Showing 4731 - 4740 of 5831 Items
A dominant allele of arabidopsis pectin-binding wall-associated kinase induces a stress response suppressed by MPK6 but not MPK3 mutations
Date: 2012-01-01
Creator: Bruce D. Kohorn, Susan L. Kohorn, Tanya Todorova, Gillian Baptiste, Kevin, Stansky, Meghan McCullough
Access: Open access
- The plant cell wall is composed of a matrix of cellulose fibers, flexible pectin polymers, and an array of assorted carbohydrates and proteins. The receptor-like Wall-Associated Kinases (WAKs) of Arabidopsis bind pectin in the wall, and are necessary both for cell expansion during development and for a response to pathogens and wounding. Mitogen Activated Protein Kinases (MPKs) form a major signaling link between cell surface receptors and both transcriptional and enzyme regulation in eukaryotes, and Arabidopsis MPK6 and MPK3 indeed have important roles in development and the response to stress and pathogens. A dominant allele of WAK2 requires kinase activity and activates a stress response that includes an increased ROS accumulation and the up-regulation of numerous genes involved in pathogen resistance, wounding, and cell wall biogenesis. This dominant allele requires a functional pectin binding and kinase domain, indicating that it is engaged in a WAK signaling pathway. A null mutant of the major plasma membrane ROS-producing enzyme complex, rbohd/f does not suppress the WAK2cTAP-induced phenotype. A mpk6, but not a mpk3, null allele is able to suppress the effects of this dominant WAK2 mutation, thus distinguishing MPK3 and MPK6, whose activity previously was thought to be redundant. Pectin activation of gene expression is abated in a wak2-null, but is tempered by the WAK-dominant allele that induces elevated basal stress-related transcript levels. The results suggest a mechanism in which changes to the cell wall can lead to a large change in cellular responses and help to explain how pathogens and wounding can have general effects on growth. The Author 2011. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPB and IPPE, SIBS, CAS.2011 © The Author 2011. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPB and IPPE, SIBS, CAS.
Automorphisms of higher rank lamplighter groups
Date: 2015-12-01
Creator: Melanie Stein, Jennifer Taback, Peter Wong
Access: Open access
- Let τd(q) denote the group whose Cayley graph with respect to a particular generating set is the Diestel-Leader graph DLd(q), as described by Bartholdi, Neuhauser and Woess. We compute both Aut(τd(q)) and Out(τd(q)) for d ≥ 2, and apply our results to count twisted conjugacy classes in these groups when d ≥ 3. Specifically, we show that when d ≥ 3, the groups τd(q) have property R∞, that is, every automorphism has an infinite number of twisted conjugacy classes. In contrast, when d = 2 the lamplighter groups τ2(q) = Lq = Zq Z have property R∞ if and only if (q, 6)≠1.
Microevolution of Candida albicans in Macrophages Restores Filamentation in a Nonfilamentous Mutant
Date: 2014-12-01
Creator: Anja Wartenberg, Jörg Linde, Ronny Martin, Maria Schreiner, Fabian, Horn, Ilse D. Jacobsen, Sabrina Jenull, Thomas Wolf, Karl Kuchler, Reinhard Guthke, Oliver Kurzai, Anja Forche, Christophe d'Enfert, Sascha Brunke, Bernhard Hube
Access: Open access
- Following antifungal treatment, Candida albicans, and other human pathogenic fungi can undergo microevolution, which leads to the emergence of drug resistance. However, the capacity for microevolutionary adaptation of fungi goes beyond the development of resistance against antifungals. Here we used an experimental microevolution approach to show that one of the central pathogenicity mechanisms of C. albicans, the yeast-to-hyphae transition, can be subject to experimental evolution. The C. albicans cph1Δ/efg1Δ mutant is nonfilamentous, as central signaling pathways linking environmental cues to hyphal formation are disrupted. We subjected this mutant to constant selection pressure in the hostile environment of the macrophage phagosome. In a comparatively short time-frame, the mutant evolved the ability to escape macrophages by filamentation. In addition, the evolved mutant exhibited hyper-virulence in a murine infection model and an altered cell wall composition compared to the cph1Δ/efg1Δ strain. Moreover, the transcriptional regulation of hyphae-associated, and other pathogenicity-related genes became re-responsive to environmental cues in the evolved strain. We went on to identify the causative missense mutation via whole genome- and transcriptome-sequencing: a single nucleotide exchange took place within SSN3 that encodes a component of the Cdk8 module of the Mediator complex, which links transcription factors with the general transcription machinery. This mutation was responsible for the reconnection of the hyphal growth program with environmental signals in the evolved strain and was sufficient to bypass Efg1/Cph1-dependent filamentation. These data demonstrate that even central transcriptional networks can be remodeled very quickly under appropriate selection pressure.
Symmetric-group decomposition of SU(N) group-theory constraints on four-, five-, and six-point color-ordered amplitudes at all loop orders
Date: 2012-01-01
Creator: Alexander C. Edison, Stephen G. Naculich
Access: Open access
- Color-ordered amplitudes for the scattering of n particles in the adjoint representation of SU(N) gauge theory satisfy constraints that arise from group theory alone. These constraints break into subsets associated with irreducible representations of the symmetric group Sn, which allows them to be presented in a compact and natural way. Using an iterative approach, we derive the constraints for six-point amplitudes at all loop orders, extending earlier results for n = 4 and n = 5. We then decompose the four-, five-, and six-point group-theory constraints into their irreducible Sn subspaces. We comment briefly on higher-point two-loop amplitudes. © SISSA 2012.
Convergence of successive approximation methods with parameter target sets
Date: 2005-01-01
Creator: A.B. Levy
Access: Open access
Rockwell Kent Collection
Date: 1972-01-01
Creator: Richard V. West
Access: Open access
- Includes an essay by Richard V. West.