Expression of Quaking RNA-Binding Protein in the Adult and Developing Mouse Retina.Report as inadecuate




Expression of Quaking RNA-Binding Protein in the Adult and Developing Mouse Retina. - Download this document for free, or read online. Document in PDF available to download.

Journal Title:

PLoS ONE

Volume:

Volume 11, Number 5

Publisher:

Public Library of Science | 2016, Pages e0156033-e0156033

Type of Work:

Article | Final Publisher PDF

Abstract: Quaking QKI, which belongs to the STAR family of KH domain-containing RNA-binding proteins, functions in pre-mRNA splicing, microRNA regulation, and formation of circular RNA. QKI plays critical roles in myelinogenesis in the central and peripheral nervous systems and has been implicated neuron-glia fate decision in the brain; however, neither the expression nor function of QKI in the neural retina is known. Here we report the expression of QKI RNA-binding protein in the developing and mature mouse retina. QKI was strongly expressed by Müller glial cells in both the developing and adult retina. Intriguingly, during development, QKI was expressed in early differentiating neurons, such as the horizontal and amacrine cells, and subsequently in later differentiating bipolar cells, but not in photoreceptors. Neuronal expression was uniformly weak in the adult. Among QKI isoforms 5, 6, and 7, QKI-5 was the predominantly expressed isoform in the adult retina. To study the function of QKI in the mouse retina, we examined quakingviableqkv mice, which have a dysmyelination phenotype that results from deficiency of QKI expression and reduced numbers of mature oligodendrocytes. In homozygous qkv mutant mice qkv-qkv, the optic nerve expression levels of QKI-6 and 7, but not QKI-5 were reduced. In the retina of the mutant homozygote, QKI-5 levels were unchanged, and QKI-6 and 7 levels, already low, were also unaffected. We conclude that QKI is expressed in developing and adult Müller glia. QKI is additionally expressed in progenitors and in differentiating neurons during retinal development, but expression weakened or diminished during maturation. Among QKI isoforms, we found that QKI-5 predominated in the adult mouse retina. Since Müller glial cells are thought to share properties with retinal progenitor cells, our data suggest that QKI may contribute to maintaining retinal progenitors prior to differentiation into neurons. On the other hand, the expression of QKI in different retinal neurons may suggest a role in neuronal cell type specific fate determination and maturation. The data raises the possibility that QKI may function in retinal cell fate determination and maturation in both glia and neurons.

Subjects: Health Sciences, Pharmacology - Biology, Neuroscience - Research Funding: Japan Science and Technology Agency PRESTO to Chieko Koike.

Ministry of Education, Culture, Sports, Science, and Technology Grants-in-Aid for Scientific Research B to Chieko Koike.

Ministry of Education, Culture, Sports, Science, and Technology Industry to support private universities building up their foundations of strategic research to Chieko Koike.

Takeda Science Foundation to Chieko Koike.

National Institutes of Health 1R01NS093016 to Yue Feng.

National Institutes of Health 5R01NS070526 to Yue Feng.

This work was supported by Precursory Research for Embryonic Science and Technology PRESTO from the Japan Science and Technology Agency, by grants from the Ministry of Education program Grants-in-Aid for Scientific Research B and Industry to support private universities building up their foundations of strategic research, by the Takeda Science Foundation to CK, and by NIH grants 1R01NS093016 and 5R01NS070526 to YF.





Author: Takahiko Suiko, Kensuke Kobayashi, Kentaro Aono, Togo Kawashima, Kiyoshi Inoue, Li Ku, Yue Feng, Chieko Koike,

Source: https://open.library.emory.edu/



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