Cops or robbers - a bistable society

The norm game described by Axelrod in 1985 was recently treated with the master equation formalism. Here we discuss the equations, where {\it i)} those who break the norm cannot punish and those who punish cannot break the norm, {\it ii)} the tendency to punish is suppressed if the majority breaks the norm. The second mechanism is new. For some values of the parameters the solution shows the saddle-point bifurcation. Then, two stable solutions are possible, where the majority breaks the norm or the majority punishes. This means, that the norm breaking can be discontinuous, when measured in the social scale. The bistable character is reproduced also with new computer simulations on the Erd{\H o}s--R\'enyi directed network.Comment: 8 pages, 2 figures. Some misleading sentences are removed from section

All-optical attoclock: accessing exahertz dynamics of optical tunnelling through terahertz emission

The debate regarding attosecond dynamics of optical tunneling has so far been focused on time delays associated with electron motion through the potential barrier created by intense ionizing laser fields and the atomic core. Compelling theoretical and experimental arguments have been put forward to advocate the polar opposite views, confirming or refuting the presence of tunnelling time delays. Yet, such delay, whether present or ot, is but a single quantity characterizing the tunnelling wavepacket; the underlying dynamics are richer. Here we propose to complement photo-electron detection with detecting light, focusing on the so-called Brunel adiation -- the near-instantaneous nonlinear optical response triggered by the tunnelling event. Using the combination of single-color and two-color driving fields, we determine not only the ionization delays, but also the re-shaping of the tunnelling wavepacket as it emerges from the classically forbidden region. Our work introduces a new type of attoclock for optical tunnelling, one that is based on measuring light rather than photo-electrons. All-optical detection paves the way to time-resolving multiphoton transitions across bandgaps in solids, on the attosecond time-scale

Aged B cells alter immune regulation of allografts in mice

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134428/1/eji3757-sup-0001-PRC.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134428/2/eji3757_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134428/3/eji3757.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134428/4/eji3757-sup-0002-figure1-3.pd

Effects of parasite and historic driven selection on the diversity and structure of a MHC-II gene in a small mammal species (Peromyscus leucopus) undergoing range expansion.

Abstract Genetic diversity may decrease from the centre to the margin of a species distribution range due to neutral stochastic processes. Selection may also alter genetic diversity in non-neutral markers, such as genes associated with the immune system. Both neutral processes and selection on the immune system are thus expected to affect the spatial distribution of such markers, but the relative strength of each has been scarcely studied. Here, we compared the diversity of a neutral marker (mitochondrial cytochrome b)and a selected marker (DRB gene from the MHC-II), in eastern-North American populations of white-footed mice (Peromyscus leucopus), a species known for its role of main reservoir of the Lyme disease. We observed distinct phylogeographic patterns with these two markers, which may be the result of selection pressure acting upon the DRB gene. As predicted by the central marginal hypothesis, we observed a loss of neutral genetic diversity toward the margin of the species distribution. A decrease in diversity was also observed for the DRB gene, likely due to genetic drift and positive selection operated by helminth parasites. Such a loss in genetic diversity at the range margin may slow down the ongoing expansion of P. leucopus, by counterbalancing the effect of global warming on the mouse survival at higher latitude

Yersinia pseudotuberculosis Spatially Controls Activation and Misregulation of Host Cell Rac1

Yersinia pseudotuberculosis binds host cells and modulates the mammalian Rac1 guanosine triphosphatase (GTPase) at two levels. Activation of Rac1 results from integrin receptor engagement, while misregulation is promoted by translocation of YopE and YopT proteins into target cells. Little is known regarding how these various factors interplay to control Rac1 dynamics. To investigate these competing processes, the localization of Rac1 activation was imaged microscopically using fluorescence resonance energy transfer. In the absence of translocated effectors, bacteria induced activation of the GTPase at the site of bacterial binding. In contrast, the entire cellular pool of Rac1 was inactivated shortly after translocation of YopE RhoGAP. Inactivation required membrane localization of Rac1. The translocated protease YopT had very different effects on Rac1. This protein, which removes the membrane localization site of Rac1, did not inactivate Rac1, but promoted entry of cleaved activated Rac1 molecules into the host cell nucleus, allowing Rac1 to localize with nuclear guanosine nucleotide exchange factors. As was true for YopE, membrane-associated Rac1 was the target for YopT, indicating that the two translocated effectors may compete for the same pool of target protein. Consistent with the observation that YopE inactivation requires membrane localization of Rac1, the presence of YopT in the cell interfered with the action of the YopE RhoGAP. As a result, interaction of target cells with a strain that produces both YopT and YopE resulted in two spatially distinct pools of Rac1: an inactive cytoplasmic pool and an activated nuclear pool. These studies demonstrate that competition between bacterial virulence factors for access to host substrates is controlled by the spatial arrangement of a target protein. In turn, the combined effects of translocated bacterial proteins are to generate pools of a single signaling molecule with distinct localization and activation states in a single cell