4 research outputs found
Colour-Octet Effects in Radiative Decays
We investigate the effects of colour-octet contributions to the radiative
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 . 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