Dispersion relations for η′→ηππ\eta'\to\eta\pi\pi

We present a dispersive analysis of the decay amplitude for $\eta'\to\eta\pi\pi$ that is based on the fundamental principles of analyticity and unitarity. In this framework, final-state interactions are fully taken into account. Our dispersive representation relies only on input for the $\pi\pi$ and $\pi\eta$ scattering phase shifts. Isospin symmetry allows us to describe both the charged and neutral decay channel in terms of the same function. The dispersion relation contains subtraction constants that cannot be fixed by unitarity. We determine these parameters by a fit to Dalitz-plot data from the VES and BES-III experiments. We study the prediction of a low-energy theorem and compare the dispersive fit to variants of chiral perturbation theory.Comment: 22 pages, 10 figures; v2: added footnote, version published in EPJ

Quark-mass dependence in ω→3π\omega\to3\pi decays

We study the quark-mass dependence of $\omega\to3\pi$ decays, based on a dispersion-theoretical framework. We rely on the quark-mass-dependent scattering phase shift for the pion-pion $P$-wave extracted from unitarized chiral perturbation theory. The dispersive representation then takes into account the final-state rescattering among all three pions. The described formalism may be used as an extrapolation tool for lattice QCD calculations of three-pion decays, for which $\omega\to3\pi$ can serve as a paradigm case.Comment: 12 pages, 8 figures; v2: added two references, version published in EPJ

Erratum to: Patterns of C- and CP-violation in hadronic η and η′ three-body decays

A correction to this paper has been published: https://doi.org/10.1007/JHEP02(2022)13

Analysis of rescattering effects in 3π3\pi 3 π final states

Abstract Decays into three particles are often described in terms of two-body resonances and a non-interacting spectator particle. To go beyond this simplest isobar model, crossed-channel rescattering effects need to be accounted for. We quantify the importance of these rescattering effects in three-pion systems for different decay masses and angular-momentum quantum numbers. We provide amplitude decompositions for four decay processes with total $$J^{PC} = 0^{--}$$ J PC = 0 - - , $$1^{--}$$ 1 - - , $$1^{-+}$$ 1 - + , and $$2^{++}$$ 2 + + , all of which decay predominantly as $$\rho \pi$$ ρ π states. Two-pion rescattering is described in terms of an Omnès function, which incorporates the $$\rho$$ ρ resonance. Inclusion of crossed-channel effects is achieved by solving the Khuri–Treiman integral equations. The unbinned log-likelihood estimator is used to determine the significance of the rescattering effects beyond two-body resonances; we compute the minimum number of events necessary to unambiguously find these in future Dalitz-plot analyses. Kinematic effects that enhance or dilute the rescattering are identified for the selected set of quantum numbers and various masses

Translation Initiation Factors eIF3 and HCR1 Control Translation Termination and Stop Codon Read-Through in Yeast Cells

Translation is divided into initiation, elongation, termination and ribosome recycling. Earlier work implicated several eukaryotic initiation factors (eIFs) in ribosomal recycling in vitro. Here, we uncover roles for HCR1 and eIF3 in translation termination in vivo. A substantial proportion of eIF3, HCR1 and eukaryotic release factor 3 (eRF3) but not eIF5 (a well-defined “initiation-specific” binding partner of eIF3) specifically co-sediments with 80S couples isolated from RNase-treated heavy polysomes in an eRF1-dependent manner, indicating the presence of eIF3 and HCR1 on terminating ribosomes. eIF3 and HCR1 also occur in ribosome- and RNA-free complexes with both eRFs and the recycling factor ABCE1/RLI1. Several eIF3 mutations reduce rates of stop codon read-through and genetically interact with mutant eRFs. In contrast, a slow growing deletion of hcr1 increases read-through and accumulates eRF3 in heavy polysomes in a manner suppressible by overexpressed ABCE1/RLI1. Based on these and other findings we propose that upon stop codon recognition, HCR1 promotes eRF3·GDP ejection from the post-termination complexes to allow binding of its interacting partner ABCE1/RLI1. Furthermore, the fact that high dosage of ABCE1/RLI1 fully suppresses the slow growth phenotype of hcr1? as well as its termination but not initiation defects implies that the termination function of HCR1 is more critical for optimal proliferation than its function in translation initiation. Based on these and other observations we suggest that the assignment of HCR1 as a bona fide eIF3 subunit should be reconsidered. Together our work characterizes novel roles of eIF3 and HCR1 in stop codon recognition, defining a communication bridge between the initiation and termination/recycling phases of translation