher = {ML Research Press}, title = {{SPDY: Accurate pruning with speedup guarantees}}, volume = {162}, year = {2022}, } @inproceedings{17060, abstract = {Payment channel networks (PCNs) are one of the most prominent solutions to the limited transaction throughput of blockchains. Nevertheless, PCNs suffer themselves from a throughput limitation due to the capital constraints of their channels. A similar dependence on high capital is also found in inter-bank payment settlements, where the so-called netting technique is used to mitigate liquidity demands. In this work, we alleviate this limitation by introducing the notion of transaction aggregation: instead of executing transactions sequentially through a PCN, we enable senders to aggregate multiple transactions and execute them simultaneously to benefit from several amounts that may "cancel out". Two direct advantages of our proposal is the decrease in intermediary fees paid by senders as well as the obfuscation of the transaction data from the intermediaries. We formulate the transaction aggregation as a computational problem, a generalization of the Bank Clearing Problem. We present a generic framework for the transaction aggregation execution, and thereafter we propose Wiser as an implementation of this framework in a specific hub-based setting. To overcome the NP-hardness of the transaction aggregation problem, in Wiser we propose a fixed-parameter linear algorithm for a special case of transaction aggregation as well as the Bank Clearing Problem. Wiser can also be seen as a modern variant of the Hawala money transfer system, as well as a decentralized implementation of the overseas remittance service of Wise.}, author = {Tiwari, Samarth and Yeo, Michelle X and Avarikioti, Zeta and Salem, Iosif and Pietrzak, Krzysztof Z and Schmid, Stefan}, booktitle = {Proceedings of the 4th ACM Conference on Advances in Financial Technologies}, isbn = {9781450398619}, location = {Cambridge, MA, United States}, pages = {217--231}, publisher = {Association for Computing Machinery}, title = {{Wiser: Increasing throughput in payment channel networks with transaction aggregation}}, doi = {10.1145/3558535.3559775}, year = {2022}, } @article{17061, abstract = {Across many domains of interaction, both natural and artificial, individuals use past experience to shape future behaviors. The results of such learning processes depend on what individuals wish to maximize. A natural objective is one’s own success. However, when two such “selfish” learners interact with each other, the outcome can be detrimental to both, especially when there are conflicts of interest. Here, we explore how a learner can align incentives with a selfish opponent. Moreover, we consider the dynamics that arise when learning rules themselves are subject to evolutionary pressure. By combining extensive simulations and analytical techniques, we demonstrate that selfish learning is unstable in most classical two-player repeated games. If evolution operates on the level of long-run payoffs, selection instead favors learning rules that incorporate social (other-regarding) preferences. To further corroborate these results, we analyze data from a repeated prisoner’s dilemma experiment. We find that selfish learning is insufficient to explain human behavior when there is a trade-off between payoff maximization and fairness.}, author = {McAvoy, Alex and Kates-Harbeck, Julian and Chatterjee, Krishnendu and Hilbe, Christian}, issn = {2752-6542}, journal = {PNAS Nexus}, number = {4}, publisher = {Oxford University Press}, title = {{Evolutionary instability of selfish learning in repeated games}}, doi = {10.1093/pnasnexus/pgac141}, volume = {1}, year = {2022}, } @inproceedings{17062, author = {Ibáñez, Maria and Liu, Yu and Calcabrini, Mariano}, booktitle = {Proceedings of the nanoGe Spring Meeting 2022}, location = {Spain/Virtual}, publisher = {Fundació Scito}, title = {{The importance of surface adsorbates in solution-processed thermoelectric materials}}, doi = {10.29363/nanoge.nsm.2022.159}, year = {2022}, } @article{17063, abstract = {This workshop continued a biannual series of workshops at Oberwolfach on dynamical systems that started with a meeting organized by Moser and Zehnder in 1981. Workshops in this series focus on new results and developments in dynamical systems and related areas of mathematics, with symplectic geometry playing an important role in recent years in connection with Hamiltonian dynamics. In this year special emphasis was placed on various kinds of spectra (in contact geometry, in Riemannian geometry, in dynamical systems and in symplectic topology) and their applications to dynamics.