@article{1908, abstract = {In large populations, multiple beneficial mutations may be simultaneously spreading. In asexual populations, these mutations must either arise on the same background or compete against each other. In sexual populations, recombination can bring together beneficial alleles from different backgrounds, but tightly linked alleles may still greatly interfere with each other. We show for well-mixed populations that when this interference is strong, the genome can be seen as consisting of many effectively asexual stretches linked together. The rate at which beneficial alleles fix is thus roughly proportional to the rate of recombination and depends only logarithmically on the mutation supply and the strength of selection. Our scaling arguments also allow us to predict, with reasonable accuracy, the fitness distribution of fixed mutations when the mutational effect sizes are broad. We focus on the regime in which crossovers occur more frequently than beneficial mutations, as is likely to be the case for many natural populations.}, author = {Weissman, Daniel and Hallatschek, Oskar}, journal = {Genetics}, number = {4}, pages = {1167 -- 1183}, publisher = {Genetics Society of America}, title = {{The rate of adaptation in large sexual populations with linear chromosomes}}, doi = {10.1534/genetics.113.160705}, volume = {196}, year = {2014}, } @article{1909, abstract = {Summary: Phenotypes are often environmentally dependent, which requires organisms to track environmental change. The challenge for organisms is to construct phenotypes using the most accurate environmental cue. Here, we use a quantitative genetic model of adaptation by additive genetic variance, within- and transgenerational plasticity via linear reaction norms and indirect genetic effects respectively. We show how the relative influence on the eventual phenotype of these components depends on the predictability of environmental change (fast or slow, sinusoidal or stochastic) and the developmental lag τ between when the environment is perceived and when selection acts. We then decompose expected mean fitness into three components (variance load, adaptation and fluctuation load) to study the fitness costs of within- and transgenerational plasticity. A strongly negative maternal effect coefficient m minimizes the variance load, but a strongly positive m minimises the fluctuation load. The adaptation term is maximized closer to zero, with positive or negative m preferred under different environmental scenarios. Phenotypic plasticity is higher when τ is shorter and when the environment changes frequently between seasonal extremes. Expected mean population fitness is highest away from highest observed levels of phenotypic plasticity. Within- and transgenerational plasticity act in concert to deliver well-adapted phenotypes, which emphasizes the need to study both simultaneously when investigating phenotypic evolution.}, author = {Ezard, Thomas and Prizak, Roshan and Hoyle, Rebecca}, journal = {Functional Ecology}, number = {3}, pages = {693 -- 701}, publisher = {Wiley-Blackwell}, title = {{The fitness costs of adaptation via phenotypic plasticity and maternal effects}}, doi = {10.1111/1365-2435.12207}, volume = {28}, year = {2014}, } @article{1910, abstract = {angerhans cells (LCs) are a unique subset of dendritic cells (DCs) that express epithelial adhesion molecules, allowing them to form contacts with epithelial cells and reside in epidermal/epithelial tissues. The dynamic regulation of epithelial adhesion plays a decisive role in the life cycle of LCs. It controls whether LCs remain immature and sessile within the epidermis or mature and egress to initiate immune responses. So far, the molecular machinery regulating epithelial adhesion molecules during LC maturation remains elusive. Here, we generated pure populations of immature human LCs in vitro to systematically probe for gene-expression changes during LC maturation. LCs down-regulate a set of epithelial genes including E-cadherin, while they upregulate the mesenchymal marker N-cadherin known to facilitate cell migration. In addition, N-cadherin is constitutively expressed by monocyte-derived DCs known to exhibit characteristics of both inflammatory-type and interstitial/dermal DCs. Moreover, the transcription factors ZEB1 and ZEB2 (ZEB is zinc-finger E-box-binding homeobox) are upregulated in migratory LCs. ZEB1 and ZEB2 have been shown to induce epithelial-to-mesenchymal transition (EMT) and invasive behavior in cancer cells undergoing metastasis. Our results provide the first hint that the molecular EMT machinery might facilitate LC mobilization. Moreover, our study suggests that N-cadherin plays a role during DC migration.