Ca2+/recoverin dependent regulation of phosphorylation of the rhodopsin mutant R135L associated with retinitis pigmentosa

Ivan I. Senin, Laia Bosch, Eva Ramon, Evgeni Yu Zernii, Joan Manyosa, Pavel P. Philippov, Pere Garriga

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Abstract

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 Ca2+/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 Ca2+/recoverin than wild-type rhodopsin. This suggests an involvement of Ca2+/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 Ca2+/recoverin may be one of the specific features of the proposed new Type III class or rhodopsin mutations associated with retinitis pigmentosa. © 2006 Elsevier Inc. All rights reserved.
Original languageEnglish
Pages (from-to)345-352
JournalBiochemical and Biophysical Research Communications
Volume349
DOIs
Publication statusPublished - 13 Oct 2006

Keywords

  • Calcium
  • Recoverin
  • Retinitis pigmentosa
  • Rhodopsin kinase
  • Rhodopsin mutation
  • Rhodopsin phosphorylation
  • Transducin activation
  • Visual phototransduction

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    Senin, I. I., Bosch, L., Ramon, E., Zernii, E. Y., Manyosa, J., Philippov, P. P., & Garriga, P. (2006). Ca2+/recoverin dependent regulation of phosphorylation of the rhodopsin mutant R135L associated with retinitis pigmentosa. Biochemical and Biophysical Research Communications, 349, 345-352. https://doi.org/10.1016/j.bbrc.2006.08.048