New limits on "odderon" amplitudes from analyticity constraints

In studies of high energy $pp$ and $\bar pp$ scattering, the odd (under crossing) forward scattering amplitude accounts for the difference between the $pp$ and $\bar pp$ cross sections. Typically, it is taken as $f_-=-\frac{p}{4\pi}Ds^{\alpha-1}e^{i\pi(1-\alpha)/2}$ ($\alpha\sim 0.5$), which has $\Delta\sigma, \Delta\rho\to0$ as $s\to\infty$, where $\rho$ is the ratio of the real to the imaginary portion of the forward scattering amplitude. However, the odd-signatured amplitude can have in principle a strikingly different behavior, ranging from having $\Delta\sigma\to$non-zero constant to having $\Delta\sigma \to \ln s/s_0$ as $s\to\infty$, the maximal behavior allowed by analyticity and the Froissart bound. We reanalyze high energy $pp$ and $\bar pp$ scattering data, using new analyticity constraints, in order to put new and precise limits on the magnitude of ``odderon'' amplitudes.Comment: 13 pages LaTex, 6 figure

Odderon in the Color Glass Condensate

We discuss the definition and the energy evolution of scattering amplitudes with $C$-odd ("odderon") quantum numbers within the effective theory for the Color Glass Condensate (CGC) endowed with the functional, JIMWLK, evolution equation. We explicitly construct gauge-invariant amplitudes describing multiple odderon exchanges in the scattering between the CGC and two types of projectiles: a color--singlet quark--antiquark pair (or `color dipole') and a system of three quarks in a colorless state. We deduce the energy evolution of these amplitudes from the general JIMWLK equation, which for this purpose is recast in a more synthetic form, which is manifestly infrared finite. For the dipole odderon, we confirm and extend the non--linear evolution equations recently proposed by Kovchegov, Szymanowski and Wallon, which couple the evolution of the odderon to that of the pomeron, and predict the rapid suppression of the odderon exchanges in the saturation regime at high energy. For the 3--quark system, we focus on the linear regime at relatively low energy, where our general equations are shown to reduce to the Bartels--Kwiecinski--Praszalowicz equation. Our gauge--invariant amplitudes, and the associated evolution equations, stay explicitly outside the M\"obius representation, which is the Hilbert space where the BFKL Hamiltonian exhibits holomorphic separability.Comment: 43 pages, 1 figur

The spin dependence of high energy proton scattering

Motivated by the need for an absolute polarimeter to determine the beam polarization for the forthcoming RHIC spin program, we study the spin dependence of the proton-proton elastic scattering amplitudes at high energy and small momentum transfer.We examine experimental evidence for the existence of an asymptotic part of the helicity-flip amplitude phi_5 which is not negligible relative to the largely imaginary average non-flip amplitude phi_+. We discuss theoretical estimates of r_5, essentially the ratio of phi_5 to phi_+, based upon extrapolation of low and medium energy Regge phenomenological results to high energies, models based on a hybrid of perturbative QCD and non-relativistic quark models, and models based on eikonalization techniques. We also apply the model-independent methods of analyticity and unitarity.The preponderence of evidence at available energy indicates that r_5 is small, probably less than 10%. The best available experimental limit comes from Fermilab E704:those data indicate that |r_5|<15%. These bounds are important because rigorous methods allow much larger values. In contradiction to a widely-held prejudice that r_5 decreases with energy, general principles allow it to grow as fast as ln(s) asymptotically, and some models show an even faster growth in the RHIC range. One needs a more precise measurement of r_5 or to bound it to be smaller than 5% in order to use the classical Coulomb-nuclear interference technique for RHIC polarimetry. As part of this study, we demonstrate the surprising result that proton-proton elastic scattering is self-analysing, in the sense that all the helicity amplitudes can, in principle, be determined experimentally at small momentum transfer without a knowledge of the magnitude of the beam and target polarization

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]

A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function

Identification of genes required for eye development by high-throughput screening of mouse knockouts.

Despite advances in next generation sequencing technologies, determining the genetic basis of ocular disease remains a major challenge due to the limited access and prohibitive cost of human forward genetics. Thus, less than 4,000 genes currently have available phenotype information for any organ system. Here we report the ophthalmic findings from the International Mouse Phenotyping Consortium, a large-scale functional genetic screen with the goal of generating and phenotyping a null mutant for every mouse gene. Of 4364 genes evaluated, 347 were identified to influence ocular phenotypes, 75% of which are entirely novel in ocular pathology. This discovery greatly increases the current number of genes known to contribute to ophthalmic disease, and it is likely that many of the genes will subsequently prove to be important in human ocular development and disease

Identification of genes required for eye development by high-throughput screening of mouse knockouts

International audienc

The Regulatory Factor ZFHX3 Modifies Circadian Function in SCN via an AT Motif-Driven Axis

SummaryWe identified a dominant missense mutation in the SCN transcription factor Zfhx3, termed short circuit (Zfhx3Sci), which accelerates circadian locomotor rhythms in mice. ZFHX3 regulates transcription via direct interaction with predicted AT motifs in target genes. The mutant protein has a decreased ability to activate consensus AT motifs in vitro. Using RNA sequencing, we found minimal effects on core clock genes in Zfhx3Sci/+ SCN, whereas the expression of neuropeptides critical for SCN intercellular signaling was significantly disturbed. Moreover, mutant ZFHX3 had a decreased ability to activate AT motifs in the promoters of these neuropeptide genes. Lentiviral transduction of SCN slices showed that the ZFHX3-mediated activation of AT motifs is circadian, with decreased amplitude and robustness of these oscillations in Zfhx3Sci/+ SCN slices. In conclusion, by cloning Zfhx3Sci, we have uncovered a circadian transcriptional axis that determines the period and robustness of behavioral and SCN molecular rhythms

The Regulatory Factor ZFHX3 Modifies Circadian Function in SCN via an at Motif-Driven Axis

We identified a dominant missense mutation in the SCN transcription factor Zfhx3, termed short circuit (Zfhx3Sci), which accelerates circadian locomotor rhythms in mice. ZFHX3 regulates transcription via direct interaction with predicted AT motifs in target genes. The mutant protein has a decreased ability to activate consensus AT motifs in vitro. Using RNA sequencing, we found minimal effects on core clock genes in Zfhx3Sci/+ SCN, whereas the expression of neuropeptides critical for SCN intercellular signaling was significantly disturbed. Moreover, mutant ZFHX3 had a decreased ability to activate AT motifs in the promoters of these neuropeptide genes. Lentiviral transduction of SCN slices showed that the ZFHX3-mediated activation of AT motifs is circadian, with decreased amplitude and robustness of these oscillations in Zfhx3Sci/+ SCN slices. In conclusion, by cloning Zfhx3Sci, we have uncovered a circadian transcriptional axis that determines the period and robustness of behavioral and SCN molecular rhythms