}, author = {Konradi, Sabine and Yasmin, Nighat and Haslwanter, Denise and Weber, Michele and Gesslbauer, Bernd and Sixt, Michael K and Strobl, Herbert}, journal = {European Journal of Immunology}, number = {2}, pages = {553 -- 560}, publisher = {Wiley-Blackwell}, title = {{Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2}}, doi = {10.1002/eji.201343681}, volume = {44}, year = {2014}, } @article{1911, abstract = {The topological Tverberg theorem has been generalized in several directions by setting extra restrictions on the Tverberg partitions. Restricted Tverberg partitions, defined by the idea that certain points cannot be in the same part, are encoded with graphs. When two points are adjacent in the graph, they are not in the same part. If the restrictions are too harsh, then the topological Tverberg theorem fails. The colored Tverberg theorem corresponds to graphs constructed as disjoint unions of small complete graphs. Hell studied the case of paths and cycles. In graph theory these partitions are usually viewed as graph colorings. As explored by Aharoni, Haxell, Meshulam and others there are fundamental connections between several notions of graph colorings and topological combinatorics. For ordinary graph colorings it is enough to require that the number of colors q satisfy q>Δ, where Δ is the maximal degree of the graph. It was proven by the first author using equivariant topology that if q>Δ 2 then the topological Tverberg theorem still works. It is conjectured that q>KΔ is also enough for some constant K, and in this paper we prove a fixed-parameter version of that conjecture. The required topological connectivity results are proven with shellability, which also strengthens some previous partial results where the topological connectivity was proven with the nerve lemma.}, author = {Engström, Alexander and Noren, Patrik}, journal = {Discrete & Computational Geometry}, number = {1}, pages = {207 -- 220}, publisher = {Springer}, title = {{Tverberg's Theorem and Graph Coloring}}, doi = {10.1007/s00454-013-9556-3}, volume = {51}, year = {2014}, } @article{1912, abstract = {Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the embryo along its left-right (LR) axis. Regional differences in cell shape within the lumen-lining KV epithelium are essential for its LR patterning function. However, the processes by which KV cells acquire their characteristic shapes are largely unknown. Here, we show that the notochord induces regional differences in cell shape within KV by triggering extracellular matrix (ECM) accumulation adjacent to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen growth. Our study provides mechanistic insight into the processes by which KV translates global embryonic patterning into regional cell shape differences required for its LR symmetry-breaking function.}, author = {Compagnon, Julien and Barone, Vanessa and Rajshekar, Srivarsha and Kottmeier, Rita and Pranjic-Ferscha, Kornelija and Behrndt, Martin and Heisenberg, Carl-Philipp J}, journal = {Developmental Cell}, number = {6}, pages = {774 -- 783}, publisher = {Cell Press}, title = {{The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ}}, doi = {10.1016/j.devcel.2014.11.003}, volume = {31}, year = {2014}, } @article{1913, abstract = {Deposits of phosphorylated tau protein and convergence of pathology in the hippocampus are the hallmarks of neurodegenerative tauopathies. Thus we aimed to evaluate whether regional and cellular vulnerability patterns in the hippocampus distinguish tauopathies or are influenced by their concomitant presence. Methods: We created a heat map of phospho-tau (AT8) immunoreactivity patterns in 24 hippocampal subregions/layers in individuals with Alzheimer's disease (AD)-related neurofibrillary degeneration (n = 40), Pick's disease (n = 8), progressive supranuclear palsy (n = 7), corticobasal degeneration (n = 6), argyrophilic grain disease (AGD, n = 18), globular glial tauopathy (n = 5), and tau-astrogliopathy of the elderly (n = 10). AT8 immunoreactivity patterns were compared by mathematical analysis. Results: