TY - JOUR AB - 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. AU - Goodrich, Carl Peter AU - Liu, Andrea J. AU - Nagel, Sidney R. ID - 7776 IS - 9 JF - Physical Review Letters SN - 0031-9007 TI - Finite-size scaling at the jamming transition VL - 109 ER - TY - JOUR AB - 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. AU - Engel, Jakob AU - Schmalhorst, Philipp S AU - Routier, Françoise ID - 801 IS - 53 JF - Journal of Biological Chemistry TI - Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose VL - 287 ER - TY - JOUR AB - 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. AU - Hennequin, Guillaume AU - Vogels, Tim P AU - Gerstner, Wulfram ID - 8024 IS - 1 JF - Physical Review E SN - 1539-3755 TI - Non-normal amplification in random balanced neuronal networks VL - 86 ER - TY - JOUR AB - 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. AU - Vinzenz, Marlene AU - Nemethova, Maria AU - Schur, Florian AU - Mueller, Jan AU - Narita, Akihiro AU - Urban, Edit AU - Winkler, Christoph AU - Schmeiser, Christian AU - Koestler, Stefan AU - Rottner, Klemens AU - Resch, Guenter AU - Maéda, Yuichiro AU - Small, John ID - 808 IS - 11 JF - Journal of Cell Science TI - Actin branching in the initiation and maintenance of lamellipodia VL - 125 ER - TY - JOUR AB - 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. AU - Dengler, Vanina AU - Meier, Patricia Stutzmann AU - Heusser, Ronald AU - Kupferschmied, Peter AU - Fazekas, Judit AU - Friebe, Sarah AU - Staufer, Sibylle Burger AU - Majcherczyk, Paul A. AU - Moreillon, Philippe AU - Berger-Bächi, Brigitte AU - McCallum, Nadine ID - 8246 IS - 2 JF - FEMS Microbiology Letters SN - 0378-1097 TI - Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response VL - 333 ER -