@article{767, abstract = {Synchronous distributed algorithms are easier to design and prove correct than algorithms that tolerate asynchrony. Yet, in the real world, networks experience asynchrony and other timing anomalies. In this paper, we address the question of how to efficiently transform an algorithm that relies on synchronous timing into an algorithm that tolerates asynchronous executions. We introduce a transformation technique from synchronous algorithms to indulgent algorithms (Guerraoui, in PODC, pp. 289-297, 2000), which induces only a constant overhead in terms of time complexity in well-behaved executions. Our technique is based on a new abstraction we call an asynchrony detector, which the participating processes implement collectively. The resulting transformation works for the class of colorless distributed tasks, including consensus and set agreement. Interestingly, we also show that our technique is relevant for colored tasks, by applying it to the renaming problem, to obtain the first indulgent renaming algorithm.}, author = {Alistarh, Dan-Adrian and Gilbert, Seth and Guerraoui, Rachid and Travers, Corentin}, journal = {Theory of Computing Systems}, number = {4}, pages = {404 -- 424}, publisher = {Elsevier}, title = {{Generating Fast Indulgent Algorithms}}, doi = {10.1007/s00224-012-9407-2}, volume = {51}, year = {2012}, } @article{7749, abstract = {Although studies on laboratory species and natural populations of vertebrates have shown reproduction to impair later performance, little is known of the age‐specific associations between reproduction and survival, and how such findings apply to the ageing of large, long‐lived species. Herein we develop a framework to examine population‐level patterns of reproduction and survival across lifespan in long‐lived organisms, and decompose those changes into individual‐level effects, and the effects of age‐specific trade‐offs between fitness components. We apply this to an extensive longitudinal dataset on female semi‐captive Asian timber elephants (Elephas maximus) and report the first evidence of age‐specific fitness declines that are driven by age‐specific associations between fitness components in a long‐lived mammal. Associations between reproduction and survival are positive in early life, but negative in later life with up to 71% of later‐life survival declines associated with investing in the production of offspring within this population of this critically endangered species.}, author = {Robinson, Matthew Richard and Mar, Khyne U and Lummaa, Virpi}, issn = {1461-023X}, journal = {Ecology Letters}, number = {3}, pages = {260--266}, publisher = {Wiley}, title = {{Senescence and age-specific trade-offs between reproduction and survival in female Asian elephants}}, doi = {10.1111/j.1461-0248.2011.01735.x}, volume = {15}, year = {2012}, } @article{7748, abstract = {Female mate choice acts as an important evolutionary force, yet the influence of the environment on both its expression and the selective pressures acting upon it remains unknown. We found consistent heritable differences between females in their choice of mate based on ornament size during a 25‐year study of a population of collared flycatchers. However, the fitness consequences of mate choice were dependent on environmental conditions experienced whilst breeding. Females breeding with highly ornamented males experienced high relative fitness during dry summer conditions, but low relative fitness during wetter years. Our results imply that sexual selection within a population can be highly variable and dependent upon the prevailing weather conditions experienced by individuals.}, author = {Robinson, Matthew Richard and Sander van Doorn, G. and Gustafsson, Lars and Qvarnström, Anna}, issn = {1461-023X}, journal = {Ecology Letters}, number = {6}, pages = {611--618}, publisher = {Wiley}, title = {{Environment-dependent selection on mate choice in a natural population of birds}}, doi = {10.1111/j.1461-0248.2012.01780.x}, volume = {15}, year = {2012}, } @article{7776, abstract = {We present an analysis of finite-size effects in jammed packings of N soft, frictionless spheres at zero temperature. There is a 1/N correction to the discrete jump in the contact number at the transition so that jammed packings exist only above isostaticity. As a result, the canonical power-law scalings of the contact number and elastic moduli break down at low pressure. These quantities exhibit scaling collapse with a nontrivial scaling function, demonstrating that the jamming transition can be considered a phase transition. Scaling is achieved as a function of N in both two and three dimensions, indicating an upper critical dimension of 2.}, author = {Goodrich, Carl Peter and Liu, Andrea J. and Nagel, Sidney R.