Our study reveals disease-specific hot spots and regional selective vulnerability for these disorders. The pattern of hippocampal AD-related tau pathology is strongly influenced by concomitant AGD. Mathematical analysis reveals that hippocampal involvement in primary tauopathies is distinguishable from early-stage AD-related neurofibrillary degeneration. Conclusion: Our data demonstrate disease-specific AT8 immunoreactivity patterns and hot spots in the hippocampus even in tauopathies, which primarily do not affect the hippocampus. These hot spots can be shifted to other regions by the co-occurrence of tauopathies like AGD. Our observations support the notion that globular glial tauopathies and tau-astrogliopathy of the elderly are distinct entities.}, author = {Milenković, Ivan and Petrov, Tatjana and Kovács, Gábor}, issn = {1420-8008}, journal = {Dementia and Geriatric Cognitive Disorders}, number = {5-6}, pages = {375 -- 388}, publisher = {Karger Publishers}, title = {{Patterns of hippocampal tau pathology differentiate neurodegenerative dementias}}, doi = {10.1159/000365548}, volume = {38}, year = {2014}, } @article{1914, abstract = {Targeting membrane proteins for degradation requires the sequential action of ESCRT sub-complexes ESCRT-0 to ESCRT-III. Although this machinery is generally conserved among kingdoms, plants lack the essential ESCRT-0 components. A new report closes this gap by identifying a novel protein family that substitutes for ESCRT-0 function in plants.}, author = {Sauer, Michael and Friml, Jirí}, journal = {Current Biology}, number = {1}, pages = {R27 -- R29}, publisher = {Cell Press}, title = {{Plant biology: Gatekeepers of the road to protein perdition}}, doi = {10.1016/j.cub.2013.11.019}, volume = {24}, year = {2014}, } @article{1915, abstract = {ROPs (Rho of plants) belong to a large family of plant-specific Rho-like small GTPases that function as essential molecular switches to control diverse cellular processes including cytoskeleton organization, cell polarization, cytokinesis, cell differentiation and vesicle trafficking. Although the machineries of vesicle trafficking and cell polarity in plants have been individually well addressed, how ROPs co-ordinate those processes is still largely unclear. Recent progress has been made towards an understanding of the coordination of ROP signalling and trafficking of PIN (PINFORMED) transporters for the plant hormone auxin in both root and leaf pavement cells. PIN transporters constantly shuttle between the endosomal compartments and the polar plasma membrane domains, therefore the modulation of PIN-dependent auxin transport between cells is a main developmental output of ROP-regulated vesicle trafficking. The present review focuses on these cellular mechanisms, especially the integration of ROP-based vesicle trafficking and plant cell polarity.}, author = {Chen, Xu and Friml, Jirí}, issn = {1470-8752}, journal = {Biochemical Society Transactions}, number = {1}, pages = {212 -- 218}, publisher = {Portland Press}, title = {{Rho-GTPase-regulated vesicle trafficking in plant cell polarity}}, doi = {10.1042/BST20130269}, volume = {42}, year = {2014}, } @article{1916, abstract = {Hereditary spastic paraplegias (HSPs) are neurodegenerative motor neuron diseases characterized by progressive age-dependent loss of corticospinal motor tract function. Although the genetic basis is partly understood, only a fraction of cases can receive a genetic diagnosis, and a global view of HSP is lacking. By using whole-exome sequencing in combination with network analysis, we identified 18 previously unknown putative HSP genes and validated nearly all of these genes functionally or genetically. The pathways highlighted by these mutations link HSP to cellular transport, nucleotide metabolism, and synapse and axon development. Network analysis revealed a host of further candidate genes, of which three were mutated in our cohort. Our analysis links HSP to other neurodegenerative disorders and can facilitate gene discovery and mechanistic understanding of disease.