ArticleInvestigative ophthalmology & visual science2015
Loss of citron kinase affects a subset of progenitor cells that alters late but not early neurogenesis in the developing rat retina.
Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Loss of U11 small nuclear RNA in the developing mouse limb results in micromelia.Development (Cambridge, England) · 2020Article
- Of rings and spines: The multiple facets of Citron proteins in neural development.Small GTPases · 2020Review
- Minor spliceosome inactivation causes microcephaly, owing to cell cycle defects and death of self-amplifying radial glial cells.Development (Cambridge, England) · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo understand how loss of citron kinase (CitK) affects retinal progenitor cells (RPCs) in the developing rat retina.
methodsWe compared knockout (KO) and wild-type (WT) retinae by immunohistochemistry. The TdT-mediated dUTP terminal nick-end labeling (TUNEL) assay was performed to determine cell death. Pulse-chase experiments using 5-ethynyl-2'-deoxyuridine (EdU) were carried out to interrogate RPC behavior and in turn neurogenesis.
resultsReverse transcription-polymerase chain reaction analysis showed that CitK was expressed at embryonic day (E)12 and was turned off at approximately postnatal day (P)4. Immunohistochemistry showed CitK being localized as puncta at the apical end of the outer neuroblastic layer (ONBL). Analyses during embryonic development showed that the KO retina was of comparable size to that of WT until E13. However, by E14, there was a reduction in the number of S-phase RPCs with a concomitant increase in TUNEL+ cells in the KO retina. Moreover, early neurogenesis, as reflected by retinal ganglion cell production, was not affected. Postnatal analysis of the retina showed that ONBL in the KO retina was reduced to half the size of that in WT and showed further degeneration. Immunohistochemistry revealed absence of Islet1+ bipolar cells at P2, which was further confirmed by EdU pulse-chase experiments. The CitK KO retinae underwent complete degeneration by P14.
conclusionsOur study showed that CitK is not required for a subset of RPCs before E14, but is necessary for RPC survival post E14. This in turn results in normal early embryonic neurogenesis, but severely compromised later embryonic and postnatal neurogenesis.
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