Decay spectroscopy of Cd-129

Excited states of $^{129}$In populated following the $\beta$-decay of $^{129}$Cd were experimentally studied with the GRIFFIN spectrometer at the ISAC facility of TRIUMF, Canada. A 480-MeV proton beam was impinged on a uranium carbide target and $^{129}$Cd was extracted using the Ion Guide Laser Ion Source (IG-LIS). $\beta$- and $\gamma$-rays following the decay of $^{129}$Cd were detected with the GRIFFIN spectrometer comprising the plastic scintillator SCEPTAR and 16 high-purity germanium (HPGe) clover-type detectors. %, along with the $\beta$-particles were detected with SCEPTAR. From the $\beta$-$\gamma$-$\gamma$ coincidence analysis, 32 new transitions and 7 new excited states were established, expanding the previously known level scheme of $^{129}$In. The $\log ft$ values deduced from the $\beta$-feeding intensities suggest that some of the high-lying states were populated by the $\nu 0 g_{7/2} \rightarrow \pi 0 g_{9/2}$ allowed Gamow-Teller (GT) transition, which indicates that the allowed GT transition is more dominant in the $^{129}$Cd decay than previously reported. Observation of fragmented Gamow-Teller strengths is consistent with theoretical calculations.Comment: 13 pages, 9 figures, to be published in Physical Review

Cornelia-de Lange syndrome-associated mutations cause a DNA damage signalling and repair defect

Cornelia de Lange syndrome is a multisystem developmental disorder typically caused by mutations in the gene encoding the cohesin loader NIPBL. The associated phenotype is generally assumed to be the consequence of aberrant transcriptional regulation. Recently, we identified a missense mutation in BRD4 associated with a Cornelia de Lange-like syndrome that reduces BRD4 binding to acetylated histones. Here we show that, although this mutation reduces BRD4-occupancy at enhancers it does not affect transcription of the pluripotency network in mouse embryonic stem cells. Rather, it delays the cell cycle, increases DNA damage signalling, and perturbs regulation of DNA repair in mutant cells. This uncovers a role for BRD4 in DNA repair pathway choice. Furthermore, we find evidence of a similar increase in DNA damage signalling in cells derived from NIPBL-deficient individuals, suggesting that defective DNA damage signalling and repair is also a feature of typical Cornelia de Lange syndrome