}, author = {Novarino, Gaia and Fenstermaker, Ali and Zaki, Maha and Hofree, Matan and Silhavy, Jennifer and Heiberg, Andrew and Abdellateef, Mostafa and Rosti, Başak and Scott, Eric and Mansour, Lobna and Masri, Amira and Kayserili, Hülya and Al Aama, Jumana and Abdel Salam, Ghada and Karminejad, Ariana and Kara, Majdi and Kara, Bülent and Bozorgmehri, Bita and Ben Omran, Tawfeg and Mojahedi, Faezeh and Mahmoud, Iman and Bouslam, Naïma and Bouhouche, Ahmed and Benomar, Ali and Hanein, Sylvain and Raymond, Laure and Forlani, Sylvie and Mascaro, Massimo and Selim, Laila and Shehata, Nabil and Al Allawi, Nasir and Bindu, Parayil and Azam, Matloob and Günel, Murat and Caglayan, Ahmet and Bilgüvar, Kaya and Tolun, Aslihan and Issa, Mahmoud and Schroth, Jana and Spencer, Emily and Rosti, Rasim and Akizu, Naiara and Vaux, Keith and Johansen, Anide and Koh, Alice and Megahed, Hisham and Dürr, Alexandra and Brice, Alexis and Stévanin, Giovanni and Gabriel, Stacy and Ideker, Trey and Gleeson, Joseph}, journal = {Science}, number = {6170}, pages = {506 -- 511}, publisher = {American Association for the Advancement of Science}, title = {{Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders}}, doi = {10.1126/science.1247363}, volume = {343}, year = {2014}, } @article{1917, abstract = {Auxin-binding protein 1 (ABP1) was discovered nearly 40 years ago and was shown to be essential for plant development and morphogenesis, but its mode of action remains unclear. Here, we report that the plasma membrane-localized transmembrane kinase (TMK) receptor-like kinases interact with ABP1 and transduce auxin signal to activate plasma membrane-associated ROPs [Rho-like guanosine triphosphatases (GTPase) from plants], leading to changes in the cytoskeleton and the shape of leaf pavement cells in Arabidopsis. The interaction between ABP1 and TMK at the cell surface is induced by auxin and requires ABP1 sensing of auxin. These findings show that TMK proteins and ABP1 form a cell surface auxin perception complex that activates ROP signaling pathways, regulating nontranscriptional cytoplasmic responses and associated fundamental processes.}, author = {Xu, Tongda and Dai, Ning and Chen, Jisheng and Nagawa, Shingo and Cao, Min and Li, Hongjiang and Zhou, Zimin and Chen, Xu and De Rycke, Riet and Rakusová, Hana and Wang, Wen and Jones, Alan and Friml, Jirí and Patterson, Sara and Bleecker, Anthony and Yang, Zhenbiao}, journal = {Science}, number = {6174}, pages = {1025 -- 1028}, publisher = {American Association for the Advancement of Science}, title = {{Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling}}, doi = {10.1126/science.1245125}, volume = {343}, year = {2014}, } @article{1918, abstract = {As the nuclear charge Z is continuously decreased an N-electron atom undergoes a binding-unbinding transition. We investigate whether the electrons remain bound and whether the radius of the system stays finite as the critical value Zc is approached. Existence of a ground state at Zc is shown under the condition Zc < N-K, where K is the maximal number of electrons that can be removed at Zc without changing the energy.}, author = {Bellazzini, Jacopo and Frank, Rupert and Lieb, Élliott and Seiringer, Robert}, journal = {Reviews in Mathematical Physics}, number = {1}, publisher = {World Scientific Publishing}, title = {{Existence of ground states for negative ions at the binding threshold}}, doi = {10.1142/S0129055X13500219}, volume = {26}, year = {2014}, } @article{1919, abstract = {Long-lasting memories are formed when the stimulus is temporally distributed (spacing effect). However, the synaptic mechanisms underlying this robust phenomenon and the precise time course of the synaptic modifications that occur during learning remain unclear. Here we examined the adaptation of horizontal optokinetic response in mice that underwent 1 h of massed and spaced training at varying intervals. Despite similar acquisition by all training protocols, 1 h of spacing produced the highest memory retention at 24 h, which lasted for 1 mo. The distinct kinetics of memory are strongly correlated with the reduction of floccular parallel fiber-Purkinje cell synapses but not with AMPA receptor (AMPAR) number and synapse size. After the spaced training, we observed 25%, 23%, and 12% reduction in AMPAR density, synapse size, and synapse number, respectively. Four hours after the spaced training, half of the synapses and Purkinje cell spines had been eliminated, whereas AMPAR density and synapse size were recovered in remaining synapses. Surprisingly, massed training also produced long-term memory and halving of synapses; however, this occurred slowly over days, and the memory lasted for only 1 wk. This distinct kinetics of structural plasticity may serve as a basis for unique temporal profiles in the formation and decay of memory with or without intervals.