}, issn = {0031-9007}, journal = {Physical Review Letters}, number = {9}, publisher = {American Physical Society}, title = {{Finite-size scaling at the jamming transition}}, doi = {10.1103/physrevlett.109.095704}, volume = {109}, year = {2012}, } @article{801, abstract = {Fungal cell walls frequently contain a polymer of mannose and galactose called galactomannan. In the pathogenic filamentous fungus Aspergillus fumigatus, this polysaccharide is made of a linear mannan backbone with side chains of galactofuran and is anchored to the plasma membrane via a glycosylphosphatidylinositol or is covalently linked to the cell wall. To date, the biosynthesis and significance of this polysaccharide are unknown. The present data demonstrate that deletion of the Golgi UDP-galactofuranose transporter GlfB or the GDP-mannose transporter GmtA leads to the absence of galactofuran or galactomannan, respectively. This indicates that the biosynthesis of galactomannan probably occurs in the lumen of the Golgi apparatus and thus contrasts with the biosynthesis of other fungal cell wall polysaccharides studied to date that takes place at the plasma membrane. Transglycosylation of galactomannan from the membrane to the cell wall is hypothesized because both the cell wall-bound and membrane-bound polysaccharide forms are affected in the generated mutants. Considering the severe growth defect of the A. fumigatus GmtA-deficient mutant, proving this paradigm might provide new targets for antifungal therapy.}, author = {Engel, Jakob and Schmalhorst, Philipp S and Routier, Françoise}, journal = {Journal of Biological Chemistry}, number = {53}, pages = {44418 -- 44424}, publisher = {American Society for Biochemistry and Molecular Biology}, title = {{Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose}}, doi = {10.1074/jbc.M112.398321}, volume = {287}, year = {2012}, } @article{8024, abstract = {In dynamical models of cortical networks, the recurrent connectivity can amplify the input given to the network in two distinct ways. One is induced by the presence of near-critical eigenvalues in the connectivity matrix W, producing large but slow activity fluctuations along the corresponding eigenvectors (dynamical slowing). The other relies on W not being normal, which allows the network activity to make large but fast excursions along specific directions. Here we investigate the trade-off between non-normal amplification and dynamical slowing in the spontaneous activity of large random neuronal networks composed of excitatory and inhibitory neurons. We use a Schur decomposition of W to separate the two amplification mechanisms. Assuming linear stochastic dynamics, we derive an exact expression for the expected amount of purely non-normal amplification. We find that amplification is very limited if dynamical slowing must be kept weak. We conclude that, to achieve strong transient amplification with little slowing, the connectivity must be structured. We show that unidirectional connections between neurons of the same type together with reciprocal connections between neurons of different types, allow for amplification already in the fast dynamical regime. Finally, our results also shed light on the differences between balanced networks in which inhibition exactly cancels excitation and those where inhibition dominates.}, author = {Hennequin, Guillaume and Vogels, Tim P and Gerstner, Wulfram}, issn = {1539-3755}, journal = {Physical Review E}, number = {1}, publisher = {American Physical Society}, title = {{Non-normal amplification in random balanced neuronal networks}}, doi = {10.1103/physreve.86.011909}, volume = {86}, year = {2012}, } @article{808, abstract = {Using correlated live-cell imaging and electron tomography we found that actin branch junctions in protruding and treadmilling lamellipodia are not concentrated at the front as previously supposed, but link actin filament subsets in which there is a continuum of distances from a junction to the filament plus ends, for up to at least 1 mm. When branch sites were observed closely spaced on the same filament their separation was commonly a multiple of the actin helical repeat of 36 nm. Image averaging of branch junctions in the tomograms yielded a model for the in vivo branch at 2.9 nm resolution, which was comparable with that derived for the in vitro actin- Arp2/3 complex. Lamellipodium initiation was monitored in an intracellular wound-healing model and was found to involve branching from the sides of actin filaments oriented parallel to the plasmalemma. Many filament plus ends, presumably capped, terminated behind the lamellipodium tip and localized on the dorsal and ventral surfaces of the actin network. These findings reveal how branching events initiate and maintain a network of actin filaments of variable length, and provide the first structural model of the branch junction in vivo. A possible role of filament capping in generating the lamellipodium leaflet is discussed and a mathematical model of protrusion is also presented.