}, author = {Arnaud, Marie-Claude and Hofer, Helmut W. and Hutchings, Michael and Kaloshin, Vadim}, issn = {1660-8941}, journal = {Oberwolfach Reports}, number = {3}, pages = {1735--1803}, publisher = {European Mathematical Society}, title = {{Dynamische Systeme}}, doi = {10.4171/owr/2021/33}, volume = {18}, year = {2022}, } @article{17065, abstract = {Past work on optimizing fabrication plans given a carpentry design can provide Pareto-optimal plans trading off between material waste, fabrication time, precision, and other considerations. However, when developing fabrication plans, experts rarely restrict to a single design, instead considering families of design variations, sometimes adjusting designs to simplify fabrication. Jointly exploring the design and fabrication plan spaces for each design is intractable using current techniques. We present a new approach to jointly optimize design and fabrication plans for carpentered objects. To make this bi-level optimization tractable, we adapt recent work from program synthesis based on equality graphs (e-graphs), which encode sets of equivalent programs. Our insight is that subproblems within our bi-level problem share significant substructures. By representing both designs and fabrication plans in a new bag of parts (BOP) e-graph, we amortize the cost of optimizing design components shared among multiple candidates. Even using BOP e-graphs, the optimization space grows quickly in practice. Hence, we also show how a feedback-guided search strategy dubbed Iterative Contraction and Expansion on E-graphs (ICEE) can keep the size of the e-graph manageable and direct the search towards promising candidates. We illustrate the advantages of our pipeline through examples from the carpentry domain.}, author = {Zhao, Haisen and Willsey, Max and Zhu, Amy and Nandi, Chandrakana and Tatlock, Zachary and Solomon, Justin and Schulz, Adriana}, issn = {1557-7368}, journal = {ACM Transactions on Graphics}, number = {3}, publisher = {Association for Computing Machinery}, title = {{Co-optimization of design and fabrication plans for carpentry}}, doi = {10.1145/3508499}, volume = {41}, year = {2022}, } @article{17066, abstract = {A cell’s size affects the likelihood that it will die. But how is cell size controlled in this context and how does cell size impact commitment to the cell death fate? We present evidence that the caspase CED-3 interacts with the RhoGEF ECT-2 in Caenorhabditis elegans neuroblasts that generate “unwanted” cells. We propose that this interaction promotes polar actomyosin contractility, which leads to unequal neuroblast division and the generation of a daughter cell that is below the critical “lethal” size threshold. Furthermore, we find that hyperactivation of ECT-2 RhoGEF reduces the sizes of unwanted cells. Importantly, this suppresses the “cell death abnormal” phenotype caused by the partial loss of ced-3 caspase and therefore increases the likelihood that unwanted cells die. A putative null mutation of ced-3 caspase, however, is not suppressed, which indicates that cell size affects CED-3 caspase activation and/or activity. Therefore, we have uncovered novel sequential and reciprocal interactions between the apoptosis pathway and cell size that impact a cell’s commitment to the cell death fate.}, author = {Sethi, Aditya and Wei, Hai and Mishra, Nikhil and Segos, Ioannis and Lambie, Eric J. and Zanin, Esther and Conradt, Barbara}, issn = {1545-7885}, journal = {PLOS Biology}, number = {10}, publisher = {Public Library of Science}, title = {{A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans}}, doi = {10.1371/journal.pbio.3001786}, volume = {20}, year = {2022}, } @article{17067, abstract = {Human doublecortin (DCX) mutations are associated with severe brain malformations leading to aberrant neuron positioning (heterotopia), intellectual disability and epilepsy. DCX is a microtubule-associated protein which plays a key role during neurodevelopment in neuronal migration and differentiation. Dcx knockout (KO) mice show disorganized hippocampal pyramidal neurons. The CA2/CA3 pyramidal cell layer is present as two abnormal layers and disorganized CA3 KO pyramidal neurons are also more excitable than wild-type (WT) cells. To further identify abnormalities, we characterized Dcx KO hippocampal neurons at subcellular, molecular and ultrastructural