}, author = {Aziz, Wajeeha and Wang, Wen and Kesaf, Sebnem and Mohamed, Alsayed and Fukazawa, Yugo and Shigemoto, Ryuichi}, journal = {PNAS}, number = {1}, pages = {E194 -- E202}, publisher = {National Academy of Sciences}, title = {{Distinct kinetics of synaptic structural plasticity, memory formation, and memory decay in massed and spaced learning}}, doi = {10.1073/pnas.1303317110}, volume = {111}, year = {2014}, } @article{1920, abstract = {Cerebellar motor learning is suggested to be caused by long-term plasticity of excitatory parallel fiber-Purkinje cell (PF-PC) synapses associated with changes in the number of synaptic AMPA-type glutamate receptors (AMPARs). However, whether the AMPARs decrease or increase in individual PF-PC synapses occurs in physiological motor learning and accounts for memory that lasts over days remains elusive. We combined quantitative SDS-digested freeze-fracture replica labeling for AMPAR and physical dissector electron microscopy with a simple model of cerebellar motor learning, adaptation of horizontal optokinetic response (HOKR) in mouse. After 1-h training of HOKR, short-term adaptation (STA) was accompanied with transient decrease in AMPARs by 28% in target PF-PC synapses. STA was well correlated with AMPAR decrease in individual animals and both STA and AMPAR decrease recovered to basal levels within 24 h. Surprisingly, long-termadaptation (LTA) after five consecutive daily trainings of 1-h HOKR did not alter the number of AMPARs in PF-PC synapses but caused gradual and persistent synapse elimination by 45%, with corresponding PC spine loss by the fifth training day. Furthermore, recovery of LTA after 2 wk was well correlated with increase of PF-PC synapses to the control level. Our findings indicate that the AMPARs decrease in PF-PC synapses and the elimination of these synapses are in vivo engrams in short- and long-term motor learning, respectively, showing a unique type of synaptic plasticity that may contribute to memory consolidation.}, author = {Wang, Wen and Nakadate, Kazuhiko and Masugi Tokita, Miwako and Shutoh, Fumihiro and Aziz, Wajeeha and Tarusawa, Etsuko and Lörincz, Andrea and Molnár, Elek and Kesaf, Sebnem and Li, Yunqing and Fukazawa, Yugo and Nagao, Soichi and Shigemoto, Ryuichi}, journal = {PNAS}, number = {1}, pages = {E188 -- E193}, publisher = {National Academy of Sciences}, title = {{Distinct cerebellar engrams in short-term and long-term motor learning}}, doi = {10.1073/pnas.1315541111}, volume = {111}, year = {2014}, } @article{1921, abstract = {Cell polarity manifested by asymmetric distribution of cargoes, such as receptors and transporters, within the plasma membrane (PM) is crucial for essential functions in multicellular organisms. In plants, cell polarity (re)establishment is intimately linked to patterning processes. Despite the importance of cell polarity, its underlying mechanisms are still largely unknown, including the definition and distinctiveness of the polar domains within the PM. Here, we show in Arabidopsis thaliana that the signaling membrane components, the phosphoinositides phosphatidylinositol 4-phosphate (PtdIns4P) and phosphatidylinositol 4, 5-bisphosphate [PtdIns(4, 5)P2] as well as PtdIns4P 5-kinases mediating their interconversion, are specifically enriched at apical and basal polar plasma membrane domains. The PtdIns4P 5-kinases PIP5K1 and PIP5K2 are redundantly required for polar localization of specifically apical and basal cargoes, such as PIN-FORMED transporters for the plant hormone auxin. As a consequence of the polarity defects, instructive auxin gradients as well as embryonic and postembryonic patterning are severely compromised. Furthermore, auxin itself regulates PIP5K transcription and PtdIns4P and PtdIns(4, 5)P2 levels, in particular their association with polar PM domains. Our results provide insight into the polar domain-delineating mechanisms in plant cells that depend on apical and basal distribution of membrane lipids and are essential for embryonic and postembryonic patterning.