September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Analysis of FGFR2 Regulated Transcripts in the Newborn Mouse Lens
Author Affiliations & Notes
  • Michael L Robinson
    Biology, Miami University, Oxford, Ohio, United States
  • Stephanie L. Padula
    Biology, Miami University, Oxford, Ohio, United States
  • Thanh Hoang
    Biology, Miami University, Oxford, Ohio, United States
  • Lin Liu
    Biology, Miami University, Oxford, Ohio, United States
  • Chun Liang
    Biology, Miami University, Oxford, Ohio, United States
  • Footnotes
    Commercial Relationships   Michael Robinson, None; Stephanie Padula, None; Thanh Hoang, None; Lin Liu, None; Chun Liang, None
  • Footnotes
    Support  NIH Grant EY012995
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Michael L Robinson, Stephanie L. Padula, Thanh Hoang, Lin Liu, Chun Liang; Analysis of FGFR2 Regulated Transcripts in the Newborn Mouse Lens. Invest. Ophthalmol. Vis. Sci. 2016;57(12):No Pagination Specified.

      Download citation file:

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

  • Supplements

Purpose : FGF receptor signaling plays an indispensable role in lens development. Deletion of Fgfr2 during lens placode formation results in apoptosis, prenatal cataract formation and microphthalmia. The severity of these phenotypes decreases upon the simultaneous deletion of Pten, suggesting an important genetic interaction. Despite obvious phenotypic abnormalities in FGFR2-deficient lenses, the transcriptional targets of FGFR2 signaling in the lens remain incomplete. Here we provide information on deregulated lens transcripts in the absence of Fgfr2, Pten, or both Fgfr2 and Pten.

Methods : Pooled mRNA from 6 newborn mouse lenses per biological replicate was collected for each of the 3 genotypes tested (mice deleted for (1)Fgfr2, (2)Pten, (3)Pten and Fgfr2). All mice were on an FVB/N background. Since gene deletion was mediated by the Le-Cre transgene, we prepared control mRNA from both (4)FVB/N and (5)Le-Cre hemizygous samples. Three biological replicates from each genotype (15 total pooled mRNA samples) were analyzed by RNA-Seq. RNA-Seq sequence reads were analyzed by Salmon 0.5.1 software that quantifies transcript expression using transcriptome reference data (ENSEMB Mouse cDNAs Release 82). Differentially expressed transcripts were determined by DESeq2 with cut-offs of ≥1.5 fold change and adjusted p values ≤0.05. Functional analysis of differentially regulated genes from each comparison was conducted with DAVID 6.7.

Results : Overall, PTEN-deficient lenses differentially expressed 462 transcript isoforms from 432 different genes, with many genes relevant to p53 signaling, alternative splicing and phosphoproteins. FGFR2-deficient lenses differentially expressed 1,233 transcript isoforms from 1,092 different genes, with many genes relevant to ribosomes and ribosomal proteins, acetylation and phosphoproteins. FGFR2-deficient lenses down regulated many lens structural genes including Bfsp1, Bfsp2, Cdh1, Crybb1, and the entire gamma crystallin cluster (Cryga-f). Lenses missing both FGFR2 and PTEN differentially expressed 724 transcript isoforms from 663 different genes.The FGFR2/PTEN knockout lenses uniquely induced two transcript isoforms of Caprin2 and restored normal expression of lens structural genes deregulated in the Fgfr2 deleted lenses.

Conclusions : FGFR signaling and PTEN signaling interact genetically. Deletion of Pten ameliorates some of the transcriptional dysregulation resulting from Fgfr2 deletion in lenses.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.