levels. Severe defects were observed in mitochondria, affecting number and distribution. Also, the Golgi apparatus was visibly abnormal, increased in volume and abnormally organized. Transcriptome analyses from laser microdissected hippocampal tissue at postnatal day 60 (P60) highlighted organelle abnormalities. Ultrastructural studies of CA3 cells performed in P60 (young adult) and > 9 months (mature) tissue showed that organelle defects are persistent throughout life. Locomotor activity and fear memory of young and mature adults were also abnormal: Dcx KO mice consistently performed less well than WT littermates, with defects becoming more severe with age. Thus, we show that disruption of a neurodevelopmentally-regulated gene can lead to permanent organelle anomalies contributing to abnormal adult behavior.}, author = {Stouffer, Melissa A and Khalaf-Nazzal, R. and Cifuentes-Diaz, C. and Albertini, G. and Bandet, E. and Grannec, G. and Lavilla, V. and Deleuze, J.-F. and Olaso, R. and Nosten-Bertrand, M. and Francis, F.}, issn = {0969-9961}, journal = {Neurobiology of Disease}, publisher = {Elsevier}, title = {{Doublecortin mutation leads to persistent defects in the Golgi apparatus and mitochondria in adult hippocampal pyramidal cells}}, doi = {10.1016/j.nbd.2022.105702}, volume = {168}, year = {2022}, } @article{17068, abstract = {In plants, the antagonism between growth and defense is hardwired by hormonal signaling. The perception of pathogen-associated molecular patterns (PAMPs) from invading microorganisms inhibits auxin signaling and plant growth. Conversely, pathogens manipulate auxin signaling to promote disease, but how this hormone inhibits immunity is not fully understood. Ustilago maydis is a maize pathogen that induces auxin signaling in its host. We characterized a U. maydis effector protein, Naked1 (Nkd1), that is translocated into the host nucleus. Through its native ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motif, Nkd1 binds to the transcriptional co-repressors TOPLESS/TOPLESS-related (TPL/TPRs) and prevents the recruitment of a transcriptional repressor involved in hormonal signaling, leading to the de-repression of auxin and jasmonate signaling and thereby promoting susceptibility to (hemi)biotrophic pathogens. A moderate upregulation of auxin signaling inhibits the PAMP-triggered reactive oxygen species (ROS) burst, an early defense response. Thus, our findings establish a clear mechanism for auxin-induced pathogen susceptibility. Engineered Nkd1 variants with increased expression or increased EAR-mediated TPL/TPR binding trigger typical salicylic-acid-mediated defense reactions, leading to pathogen resistance. This implies that moderate binding of Nkd1 to TPL is a result of a balancing evolutionary selection process to enable TPL manipulation while avoiding host recognition.}, author = {Navarrete, Fernando and Gallei, Michelle C and Kornienko, Aleksandra E. and Saado, Indira and Khan, Mamoona and Chia, Khong-Sam and Darino, Martin A. and Bindics, Janos and Djamei, Armin}, issn = {2590-3462}, journal = {Plant Communications}, number = {2}, publisher = {Elsevier}, title = {{TOPLESS promotes plant immunity by repressing auxin signaling and is targeted by the fungal effector Naked1}}, doi = {10.1016/j.xplc.2021.100269}, volume = {3}, year = {2022}, } @article{17069, abstract = {Fertilization of an egg by multiple sperm (polyspermy) leads to lethal genome imbalance and chromosome segregation defects. In Arabidopsis thaliana, the block to polyspermy is facilitated by a mechanism that prevents polytubey (the arrival of multiple pollen tubes to one ovule). We show here that FERONIA, ANJEA, and HERCULES RECEPTOR KINASE 1 receptor-like kinases located at the septum interact with pollen tube–specific RALF6, 7, 16, 36, and 37 peptide ligands to establish this polytubey block. The same combination of RALF (rapid alkalinization factor) peptides and receptor complexes controls pollen tube reception and rupture inside the targeted ovule. Pollen tube rupture releases the polytubey block at the septum, which allows the emergence of secondary pollen tubes upon fertilization failure. Thus, orchestrated steps in the fertilization process in Arabidopsis are coordinated by the same signaling components to guarantee and optimize reproductive success.