}, author = {Tejos, Ricardo and Sauer, Michael and Vanneste, Steffen and Palacios-Gomez, MiriamPalacios and Li, Hongjiang and Heilmann, Mareike and Van Wijk, Ringo and Vermeer, Joop and Heilmann, Ingo and Munnik, Teun and Friml, Jirí}, journal = {Plant Cell}, number = {5}, pages = {2114 -- 2128}, publisher = {American Society of Plant Biologists}, title = {{Bipolar plasma membrane distribution of phosphoinositides and their requirement for auxin-mediated cell polarity and patterning in Arabidopsis}}, doi = {10.1105/tpc.114.126185}, volume = {26}, year = {2014}, } @article{1922, abstract = {Germination of Arabidopsis seeds in darkness induces apical hook development, based on a tightly regulated differential growth coordinated by a multiple hormone cross-talk. Here, we endeavoured to clarify the function of brassinosteroids (BRs) and cross-talk with ethylene in hook development. An automated infrared imaging system was developed to study the kinetics of hook development in etiolated Arabidopsis seedlings. To ascertain the photomorphogenic control of hook opening, the system was equipped with an automatic light dimmer. We demonstrate that ethylene and BRs are indispensable for hook formation and maintenance. Ethylene regulation of hook formation functions partly through BRs, with BR feedback inhibition of ethylene action. Conversely, BR-mediated extension of hook maintenance functions partly through ethylene. Furthermore, we revealed that a short light pulse is sufficient to induce rapid hook opening. Our dynamic infrared imaging system allows high-resolution, kinetic imaging of up to 112 seedlings in a single experimental run. At this high throughput, it is ideally suited to rapidly gain insight in pathway networks. We demonstrate that BRs and ethylene cooperatively regulate apical hook development in a phase-dependent manner. Furthermore, we show that light is a predominant regulator of hook opening, inhibiting ethylene- and BR-mediated postponement of hook opening.}, author = {Smet, Dajo and Žádníková, Petra and Vandenbussche, Filip and Benková, Eva and Van Der Straeten, Dominique}, journal = {New Phytologist}, number = {4}, pages = {1398 -- 1411}, publisher = {Wiley-Blackwell}, title = {{Dynamic infrared imaging analysis of apical hook development in Arabidopsis: The case of brassinosteroids}}, doi = {10.1111/nph.12751}, volume = {202}, year = {2014}, } @article{1923, abstract = {We derive the equations for a thin, axisymmetric elastic shell subjected to an internal active stress giving rise to active tension and moments within the shell. We discuss the stability of a cylindrical elastic shell and its response to a localized change in internal active stress. This description is relevant to describe the cellular actomyosin cortex, a thin shell at the cell surface behaving elastically at a short timescale and subjected to active internal forces arising from myosin molecular motor activity. We show that the recent observations of cell deformation following detachment of adherent cells (Maître J-L et al 2012 Science 338 253-6) are well accounted for by this mechanical description. The actin cortex elastic and bending moduli can be obtained from a quantitative analysis of cell shapes observed in these experiments. Our approach thus provides a non-invasive, imaging-based method for the extraction of cellular physical parameters.}, author = {Berthoumieux, Hélène and Maître, Jean-Léon and Heisenberg, Carl-Philipp J and Paluch, Ewa and Julicher, Frank and Salbreux, Guillaume}, journal = {New Journal of Physics}, publisher = {IOP Publishing Ltd.}, title = {{Active elastic thin shell theory for cellular deformations}}, doi = {10.1088/1367-2630/16/6/065005}, volume = {16}, year = {2014}, } @article{1924, abstract = {Stomata are two-celled valves that control epidermal pores whose spacing optimizes shoot-atmosphere gas exchange. They develop from protodermal cells after unequal divisions followed by an equal division and differentiation. The concentration of the hormone auxin, a master plant developmental regulator, is tightly controlled in time and space, but its role, if any, in stomatal formation is obscure. Here dynamic changes of auxin activity during stomatal development are monitored using auxin input (DII-VENUS) and output (DR5:VENUS) markers by time-lapse imaging. A decrease in auxin levels in the smaller daughter cell after unequal division presages the acquisition of a guard mother cell fate whose equal division produces the two guard cells. Thus, stomatal patterning requires auxin pathway control of stem cell compartment size, as well as auxin depletion that triggers a developmental switch from unequal to equal division.