67 research outputs found
Quantised Vortices in an Exciton-Polariton Fluid
One of the most striking quantum effects in a low temperature interacting
Bose gas is superfluidity. First observed in liquid 4He, this phenomenon has
been intensively studied in a variety of systems for its amazing features such
as the persistence of superflows and the quantization of the angular momentum
of vortices. The achievement of Bose-Einstein condensation (BEC) in dilute
atomic gases provided an exceptional opportunity to observe and study
superfluidity in an extremely clean and controlled environment. In the solid
state, Bose-Einstein condensation of exciton polaritons has now been reported
several times. Polaritons are strongly interacting light-matter
quasi-particles, naturally occurring in semiconductor microcavities in the
strong coupling regime and constitute a very interesting example of composite
bosons. Even though pioneering experiments have recently addressed the
propagation of a fluid of coherent polaritons, still no conclusive evidence is
yet available of its superfluid nature. In the present Letter, we report the
observation of spontaneous formation of pinned quantised vortices in the
Bose-condensed phase of a polariton fluid by means of phase and amplitude
imaging. Theoretical insight into the possible origin of such vortices is
presented in terms of a generalised Gross-Pitaevskii equation. The implications
of our observations concerning the superfluid nature of the non-equilibrium
polariton fluid are finally discussed.Comment: 14 pages, 4 figure
Role of RecA and the SOS Response in Thymineless Death in Escherichia coli
Thymineless death (TLD) is a classic and enigmatic phenomenon, documented in bacterial, yeast, and human cells, whereby cells lose viability rapidly when deprived of thymine. Despite its being the essential mode of action of important chemotherapeutic agents, and despite having been studied extensively for decades, the basic mechanisms of TLD have remained elusive. In Escherichia coli, several proteins involved in homologous recombination (HR) are required for TLD, however, surprisingly, RecA, the central HR protein and activator of the SOS DNA–damage response was reported not to be. We demonstrate that RecA and the SOS response are required for a substantial fraction of TLD. We show that some of the Rec proteins implicated previously promote TLD via facilitating activation of the SOS response and that, of the roughly 40 proteins upregulated by SOS, SulA, an SOS–inducible inhibitor of cell division, accounts for most or all of how SOS causes TLD. The data imply that much of TLD results from an irreversible cell-cycle checkpoint due to blocked cell division. FISH analyses of the DNA in cells undergoing TLD reveal blocked replication and apparent DNA loss with the region near the replication origin underrepresented initially and the region near the terminus lost later. Models implicating formation of single-strand DNA at blocked replication forks, a SulA-blocked cell cycle, and RecQ/RecJ-catalyzed DNA degradation and HR are discussed. The data predict the importance of DNA damage-response and HR networks to TLD and chemotherapy resistance in humans
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