}, author = {Zhong, Sheng and Li, Ling and Wang, Zhijuan and Ge, Zengxiang and Li, Qiyun and Bleckmann, Andrea and Wang, Jizong and Song, Zihan and Shi, Yihao and Liu, Tianxu and Li, Luhan and Zhou, Huabin and Wang, Yanyan and Zhang, Li and Wu, Hen-Ming and Lai, Luhua and Gu, Hongya and Dong, Juan and Cheung, Alice Y. and Dresselhaus, Thomas and Qu, Li-Jia}, issn = {1095-9203}, journal = {Science}, number = {6578}, pages = {290--296}, publisher = {American Association for the Advancement of Science}, title = {{RALF peptide signaling controls the polytubey block in Arabidopsis}}, doi = {10.1126/science.abl4683}, volume = {375}, year = {2022}, } @article{17070, abstract = {We investigate the formation of magnetic Bose polaron, an impurity atom dressed by spin-wave excitations, in a one-dimensional spinor Bose gas. Within an effective potential model, the impurity is strongly confined by the host excitations which can even overcome the impurity-medium repulsion leading to a self-localized quasi-particle state. The phase diagram of the attractive and self-bound repulsive magnetic polaron, repulsive non-magnetic (Fröhlich-type) polaron and impurity-medium phase-separation regimes is explored with respect to the Rabi-coupling between the spin components, spin–spin interactions and impurity-medium coupling. The residue of such magnetic polarons decreases substantially in both strong attractive and repulsive branches with strong impurity-spin interactions, illustrating significant dressing of the impurity. The impurity can be used to probe and maneuver the spin polarization of the magnetic medium while suppressing ferromagnetic spin–spin correlations. It is shown that mean-field theory fails as the spinor gas approaches immiscibility since the generated spin-wave excitations are prominent. Our findings illustrate that impurities can be utilized to generate controllable spin–spin correlations and magnetic polaron states which can be realized with current cold atom setups.}, author = {Mistakidis, S I and Koutentakis, Georgios and Grusdt, F and Schmelcher, P and Sadeghpour, H R}, issn = {1367-2630}, journal = {New Journal of Physics}, number = {8}, publisher = {IOP Publishing}, title = {{Inducing spin-order with an impurity: phase diagram of the magnetic Bose polaron}}, doi = {10.1088/1367-2630/ac836c}, volume = {24}, year = {2022}, } @article{17071, abstract = {The eukaryotic nucleus pro­tects the genome and is enclosed by the two membranes of the nuclear envelope. Nuclear pore complexes (NPCs) perforate the nuclear envelope to facilitate nucleocytoplasmic transport. With a molecular weight of ∼120 MDa, the human NPC is one of the larg­est protein complexes. Its ~1000 proteins are taken in multiple copies from a set of about 30 distinct nucleoporins (NUPs). They can be roughly categorized into two classes. Scaf­fold NUPs contain folded domains and form a cylindrical scaffold architecture around a central channel. Intrinsically disordered NUPs line the scaffold and extend into the central channel, where they interact with cargo complexes. The NPC architecture is highly dynamic. It responds to changes in nuclear envelope tension with conforma­tional breathing that manifests in dilation and constriction movements. Elucidating the scaffold architecture, ultimately at atomic resolution, will be important for gaining a more precise understanding of NPC function and dynamics but imposes a substantial chal­lenge for structural biologists. Considerable progress has been made toward this goal by a joint effort in the field. A synergistic combination of complementary approaches has turned out to be critical. In situ structural biology techniques were used to reveal the overall layout of the NPC scaffold that defines the spatial reference for molecular modeling. High-resolution structures of many NUPs were determined in vitro. Proteomic analysis and extensive biochemical work unraveled the interaction network of NUPs. Integra­tive modeling has been used to combine the different types of data, resulting in a rough outline of the NPC scaffold. Previous struc­tural models of the human NPC, however, were patchy and limited in accuracy owing to several challenges: (i) Many of the high-resolution structures of individual NUPs have been solved from distantly related species and, consequently, do not comprehensively cover their human counterparts. (ii) The scaf­fold is interconnected by a set of intrinsically disordered linker NUPs that are not straight­forwardly accessible to common structural biology techniques. (iii) The NPC scaffold intimately embraces the fused inner and outer nuclear membranes in a distinctive topol­ogy and cannot be studied in isolation. (iv) The conformational