}, author = {Le, Jie and Liu, Xuguang and Yang, Kezhen and Chen, Xiaolan and Zhu, Lingling and Wang, Hongzhe and Wang, Ming and Vanneste, Steffen and Morita, Miyo and Tasaka, Masao and Ding, Zhaojun and Friml, Jirí and Beeckman, Tom and Sack, Fred}, journal = {Nature Communications}, publisher = {Nature Publishing Group}, title = {{Auxin transport and activity regulate stomatal patterning and development}}, doi = {10.1038/ncomms4090}, volume = {5}, year = {2014}, } @article{1925, abstract = {In the past decade carbon nanotubes (CNTs) have been widely studied as a potential drug-delivery system, especially with functionality for cellular targeting. Yet, little is known about the actual process of docking to cell receptors and transport dynamics after internalization. Here we performed single-particle studies of folic acid (FA) mediated CNT binding to human carcinoma cells and their transport inside the cytosol. In particular, we employed molecular recognition force spectroscopy, an atomic force microscopy based method, to visualize and quantify docking of FA functionalized CNTs to FA binding receptors in terms of binding probability and binding force. We then traced individual fluorescently labeled, FA functionalized CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed trajectories of directed diffusion and areas of nanotube confinement in the cytosol. Our results demonstrate the potential of a single-molecule approach for investigation of drug-delivery vehicles and their targeting capacity.}, author = {Lamprecht, Constanze and Plochberger, Birgit and Ruprecht, Verena and Wieser, Stefan and Rankl, Christian and Heister, Elena and Unterauer, Barbara and Brameshuber, Mario and Danzberger, Jürgen and Lukanov, Petar and Flahaut, Emmanuel and Schütz, Gerhard and Hinterdorfer, Peter and Ebner, Andreas}, journal = {Nanotechnology}, number = {12}, publisher = {IOP Publishing}, title = {{A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes}}, doi = {10.1088/0957-4484/25/12/125704}, volume = {25}, year = {2014}, } @article{1926, abstract = {We consider cross products of finite graphs with a class of trees that have arbitrarily but finitely long line segments, such as the Fibonacci tree. Such cross products are called tree-strips. We prove that for small disorder random Schrödinger operators on such tree-strips have purely absolutely continuous spectrum in a certain set.}, author = {Sadel, Christian}, journal = {Mathematical Physics, Analysis and Geometry}, number = {3-4}, pages = {409 -- 440}, publisher = {Springer}, title = {{Absolutely continuous spectrum for random Schrödinger operators on the Fibonacci and similar Tree-strips}}, doi = {10.1007/s11040-014-9163-4}, volume = {17}, year = {2014}, } @article{1928, abstract = {In infectious disease epidemiology the basic reproductive ratio, R0, is defined as the average number of new infections caused by a single infected individual in a fully susceptible population. Many models describing competition for hosts between non-interacting pathogen strains in an infinite population lead to the conclusion that selection favors invasion of new strains if and only if they have higher R0 values than the resident. Here we demonstrate that this picture fails in finite populations. Using a simple stochastic SIS model, we show that in general there is no analogous optimization principle. We find that successive invasions may in some cases lead to strains that infect a smaller fraction of the host population, and that mutually invasible pathogen strains exist. In the limit of weak selection we demonstrate that an optimization principle does exist, although it differs from R0 maximization. For strains with very large R0, we derive an expression for this local fitness function and use it to establish a lower bound for the error caused by neglecting stochastic effects. Furthermore, we apply this weak selection limit to investigate the selection dynamics in the presence of a trade-off between the virulence and the transmission rate of a pathogen.}, author = {Humplik, Jan and Hill, Alison and Nowak, Martin}, journal = {Journal of Theoretical Biology}, pages = {149 -- 162}, publisher = {Elsevier}, title = {{Evolutionary dynamics of infectious diseases in finite populations}}, doi = {10.1016/j.jtbi.2014.06.039}, volume = {360}, year = {2014}, }