Colour-Octet Effects in Radiative Υ\Upsilon Decays

We investigate the effects of colour-octet contributions to the radiative $\Upsilon$ decay within the Bodwin, Braaten and Lepage NRQCD factorization framework. Photons coming both from the coupling to hard processes (`direct') and by collinear emission from light quarks (`fragmentation') are consistently included at next-to-leading order (NLO) in $\alpha_s$. An estimate for the non-perturbative matrix elements which enter in the final result is then obtained. By comparing the NRQCD prediction at NLO for total decay rates with the experimental data, it is found that the non-perturbative parameters must be smaller than expected from the na\"\i ve scaling rules of NRQCD. Nevertheless, colour-octet contributions to the shape of the photon spectrum turn out to be significant.Comment: 25 pages, Latex, 8 figure

The cGMP-Dependent Protein Kinase 2 Contributes to Cone Photoreceptor Degeneration in the Cnga3-Deficient Mouse Model of Achromatopsia

Mutations in the CNGA3 gene, which encodes the A subunit of the cyclic guanosine monophosphate (cGMP)-gated cation channel in cone photoreceptor outer segments, cause total colour blindness, also referred to as achromatopsia. Cones lacking this channel protein are non-functional, accumulate high levels of the second messenger cGMP and degenerate over time after induction of ER stress. The cell death mechanisms that lead to loss of affected cones are only partially understood. Here, we explored the disease mechanisms in the Cnga3 knockout (KO) mouse model of achromatopsia. We found that another important effector of cGMP, the cGMP-dependent protein kinase 2 (Prkg2) is crucially involved in cGMP cytotoxicity of cones in Cnga3 KO mice. Virus-mediated knockdown or genetic ablation of Prkg2 in Cnga3 KO mice counteracted degeneration and preserved the number of cones. Analysis of markers of endoplasmic reticulum stress and unfolded protein response confirmed that induction of these processes in Cnga3 KO cones also depends on Prkg2. In conclusion, we identified Prkg2 as a novel key mediator of cone photoreceptor degeneration in achromatopsia. Our data suggest that this cGMP mediator could be a novel pharmacological target for future neuroprotective therapies