Ca super(2) super(+)/recoverin dependent regulation of phosphorylation of the rhodopsin mutant R135L associated with retinitis pigmentosa

• Published in: Biochemical and biophysical research communications Vol. 349; no. 1; pp. 345 - 352
• Main Authors: Senin, I I, Bosch, L, Ramon, E, Zernii, EYu, Manyosa, J, Philippov, P P, Garriga, P
• Format: Journal Article
• Language: English
• Published: 13.10.2006
• ISSN: 0006-291X
• DOI: 10.1016/j.bbrc.2006.08.048

No single molecular mechanism accounts for the effect of mutations in rhodopsin associated with retinitis pigmentosa. Here we report on the specific effect of a Ca super(2) super(+)/recoverin upon phosphorylation of the autosomal dominant retinitis pigmentosa R135L rhodopsin mutant. This mutant shows specific features like impaired G-protein signaling but enhanced phosphorylation in the shut-off process. We now report that R135L hyperphosphorylation by rhodopsin kinase is less efficiently inhibited by Ca super(2) super(+)/recoverin than wild-type rhodopsin. This suggests an involvement of Ca super(2) super(+)/recoverin into the molecular pathogenic effect of the mutation in retinitis pigmentosa which is the cause of rod photoreceptor cell degeneration. This new proposed role of Ca super(2) super(+)/recoverin may be one of the specific features of the proposed new Type III class or rhodopsin mutations associated with retinitis pigmentosa.