Compartmentalization and Ca<superscript>2+</superscript> Buffering Are Essential for Prevention of Light-Induced Retinal Degeneration.
In: Journal of Neuroscience, Jg. 32 (2012-10-17), Heft 42, S. 14696-14708
academicJournal
Zugriff:
Fly photoreceptors are polarized cells, each of which has an extended interface between its cell body and the light-signaling compartment, the rhabdomere. Upon intense illumination, rhabdomeric calcium concentration reaches millimolar levels that would be toxic if Ca2+ diffusion between the rhabdomere and cell body was not robustly attenuated. Yet, it is not clear how such effective attenuation is obtained. Here we show that Ca2+ homeostasis in the photoreceptor cell relies on the protein calphotin. This unique protein functions as an immobile Ca2+ buffer localized along the base of the rhabdomere, separating the signaling compartment from the cell body. Generation and analyses of transgenic Drosophila strains, in which calphotin-expression levels were reduced in a graded manner, showed that moderately reduced calphotin expression impaired Ca2+ homeostasis while calphotin elimination resulted in severe light-dependent photoreceptor degeneration. Electron microscopy, electrophysiology, and optical methods revealed that the degeneration was rescued by prevention of Ca2+ overload via overexpression of CalX, the Na + Ca2+ exchanger. In addition, Ca2+-imaging experiments showed that reduced calphotin levels resulted in abnormally fast kinetics of Ca2+ elevation in photoreceptor cells. Together, the data suggest that calphotin functions as a Ca2+ buffer; a possibility that we directly demonstrate by expressing calphotin in a heterologous expression system. We propose that calphotin-mediated compartmentalization and Ca2+ buffering constitute an effective strategy to protect cells from Ca2+ overload and light-induced degeneration. [ABSTRACT FROM AUTHOR]
Titel: |
Compartmentalization and Ca<superscript>2+</superscript> Buffering Are Essential for Prevention of Light-Induced Retinal Degeneration.
|
---|---|
Autor/in / Beteiligte Person: | Weiss, Shirley ; Kohn, Elkana ; Dadon, Daniela ; Katz, Ben ; Peters, Maximilian ; Lebendiker, Mario ; Kosloff, Mickey ; Colley, Nansi Jo ; Minke, Baruch |
Zeitschrift: | Journal of Neuroscience, Jg. 32 (2012-10-17), Heft 42, S. 14696-14708 |
Veröffentlichung: | 2012 |
Medientyp: | academicJournal |
ISSN: | 0270-6474 (print) |
DOI: | 10.1523/JNEUROSCI.2456-12.2012 |
Schlagwort: |
|
Sonstiges: |
|