dynamics of scaffold NUPs limits the resolution achievable in structure determination. In this study, we used artificial intelligence (AI)–based prediction to generate an exten­sive repertoire of structural models of human NUPs and their subcomplexes. The resulting models cover various domains and interfaces that so far remained structurally uncharac­terized. Benchmarking against previous and unpublished x-ray and cryo–electron micros­copy structures revealed unprecedented accu­racy. We obtained well-resolved cryo–electron tomographic maps of both the constricted and dilated conformational states of the hu­man NPC. Using integrative modeling, we fit­ted the structural models of individual NUPs into the cryo–electron microscopy maps. We explicitly included several linker NUPs and traced their trajectory through the NPC scaf­fold. We elucidated in great detail how mem­brane-associated and transmembrane NUPs are distributed across the fusion topology of both nuclear membranes. The resulting architectural model increases the structural coverage of the human NPC scaffold by about twofold. We extensively validated our model against both earlier and new experimental data. The completeness of our model has enabled microsecond-long coarse-grained molecular dynamics simulations of the NPC scaffold within an explicit membrane en­vironment and solvent. These simulations reveal that the NPC scaffold prevents the constriction of the otherwise stable double-membrane fusion pore to small diameters in the absence of membrane tension Our 70-MDa atomically re­solved model covers >90% of the human NPC scaffold. It captures conforma­tional changes that occur during dilation and constriction. It also reveals the precise anchoring sites for intrinsically disordered NUPs, the identification of which is a prerequisite for a complete and dy­namic model of the NPC. Our study exempli­fies how AI-based structure prediction may accelerate the elucidation of subcellular ar­chitecture at atomic resolution.}, author = {Mosalaganti, Shyamal and Obarska-Kosinska, Agnieszka and Siggel, Marc and Taniguchi, Reiya and Turoňová, Beata and Zimmerli, Christian E. and Buczak, Katarzyna and Schmidt, Florian and Margiotta, Erica and Mackmull, Marie-Therese and Hagen, Wim J. H. and Hummer, Gerhard and Kosinski, Jan and Beck, Martin}, issn = {1095-9203}, journal = {Science}, number = {6598}, publisher = {American Association for the Advancement of Science}, title = {{AI-based structure prediction empowers integrative structural analysis of human nuclear pores}}, doi = {10.1126/science.abm9506}, volume = {376}, year = {2022}, } @article{17072, abstract = {The collapse of polypeptides is thought important to protein folding, aggregation, intrinsic disorder, and phase separation. However, whether polypeptide collapse is modulated in cells to control protein states is unclear. Here, using integrated protein manipulation and imaging, we show that the chaperonin GroEL-ES can accelerate the folding of proteins by strengthening their collapse. GroEL induces contractile forces in substrate chains, which draws them into the cavity and triggers a general compaction and discrete folding transitions, even for slow-folding proteins. This collapse enhancement is strongest in the nucleotide-bound states of GroEL and is aided by GroES binding to the cavity rim and by the amphiphilic C-terminal tails at the cavity bottom. Collapse modulation is distinct from other proposed GroEL-ES folding acceleration mechanisms, including steric confinement and misfold unfolding. Given the prevalence of collapse throughout the proteome, we conjecture that collapse modulation is more generally relevant within the protein quality control machinery.}, author = {Naqvi, Mohsin M. and Avellaneda Sarrió, Mario and Roth, Andrew and Koers, Eline J. and Roland, Antoine and Sunderlikova, Vanda and Kramer, Günter and Rye, Hays S. and Tans, Sander J.