Floodlight Quantum Key Distribution: A Practical Route to Gbps Secret-Key Rates

The channel loss incurred in long-distance transmission places a significant burden on quantum key distribution (QKD) systems: they must defeat a passive eavesdropper who detects all the light lost in the quantum channel and does so without disturbing the light that reaches the intended destination. The current QKD implementation with the highest long-distance secret-key rate meets this challenge by transmitting no more than one photon per bit [Opt. Express 21, 24550-24565 (2013)]. As a result, it cannot achieve the Gbps secret-key rate needed for one-time pad encryption of large data files unless an impractically large amount of multiplexing is employed. We introduce floodlight QKD (FL-QKD), which floods the quantum channel with a high number of photons per bit distributed over a much greater number of optical modes. FL-QKD offers security against the optimum frequency-domain collective attack by transmitting less than one photon per mode and using photon-coincidence channel monitoring, and it is completely immune to passive eavesdropping. More importantly, FL-QKD is capable of a 2 Gbps secret-key rate over a 50 km fiber link, without any multiplexing, using available equipment, i.e., no new technology need be developed. FL-QKD achieves this extraordinary secret-key rate by virtue of its unprecedented secret-key efficiency, in bits per channel use, which exceeds those of state-of-the-art systems by two orders of magnitude.Comment: 18 pages, 5 figure

Phase-noise limitations on single-photon cross-phase modulation with differing group velocities

A framework is established for evaluating {\sc cphase} gates that use single-photon cross-phase modulation (XPM) originating from the Kerr nonlinearity. Prior work Phys. Rev. A {\bf 73,} 062305 (2006)], which assumed that the control and target pulses propagated at the same group velocity, showed that the causality-induced phase noise required by a non-instantaneous XPM response function precluded the possibility of high-fidelity $\pi$-radian conditional phase shifts. The framework presented herein incorporates the more realistic case of group-velocity disparity between the control and target pulses, as employed in existing XPM-based fiber-optical switches. Nevertheless, the causality-induced phase noise identified in [Phys. Rev. A {\bf 73,} 062305 (2006)] still rules out high-fidelity $\pi$-radian conditional phase shifts. This is shown to be so for both a reasonable theoretical model for the XPM response function and for the experimentally-measured XPM response function of silica-core fiber.Comment: 8 pages, 4 figure

Structural Basis for Type VI Secretion Effector Recognition by a Cognate Immunity Protein

The type VI secretion system (T6SS) has emerged as an important mediator of interbacterial interactions. A T6SS from Pseudomonas aeruginosa targets at least three effector proteins, type VI secretion exported 1–3 (Tse1–3), to recipient Gram-negative cells. The Tse2 protein is a cytoplasmic effector that acts as a potent inhibitor of target cell proliferation, thus providing a pronounced fitness advantage for P. aeruginosa donor cells. P. aeruginosa utilizes a dedicated immunity protein, type VI secretion immunity 2 (Tsi2), to protect against endogenous and intercellularly-transferred Tse2. Here we show that Tse2 delivered by the T6SS efficiently induces quiescence, not death, within recipient cells. We demonstrate that despite direct interaction of Tsi2 and Tse2 in the cytoplasm, Tsi2 is dispensable for targeting the toxin to the secretory apparatus. To gain insights into the molecular basis of Tse2 immunity, we solved the 1.00 Å X-ray crystal structure of Tsi2. The structure shows that Tsi2 assembles as a dimer that does not resemble previously characterized immunity or antitoxin proteins. A genetic screen for Tsi2 mutants deficient in Tse2 interaction revealed an acidic patch distal to the Tsi2 homodimer interface that mediates toxin interaction and immunity. Consistent with this finding, we observed that destabilization of the Tsi2 dimer does not impact Tse2 interaction. The molecular insights into Tsi2 structure and function garnered from this study shed light on the mechanisms of T6 effector secretion, and indicate that the Tse2–Tsi2 effector–immunity pair has features distinguishing it from previously characterized toxin–immunity and toxin–antitoxin systems

Variability in the Composition of Pacific Oyster Microbiomes Across Oyster Families Exhibiting Different Levels of Susceptibility to OsHV-1 μvar Disease

Oyster diseases are a major impediment to the profitability and growth of the oyster aquaculture industry. In recent years, geographically widespread outbreaks of disease caused by ostreid herpesvirus-1 microvariant (OsHV-1 μvar) have led to mass mortalities among Crassostrea gigas, the Pacific Oyster. Attempts to minimize the impact of this disease have been largely focused on breeding programs, and although these have shown some success in producing oyster families with reduced mortality, the mechanism(s) behind this protection is poorly understood. One possible factor is modification of the C. gigas microbiome. To explore how breeding for resistance to OsHV-1 μvar affects the oyster microbiome, we used 16S rRNA amplicon sequencing to characterize the bacterial communities associated with 35 C. gigas families, incorporating oysters with different levels of susceptibility to OsHV-1 μvar disease. The microbiomes of disease-susceptible families were significantly different to the microbiomes of disease-resistant families. OTUs assigned to the Photobacterium, Vibrio, Aliivibrio, Streptococcus, and Roseovarius genera were associated with low disease resistance. In partial support of this finding, qPCR identified a statistically significant increase of Vibrio-specific 16S rRNA gene copies in the low disease resistance families, possibly indicative of a reduced host immune response to these pathogens. In addition to these results, examination of the core microbiome revealed that each family possessed a small core community, with OTUs assigned to the Winogradskyella genus and the Bradyrhizobiaceae family consistent members across most disease-resistant families. This study examines patterns in the microbiome of oyster families exhibiting differing levels of OsHV-1 μvar disease resistance and reveals some key bacterial taxa that may provide a protective or detrimental role in OsHV-1 μvar disease outbreaks