June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Function of Zfp36l1 in mouse retinal development and maintenance
Author Affiliations & Notes
  • Xiuqian Mu
    Ophthalmology/Ross Eye Institute, University at Buffalo, Buffalo, NY
    SUNY Eye Institute, Buffalo, NY
  • Tadeusz Kaczynski
    Ophthalmology/Ross Eye Institute, University at Buffalo, Buffalo, NY
    SUNY Eye Institute, Buffalo, NY
  • Hemabindu Chintala
    Ophthalmology/Ross Eye Institute, University at Buffalo, Buffalo, NY
    SUNY Eye Institute, Buffalo, NY
  • Martin Turner
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge, United Kingdom
  • Fuguo Wu
    Ophthalmology/Ross Eye Institute, University at Buffalo, Buffalo, NY
  • Footnotes
    Commercial Relationships Xiuqian Mu, None; Tadeusz Kaczynski, None; Hemabindu Chintala, None; Martin Turner, None; Fuguo Wu, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 1471. doi:
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      Xiuqian Mu, Tadeusz Kaczynski, Hemabindu Chintala, Martin Turner, Fuguo Wu; Function of Zfp36l1 in mouse retinal development and maintenance. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1471.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Zfp36l1 is an RNA binding protein involved in mRNA degradation. Our RNA-seq analysis indicates that Zfp36l1 is highly expressed in the developing retina. Our purpose in this study is to understand the role of Zfp35l1 in the retina by investigating its expression patterns in different developmental stages and examining if its mutation leads to any retinal defects.

Methods: In situ hybridization was used to analyze the expression of Zfp36l1 during retinal development. To further determine its function, we conditionally deleted Zfp36l1 in the developing retina by crossing a Zfp36l1-flox allele with the retina-specific Six3-Cre transgenic allele. The development of Zfp36l1-null retina and its maintenance were then examined by histological and immunofluorescence analysis.

Results: By in situ hybridization, we found that Zfp36l1 was expressed in retinal development from E12 to P5. Its expression was confined to retinal progenitor cells in all these stages. In the mature retina, Zfp36l1 is only expressed in Muller glial cells. Crossing of Zfp36l1-flox with Six3-Cre efficiently deleted Zfp36l1. However, we did not observe overt defects in the development of the Zfp36l1-null retina; all cell-types were born with correct proportions and the morphology of the Zfp36l1-null retina also appeared normal at P16 and P30. Nevertheless, we observed severe retinal degeneration of the Zfp36l1-null retina at four months of age, indicating that Zfp36l1 is essential for the maintenance of the retina. We currently are further characterizing the phenotypes to understand the underlying mechanisms.

Conclusions: Zfp36l1 is expressed in retinal progenitor cells during development and Muller glial cells in the mature retina. Deletion of Zfp36l1 does not affect retinal development, likely due to redundancy with another related gene, Zfp36l2. However, Zfp36l1-null retina undergoes degeneration postnatally. This may be caused by defects in Muller glial cells.

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