}, issn = {2375-2548}, journal = {Science Advances}, number = {9}, publisher = {American Association for the Advancement of Science}, title = {{Protein chain collapse modulation and folding stimulation by GroEL-ES}}, doi = {10.1126/sciadv.abl6293}, volume = {8}, year = {2022}, } @inbook{17075, abstract = {Disorders associated with the malfunction of amino acid transporters mainly affect the function of the intestine, kidney, brain, and liver. Mutations of brain amino acid transporters, for example, alter neuronal excitability (e.g., episodic ataxia due to SLC1A3 (EAAT1) defect and hyperekplexia due to SLC6A5 (GLYT2) deficiency) or brain development (SLC1A1 (EAAT3), SLC3A2/SLC7A5 (CD98hc/LAT1), and SLC1A4 (ASCT1) deficiencies). Mutations of renal and intestinal amino acid transporters SLC3A1/SLC7A9 (rBAT/b0,+AT) and SLC1A1 (EAAT3) cause renal problems (cystinuria and dicarboxylic aminoaciduria, respectively) and malabsorption that can affect whole-body homoeostasis (Hartnup disorder SLC6A19 (B0AT1), lysinuric protein intolerance SLC3A2/SLC7A7 (CD98hc/y+LAT1), and hyperdibasic aminoaciduria type 1). Mutations in the neuronal system A amino acid transporter SLC38A8 (SNAT8) cause eye developmental and visual defects. Inborn errors associated with mitochondrial SLC25 family members such as SLC25A12 (neuronal- and muscle-specific mitochondrial aspartate/glutamate transporter 1; AGC1) (global cerebral hypomyelination), SLC25A13 (aspartate/glutamate transporter 2) (citrin deficiency), SLC25A15 (ornithine-citrulline carrier 2) (homocitrullinuria, hyperornithinemia, and hyperammonemia syndrome), and SLC25A22 (mitochondrial glutamate/H+ symporter 1, GC1) (neonatal myoclonic epilepsy) will be dealt within Chap. 43 (defects of mitochondrial carriers).}, author = {Palacín, Manuel and Bröer, Stefan and Novarino, Gaia}, booktitle = {Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases}, editor = {Blau, Nenad and Vici, Carlo Dionisi and Ferreira, Carlos R. and Vianey-Saban, Christine and van Karnebeek, Clara D.M.}, isbn = {9783030677268}, pages = {291--312}, publisher = {Springer Nature}, title = {{Amino Acid Transport Defects}}, doi = {10.1007/978-3-030-67727-5_18}, year = {2022}, } @article{17076, abstract = {Introduction: The levels of many blood proteins are associated with Alzheimer's disease (AD) or its pathological hallmarks. Elucidating the molecular factors that control circulating levels of these proteins may help to identify proteins associated with disease risk mechanisms. Methods: Genome-wide and epigenome-wide studies (nindividuals ≤1064) were performed on plasma levels of 282 AD-associated proteins, identified by a structured literature review. Bayesian penalized regression estimated contributions of genetic and epigenetic variation toward inter-individual differences in plasma protein levels. Mendelian randomization (MR) and co-localization tested associations between proteins and disease-related phenotypes. Results: Sixty-four independent genetic and 26 epigenetic loci were associated with 45 proteins. Novel findings included an association between plasma triggering receptor expressed on myeloid cells 2 (TREM2) levels and a polymorphism and cytosine-phosphate-guanine (CpG) site within the MS4A4A locus. Higher plasma tubulin-specific chaperone A (TBCA) and TREM2 levels were significantly associated with lower AD risk. Discussion: Our data inform the regulation of biomarker levels and their relationships with AD.}, author = {Hillary, Robert F. and Gadd, Danni A. and McCartney, Daniel L. and Shi, Liu and Campbell, Archie and Walker, Rosie M. and Ritchie, Craig W. and Deary, Ian J. and Evans, Kathryn L. and Nevado‐Holgado, Alejo J. and Hayward, Caroline and Porteous, David J. and McIntosh, Andrew M. and Lovestone, Simon and Robinson, Matthew Richard and Marioni, Riccardo E.}, issn = {2352-8729}, journal = {Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring}, number = {1}, publisher = {Wiley}, title = {{Genome‐ and epigenome‐wide studies of plasma protein biomarkers for Alzheimer's disease implicate TBCA and TREM2 in disease risk}}, doi = {10.1002/dad2.12280}, volume = {14}, year = {2022}, } @article{17077, abstract = {Resolving a conjecture of Füredi from 1988, we prove that with high probability, the random graph 𝔾(𝑛, 1/2) admits a friendly bisection of its vertex set, i.e., a partition of its vertex set into two parts whose sizes differ by at most one in which 𝑛 − 𝑜(𝑛) vertices have more neighbours in their own part as across. Our proof is constructive, and in the process, we develop a new method to study stochastic processes driven by degree information in random graphs; this involves combining enumeration techniques with an abstract second moment argument.}, author = {Ferber, Asaf and Kwan, Matthew Alan and Narayanan, Bhargav and Sah, Ashwin and Sawhney, Mehtaab}, issn = {2692-3688}, journal = {Communications of the American Mathematical Society}, number = {10}, pages = {380--416}, publisher = {American Mathematical Society}, title = {{Friendly bisections of random graphs}}, doi = {10.1090/cams/13}, volume = {2}, year = {2022}, }