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Jeffrey Trimarchi, Jillian Goetz; Polo-like kinase 3 plays a role in the normal development of retinal cell subtypes and connectivity . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2251.
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© ARVO (1962-2015); The Authors (2016-present)
Single-cell transcriptomic analysis of murine retinal progenitor cells has determined that Polo-like kinase 3 (Plk3) is expressed in subsets of developing retinal cells at the proper times and locations to influence retinogenesis and neuronal maturation. We tested the hypothesis that Plk3 is involved in normal retinal development by examining changes exhibited between the retinas of Plk3-deficient mice and wildtype littermates at various developmental timepoints and in mature retinas.
We have obtained a Plk3-KO mouse and investigated changes in the retina throughout retinal development as compared to wildtype littermates. Gross retinal morphology was examined using immunohistochemistry with markers of all the different retinal neurons and Muller glia. Transcriptome-wide changes in markers of retinal cell subsets were determined through microarray analysis and confirmed quantitatively using qPCR and qualitatively through in situ hybridization.
Plk3-KO mice exhibit exuberant processes leading to disorganization of the inner plexiform layer. Quantification of retinal subtypes through immunohistochemistry indicated significant changes in some retinal cell populations, including Calbindin-expressing cells in the ganglion cell layer. Additionally, transcriptomic analyses, combined with in situ hybridization-based qualitative investigation of subsets of retinal cells, have determined that markers of some retinal cell subtypes, including photoreceptors and amacrine cells, are significantly changed in the absence of Plk3. Ongoing studies are being performed to link these genetic changes with the inner plexiform phenotype in the mice.
Single-cell transcriptomics revealed the Plk3 is expressed in a subset of progenitor cells during early retinal development. Studies of Plk3-KO mice have revealed inner plexiform layer defects and possible cell fate changes of specific subsets of retinal neurons.
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