The mode of colonization of the lateral line melanophore band of the zebrafish, Brachydanio rerio, by the second wave of melanophores has been investigated. This stripe forms in two consecutive stages. First, there is an initial migration and reorientation of pigment cells in an anteroposterior wave into the site to form an interrupted stripe. Following this, a round of melanophores differentiates directly at the site and fills in the gaps between the initial cells. An analysis of the distributions of initial and second wave melanophores along the stripe site has shown that both groups of cells are selective as to localization. Initial wave melanophores colonize more anterior somite areas than do second wave melanophores. However, both groups of cells exhibit preferential colonization of the same anterior sites. It is suggested that second wave melanophores attempt to colonize the same somite areas of the stripe as the initial wave of melanophores but are forced to move to more posterior locations due to the presence of initial wave melanophores anteriorly. Observations were also made on later stages of development of the lateral line melanophore band. These melanophores retain the ability to migrate. Some of them reorient out onto the flank and contribute to the juvenile flank pigment pattern.
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http://dx.doi.org/10.1002/jez.1402270112 | DOI Listing |
Invest Ophthalmol Vis Sci
June 2016
Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States 2Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio, United States.
Purpose: The electroretinogram c-wave is generated by the summation of the positive polarity hyperpolarization of the apical RPE membrane and a negative polarity slow PIII response of Müller glia cells. Therefore, the c-wave reduction noted in prior studies of mouse models of diabetes could reflect a reduction in the RPE component or an increase in slow PIII. The present study used a genetic approach to distinguish between these two alternatives.
View Article and Find Full Text PDFExp Eye Res
May 2014
Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA. Electronic address:
Mutations in myosin VIIa (MYO7A) cause Usher Syndrome 1B (USH1B), a disease characterized by the combination of sensorineural hearing loss and visual impairment termed retinitis pigmentosa (RP). Although the shaker-1 mouse model of USH1B exists, only minor defects in the retina have been observed during its lifespan. Previous studies of the zebrafish mariner mutant, which also carries a mutation in myo7aa, revealed balance and hearing defects in the mutants but the retinal phenotype has not been described.
View Article and Find Full Text PDFMutations in MYO7A cause autosomal recessive Usher syndrome type IB (USH1B), one of the most frequent conditions that combine severe congenital hearing impairment and retinitis pigmentosa. A promising therapeutic strategy for retinitis pigmentosa is gene therapy, however its pre-clinical development is limited by the mild retinal phenotype of the shaker1 (sh1(-/-)) murine model of USH1B which lacks both retinal functional abnormalities and degeneration. Here we report a significant, early-onset delay of sh1(-/-) photoreceptor ability to recover from light desensitization as well as a progressive reduction of both b-wave electroretinogram amplitude and light sensitivity, in the absence of significant loss of photoreceptors up to 12 months of age.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
September 2007
National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Purpose: To characterize the ocular phenotype resulting from mutation of Rab38, a candidate gene for Hermansky-Pudlak syndrome.
Methods: Chocolate mice (cht, Rab38(cht/cht)) and control heterozygous (Rab38(cht/)(+)) and wild-type mice were examined clinically, histologically, ultrastructurally, and electrophysiologically. Mice homozygous for both the Rab38(cht) and the Tyrp1(b) alleles were similarly examined.
Invest Ophthalmol Vis Sci
July 2006
Northrop Grumman, Life Sciences Research and Applications, San Antonio, Texas 78228-1330, USA.
Purpose: Until reliable nonanimal systems of analysis are available, animal models will be necessary for ocular laser hazard analysis and for evaluating clinical applications. The purpose of this work was to demonstrate the utility of an in vitro system for laser bioeffects by identifying photothermal and photochemical cytotoxicity thresholds for continuous-wave (cw) and mode-locked (ml) laser exposures.
Methods: Exogenous melanosomes were added to hTERT-RPE1 cells in exposure wells 1 day before laser exposure.
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