ZFIN ID: ZDB-PUB-130729-5
transparent, a gene affecting stripe formation in Zebrafish, encodes the mitochondrial protein Mpv17 that is required for iridophore survival
Krauss, J., Astrinidis, P., Frohnhöfer, H.G., Walderich, B., and Nüsslein-Volhard, C.
Date: 2013
Source: Biology Open 2(7): 703-710 (Journal)
Registered Authors: Frohnhöfer, Hans Georg, Krauss, Jana, Nüsslein-Volhard, Christiane, Walderich, Brigitte
Keywords: Mpv17, Mitochondria, Chimeras, Iridophore
MeSH Terms: none
PubMed: 23862018 Full text @ Biol. Open
FIGURES   (current status)
ABSTRACT

In the skin of adult zebrafish, three pigment cell types arrange into alternating horizontal stripes, melanophores in dark stripes, xanthophores in light interstripes and iridophores in both stripes and interstripes. The analysis of mutants and regeneration studies revealed that this pattern depends on interactions between melanophores and xanthophores; however, the role of iridophores in this process is less understood. We describe the adult viable and fertile mutant transparent (tra), which shows a loss or strong reduction of iridophores throughout larval and adult stages. In addition, in adults only the number of melanophores is strongly reduced, and stripes break up into spots. Stripes in the fins are normal. By cell transplantations we show that tra acts cell-autonomously in iridophores, whereas the reduction in melanophores in the body occurs secondarily as a consequence of iridophore loss. We conclude that differentiated iridophores are required for the accumulation and maintenance of melanophores during pigment pattern formation. The tra mutant phenotype is caused by a small deletion in mpv17, an ubiquituously expressed gene whose protein product, like its mammalian and yeast homologs, localizes to mitochondria. Iridophore death might be the result of mitochondrial dysfunction, consistent with the mitochondrial DNA depletion syndrome observed in mammalian mpv17 mutants. The specificity of the tra phenotype is most likely due to redundancy after gene multiplication, making this mutant a valuable model to understand the molecular function of Mpv17 in mitochondria.

ADDITIONAL INFORMATION