Opening up the Quantum Three-Box Problem with Undetectable Measurements

One of the most striking features of quantum mechanics is the profound effect exerted by measurements alone. Sophisticated quantum control is now available in several experimental systems, exposing discrepancies between quantum and classical mechanics whenever measurement induces disturbance of the interrogated system. In practice, such discrepancies may frequently be explained as the back-action required by quantum mechanics adding quantum noise to a classical signal. Here we implement the 'three-box' quantum game of Aharonov and Vaidman in which quantum measurements add no detectable noise to a classical signal, by utilising state-of-the-art control and measurement of the nitrogen vacancy centre in diamond. Quantum and classical mechanics then make contradictory predictions for the same experimental procedure, however classical observers cannot invoke measurement-induced disturbance to explain this discrepancy. We quantify the residual disturbance of our measurements and obtain data that rule out any classical model by > 7.8 standard deviations, allowing us for the first time to exclude the property of macroscopic state-definiteness from our system. Our experiment is then equivalent to a Kochen-Spekker test of quantum non-contextuality that successfully addresses the measurement detectability loophole

A note on the Landauer principle in quantum statistical mechanics

The Landauer principle asserts that the energy cost of erasure of one bit of information by the action of a thermal reservoir in equilibrium at temperature T is never less than $kTlog 2$. We discuss Landauer's principle for quantum statistical models describing a finite level quantum system S coupled to an infinitely extended thermal reservoir R. Using Araki's perturbation theory of KMS states and the Avron-Elgart adiabatic theorem we prove, under a natural ergodicity assumption on the joint system S+R, that Landauer's bound saturates for adiabatically switched interactions. The recent work of Reeb and Wolf on the subject is discussed and compared

Maf1, a New Player in the Regulation of Human RNA Polymerase III Transcription

BACKGROUND: Human RNA polymerase III (pol III) transcription is regulated by several factors, including the tumor suppressors P53 and Rb, and the proto-oncogene c-Myc. In yeast, which lacks these proteins, a central regulator of pol III transcription, called Maf1, has been described. Maf1 is required for repression of pol III transcription in response to several signal transduction pathways and is broadly conserved in eukaryotes. METHODOLOGY/PRINCIPAL FINDINGS: We show that human endogenous Maf1 can be co-immunoprecipitated with pol III and associates in vitro with two pol III subunits, the largest subunit RPC1 and the α-like subunit RPAC2. Maf1 represses pol III transcription in vitro and in vivo and is required for maximal pol III repression after exposure to MMS or rapamycin, treatments that both lead to Maf1 dephosphorylation. CONCLUSIONS/SIGNIFICANCE: These data suggest that Maf1 is a major regulator of pol III transcription in human cells

A Candidate Approach Implicates the Secreted Salmonella Effector Protein SpvB in P-Body Disassembly

P-bodies are dynamic aggregates of RNA and proteins involved in several post-transcriptional regulation processes. P-bodies have been shown to play important roles in regulating viral infection, whereas their interplay with bacterial pathogens, specifically intracellular bacteria that extensively manipulate host cell pathways, remains unknown. Here, we report that Salmonella infection induces P-body disassembly in a cell type-specific manner, and independently of previously characterized pathways such as inhibition of host cell RNA synthesis or microRNA-mediated gene silencing. We show that the Salmonella-induced P-body disassembly depends on the activation of the SPI-2 encoded type 3 secretion system, and that the secreted effector protein SpvB plays a major role in this process. P-body disruption is also induced by the related pathogen, Shigella flexneri, arguing that this might be a new mechanism by which intracellular bacterial pathogens subvert host cell function

DLK induces developmental neuronal degeneration via selective regulation of proapoptotic JNK activity

DLK is part of a specialized JNK signaling complex in axons that promotes apoptosis via c-Jun but axon degeneration via distinct JNK substrates

Conformational Dynamics of Single pre-mRNA Molecules During \u3cem\u3eIn Vitro\u3c/em\u3e Splicing

The spliceosome is a complex small nuclear RNA (snRNA)-protein machine that removes introns from pre-mRNAs via two successive phosphoryl transfer reactions. The chemical steps are isoenergetic, yet splicing requires at least eight RNA-dependent ATPases responsible for substantial conformational rearrangements. To comprehensively monitor pre-mRNA conformational dynamics, we developed a strategy for single-molecule FRET (smFRET) that uses a small, efficiently spliced yeast pre-mRNA, Ubc4, in which donor and acceptor fluorophores are placed in the exons adjacent to the 5′ and 3′ splice sites. During splicing in vitro, we observed a multitude of generally reversible time-and ATP-dependent conformational transitions of individual pre-mRNAs. The conformational dynamics of branchpoint and 3′-splice site mutants differ from one another and from wild type. Because all transitions are reversible, spliceosome assembly appears to be occurring close to thermal equilibrium

Downregulation of TFPI in breast cancer cells induces tyrosine phosphorylation signaling and increases metastatic growth by stimulating cell motility

<p>Abstract</p> <p>Background</p> <p>Increased hemostatic activity is common in many cancer types and often causes additional complications and even death. Circumstantial evidence suggests that tissue factor pathway inhibitor-1 (TFPI) plays a role in cancer development. We recently reported that downregulation of TFPI inhibited apoptosis in a breast cancer cell line. In this study, we investigated the effects of TFPI on self-sustained growth and motility of these cells, and of another invasive breast cancer cell type (MDA-MB-231).</p> <p>Methods</p> <p>Stable cell lines with TFPI (both α and β) and only TFPIβ downregulated were created using RNA interference technology. We investigated the ability of the transduced cells to grow, when seeded at low densities, and to form colonies, along with metastatic characteristics such as adhesion, migration and invasion.</p> <p>Results</p> <p>Downregulation of TFPI was associated with increased self-sustained cell growth. An increase in cell attachment and spreading was observed to collagen type I, together with elevated levels of integrin α2. Downregulation of TFPI also stimulated migration and invasion of cells, and elevated MMP activity was involved in the increased invasion observed. Surprisingly, equivalent results were observed when TFPIβ was downregulated, revealing a novel function of this isoform in cancer metastasis.</p> <p>Conclusions</p> <p>Our results suggest an anti-metastatic effect of TFPI and may provide a novel therapeutic approach in cancer.</p