}, author = {Vinzenz, Marlene and Nemethova, Maria and Schur, Florian and Mueller, Jan and Narita, Akihiro and Urban, Edit and Winkler, Christoph and Schmeiser, Christian and Koestler, Stefan and Rottner, Klemens and Resch, Guenter and Maéda, Yuichiro and Small, John}, journal = {Journal of Cell Science}, number = {11}, pages = {2775 -- 2785}, publisher = {Company of Biologists}, title = {{Actin branching in the initiation and maintenance of lamellipodia}}, doi = {10.1242/jcs.107623}, volume = {125}, year = {2012}, } @article{8246, abstract = {The Staphylococcus aureus cell wall stress stimulon (CWSS) is activated by cell envelope-targeting antibiotics or depletion of essential cell wall biosynthesis enzymes. The functionally uncharacterized S. aureus LytR-CpsA-Psr (LCP) proteins, MsrR, SA0908 and SA2103, all belong to the CWSS. Although not essential, deletion of all three LCP proteins severely impairs cell division. We show here that VraSR-dependent CWSS expression was up to 250-fold higher in single, double and triple LCP mutants than in wild type S. aureus in the absence of external stress. The LCP triple mutant was virtually depleted of wall teichoic acids (WTA), which could be restored to different degrees by any of the single LCP proteins. Subinhibitory concentrations of tunicamycin, which inhibits the first WTA synthesis enzyme TarO (TagO), could partially complement the severe growth defect of the LCP triple mutant. Both of the latter findings support a role for S. aureus LCP proteins in late WTA synthesis, as in Bacillus subtilis where LCP proteins were recently proposed to transfer WTA from lipid carriers to the cell wall peptidoglycan. Intrinsic activation of the CWSS upon LCP deletion and the fact that LCP proteins were essential for WTA-loading of the cell wall, highlight their important role(s) in S. aureus cell envelope biogenesis.}, author = {Dengler, Vanina and Meier, Patricia Stutzmann and Heusser, Ronald and Kupferschmied, Peter and Fazekas, Judit and Friebe, Sarah and Staufer, Sibylle Burger and Majcherczyk, Paul A. and Moreillon, Philippe and Berger-Bächi, Brigitte and McCallum, Nadine}, issn = {0378-1097}, journal = {FEMS Microbiology Letters}, number = {2}, pages = {109--120}, publisher = {Oxford University Press}, title = {{Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response}}, doi = {10.1111/j.1574-6968.2012.02603.x}, volume = {333}, year = {2012}, } @article{826, abstract = {Plants exhibit a unique developmental flexibility to ever-changing environmental conditions. To achieve their profound adaptability, plants are able to maintain permanent stem cell populations and form new organs during the entire plant life cycle. Signaling substances, called plant hormones, such as auxin, cytokinin, abscisic acid, brassinosteroid, ethylene, gibberellin, jasmonic acid, and strigolactone, govern and coordinate these developmental processes. Physiological and genetic studies have dissected the molecular components of signal perception and transduction of the individual hormonal pathways. However, over recent years it has become evident that hormones do not act only in a linear pathway. Hormonal pathways are interconnected by a complex network of interactions and feedback circuits that determines the final outcome of the individual hormone actions. This raises questions about the molecular mechanisms underlying hormonal cross talk and about how these hormonal networks are established, maintained, and modulated throughout plant development.}, author = {Vanstraelen, Marleen and Eva Benková}, journal = {Annual Review of Cell and Developmental Biology}, pages = {463 -- 487}, publisher = {Annual Reviews}, title = {{Hormonal interactions in the regulation of plant development}}, doi = {10.1146/annurev-cellbio-101011-155741}, volume = {28}, year = {2012}, } @article{829, abstract = {The architecture of a plant's root system, established postembryonically, results from both coordinated root growth and lateral root branching. The plant hormones auxin and cytokinin are central endogenous signaling molecules that regulate lateral root organogenesis positively and negatively, respectively. Tight control and mutual balance of their antagonistic activities are particularly important during the early phases of lateral root organogenesis to ensure continuous lateral root initiation (LRI) and proper development of lateral root primordia (LRP). Here, we show that the early phases of lateral root organogenesis, including priming and initiation, take place in root zones with a repressed cytokinin response. Accordingly, ectopic overproduction of cytokinin in the root basal meristem most efficiently inhibits LRI. Enhanced cytokinin responses in pericycle cells between existing LRP might restrict LRI near existing LRP and, when compromised, ectopic LRI occurs. Furthermore, our results demonstrate that young LRP are more sensitive to perturbations in the cytokinin activity than are developmentally more advanced primordia. We hypothesize that the effect of cytokinin on the development of primordia possibly depends on the robustness and stability of the auxin gradient.}, author = {Bielach, Agnieszka and Podlesakova, Katerina and Peter Marhavy and Duclercq, Jérôme and Candela Cuesta and Muller, Bruno and Grunewald, Wim and Tarkowski, Petr and Eva Benková}, journal = {The Plant Cell}, number = {10}, pages = {3967 -- 3981}, publisher = {American Society of Plant Biologists}, title = {{Spatiotemporal regulation of lateral root organogenesis in Arabidopsis by cytokinin}}, doi = {10.1105/tpc.112.103044}, volume = {24}, year = {2012}, }