Ruth A. Frey
University of Idaho
17 Papers
287 Citations
Ruth A. Frey is an academic researcher from University of Idaho. The author has contributed to research in topics: Zebrafish & Cellular differentiation. The author has an hindex of 12, co-authored 16 publications.
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Papers
Extraretinal and retinal hedgehog signaling sequentially regulate retinal differentiation in zebrafish.
Deborah L. Stenkamp,Ruth A. Frey +1 more
TL;DR: The eye phenotype of zebrafish slow muscle-omitted (smu) mutants, which lack a functional smoothened gene, is examined, and it is found that Hh signaling from extraretinal sources is required for the initiation of retinal differentiation, but this involvement may be independent of the effects of HH signaling on optic stalk development.
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The Developmental Sequence of Gene Expression Within the Rod Photoreceptor Lineage in Embryonic Zebrafish
TL;DR: The presence of rX1 within the rod lineage and in maturing rods indicates that rx1 is not cone‐specific, as previously reported, and suggests a high degree of molecular similarity between rod and cone progenitor populations in the zebrafish.
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Embryonic retinal gene expression in sonic-you mutant zebrafish.
TL;DR: It is found that features of the eye phenotype of the sonic‐you (syu) mutant are consistent with multiple roles for the Hh signal during retinal development, and these functions provide an explanation for progressive microphthalmia in the syu‐/‐ mutant.
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Endocrine regulation of multichromatic color vision
Robert Mackin,Ruth A. Frey,Carmina Gutierrez,Ashley Alice Farre,Shoji Kawamura,Diana M. Mitchell,Deborah L. Stenkamp +6 more
TL;DR: It is demonstrated that the endocrine signal thyroid hormone (TH) is a potent endogenous regulator of the orthologous zebrafish lws1/lws2 array, and of the tandemly quadruplicated rh2-1/rh2-2/Rh2-3/rh 2-4 array, indicating TH-coordinated control of visual function during organismal growth.
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Ethanol-induced microphthalmia is not mediated by changes in retinoic acid or sonic hedgehog signaling during retinal neurogenesis.
TL;DR: These studies suggest that FASD intervention strategies based upon augmentation of RA or Shh signaling may not prevent ethanol-induced microphthalmia, and indicate that effects of ethanol on eye development are likely independent of the RA and ShH signaling pathways.
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