Inverse Cotton-Mouton effect of the Vacuum and of atomic systems

In this letter we calculate the Inverse Cotton-Mouton Effect (ICME) for the vacuum following the predictions of Quantum ElectroDynamics. We compare the value of this effect for the vacuum with the one expected for atomic systems. We finally show that ICME could be measured for the first time for noble gases using state-of-the-art laser systems and for the quantum vacuum with near-future laser facilities like ELI and HiPER, providing in particular a test of the nonlinear behaviour of quantum vacuum at intensities below the Schwinger limit of 4.5x10^33 W/m^2.Comment: Submitted to EP

Furin, a transcriptional target of NKX2-5, has an essential role in heart development and function

The homeodomain transcription factor NKX2-5 is known to be essential for both normal heart development and for heart function. But little is yet known about the identities of its downstream effectors or their function during differentiation of cardiac progenitor cells (CPCs). We have used transgenic analysis and CRISPR-mediated ablation to identify a cardiac enhancer of the Furin gene. The Furin gene, encoding a proprotein convertase, is directly repressed by NKX2-5. Deletion of Furin in CPCs is embryonic lethal, with mutant hearts showing a range of abnormalities in the outflow tract. Those defects are associated with a reduction in proliferation and premature differentiation of the CPCs. Deletion of Furin in differentiated cardiomyocytes results in viable adult mutant mice showing an elongation of the PR interval, a phenotype that is consistent with the phenotype of mice and human mutant for Nkx2-5. Our results show that Furin mediate some aspects of Nkx2-5 function in the heart

Strong laser fields as a probe for fundamental physics

Upcoming high-intensity laser systems will be able to probe the quantum-induced nonlinear regime of electrodynamics. So far unobserved QED phenomena such as the discovery of a nonlinear response of the quantum vacuum to macroscopic electromagnetic fields can become accessible. In addition, such laser systems provide for a flexible tool for investigating fundamental physics. Primary goals consist in verifying so far unobserved QED phenomena. Moreover, strong-field experiments can search for new light but weakly interacting degrees of freedom and are thus complementary to accelerator-driven experiments. I review recent developments in this field, focusing on photon experiments in strong electromagnetic fields. The interaction of particle-physics candidates with photons and external fields can be parameterized by low-energy effective actions and typically predict characteristic optical signatures. I perform first estimates of the accessible new-physics parameter space of high-intensity laser facilities such as POLARIS and ELI.Comment: 7 pages, Key Lecture at the ELI Workshop and School on "Fundamental Physics with Ultra-High Fields", 9 September - 2 October 2008 at Frauenworth Monastery, German

Quantum Vacuum Friction in Highly Magnetized Neutron Stars

In this letter we calculate the energy loss of highly magnetized neutron star due to friction with quantum vacuum, namely Quantum Vacuum Friction (QVF). Taking into account one-loop corrections in the effective Heisenberg-Euler Lagrangian of the light-light interaction, we derive an analytic expression for QVF allowing us to consider magnetic field at the surface of the star as high as $10^{11}$T. In the case of magnetars with high magnetic field above the QED critical field, we show that the energy loss by QVF dominates the energy loss process. This has important consequences, in particular on the inferred value of the magnetic field. This also indicates the need for independent measurements of magnetic field, energy loss rate, and of the braking index to fully characterize magnetars.Comment: To be published in EP

HIRA Is Required for Heart Development and Directly Regulates Tnni2 and Tnnt3

Chromatin remodelling is essential for cardiac development. Interestingly, the role of histone chaperones has not been investigated in this regard. HIRA is a member of the HUCA (HIRA/UBN1/CABIN1/ASF1a) complex that deposits the variant histone H3.3 on chromatin independently of replication. Lack of HIRA has general effects on chromatin and gene expression dynamics in embryonic stem cells and mouse oocytes. Here we describe the conditional ablation of Hira in the cardiogenic mesoderm of mice. We observed surface oedema, ventricular and atrial septal defects and embryonic lethality. We identified dysregulation of a subset of cardiac genes, notably upregulation of troponins Tnni2 and Tnnt3, involved in cardiac contractility and decreased expression of Epha3, a gene necessary for the fusion of the muscular ventricular septum and the atrioventricular cushions. We found that HIRA binds GAGA rich DNA loci in the embryonic heart, and in particular a previously described enhancer of Tnni2/Tnnt3 (TTe) bound by the transcription factor NKX2.5. HIRA-dependent H3.3 enrichment was observed at the TTe in embryonic stem cells (ESC) differentiated toward cardiomyocytes in vitro. Thus, we show here that HIRA has locus-specific effects on gene expression and that histone chaperone activity is vital for normal heart development, impinging on pathways regulated by an established cardiac transcription factor

Tbx2 and Tbx3 induce atrioventricular myocardial development and endocardial cushion formation

A key step in heart development is the coordinated development of the atrioventricular canal (AVC), the constriction between the atria and ventricles that electrically and physically separates the chambers, and the development of the atrioventricular valves that ensure unidirectional blood flow. Using knock-out and inducible overexpression mouse models, we provide evidence that the developmentally important T-box factors Tbx2 and Tbx3, in a functionally redundant manner, maintain the AVC myocardium phenotype during the process of chamber differentiation. Expression profiling and ChIP-sequencing analysis of Tbx3 revealed that it directly interacts with and represses chamber myocardial genes, and induces the atrioventricular pacemaker-like phenotype by activating relevant genes. Moreover, mutant mice lacking 3 or 4 functional alleles of Tbx2 and Tbx3 failed to form atrioventricular cushions, precursors of the valves and septa. Tbx2 and Tbx3 trigger development of the cushions through a regulatory feed-forward loop with Bmp2, thus providing a mechanism for the co-localization and coordination of these important processes in heart development

Sox4 mediates Tbx3 transcriptional regulation of the gap junction protein Cx43

Tbx3, a T-box transcription factor, regulates key steps in development of the heart and other organ systems. Here, we identify Sox4 as an interacting partner of Tbx3. Pull-down and nuclear retention assays verify this interaction and in situ hybridization reveals Tbx3 and Sox4 to co-localize extensively in the embryo including the atrioventricular and outflow tract cushion mesenchyme and a small area of interventricular myocardium. Tbx3, SOX4, and SOX2 ChIP data, identify a region in intron 1 of Gja1 bound by all tree proteins and subsequent ChIP experiments verify that this sequence is bound, in vivo, in the developing heart. In a luciferase reporter assay, this element displays a synergistic antagonistic response to co-transfection of Tbx3 and Sox4 and in vivo, in zebrafish, drives expression of a reporter in the heart, confirming its function as a cardiac enhancer. Mechanistically, we postulate that Sox4 is a mediator of Tbx3 transcriptional activity