December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Functional Mapping Of Protein Interactions Involved In Regulation Of Gene Expression In Developing Retina: Nrl Molecular Interactions
Author Affiliations & Notes
  • KP Mitton
    Eye Research Institute Oakland University Rochester MI
  • PK Swain
    Ophthalmology & Visual Sciences University of Michigan Ann Arbor MI
  • IJ Apel
    Ophthalmology & Visual Sciences University of Michigan Ann Arbor MI
  • A Swaroop
    Ophthalmology & Visual Sciences University of Michigan Ann Arbor MI
  • Footnotes
    Commercial Relationships   K.P. Mitton, None; P.K. Swain, None; I.J. Apel, None; A. Swaroop, None. Grant Identification: Support: NIH-EY11115 and EY07003, Research to Prevent Blindness
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2439. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      KP Mitton, PK Swain, IJ Apel, A Swaroop; Functional Mapping Of Protein Interactions Involved In Regulation Of Gene Expression In Developing Retina: Nrl Molecular Interactions . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2439.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: Cell-specific gene expression determines the fate of retinal progenitor cells as they differentiate into one of the six basic retinal neurons and glial cells. NRL is a transcription factor required for normal rod cell formation and is a component of the rhodopsin enhanceosome regulating the expression of rhodopsin. Protein interactions were mapped starting with different domains of NRL used as baits in yeast two-hybrid protein screening. Methods: Different domains of NRL were used as baits for multiple yeast two-hybrid screens of a bovine retina cDNA library, in addition to the previous reported screen using the NRL zipper domain (Mitton et al., 2000). Double positive clones were sequenced and evaluated by GST pull-down assay to confirm interactions. For rhodopsin promoter activation assay, CV-1 cells were co-transfected with expression constructs for NRL, interacting protein sequences, and the rhodopsin-promoter luciferase-reporter plasmid p130-Luc. Results: A second region of NRL, N-terminal to the DNA binding domain, was found to interact with CRX. Screening also identified an interactor with NRL that is a homolog of the novel mouse protein, Fiz-1. Unlike CRX, Fiz-1 is a ubiquitous signal transduction protein that can interact with the Flt-3 tyrosine kinase receptor in hematopoetic stem cells. GST pull-down assay using GST-NRL and 35S-bFiz confirmed NRL/bFiz interaction. Immunoblot analysis labeled a protein of 65 kDa in both bovine and human retina with the bFiz antiserum. Northern blotting showed human FIZ-1 transcripts in all human tissues examined and mouse Fiz-1 transcripts to be present in embryonic and postnatal mouse retina. In CV-1 cells, bFiz repressed NRL-mediated transactivation of the rhodopsin promoter in a dose dependent manner but did not affect CRX transactivation. Immunofluorescent staining of adult mouse retina with antibody to bFiz suggests ubiquitous protein distribution. Conclusion: Yeast two-hybrid trapping is useful for: 1) finding novel retinal-specific transcription factor and signal-transduction protein interactions, 2) mapping protein interactions to specific domains. Either of two regions of NRL, straddling the DNA binding domain, are sufficient for interaction with the CRX transcription factor. A novel and ubiquitous protein, Fiz1, also interacts with NRL and is present in the developing and adult mouse retina. The role of Fiz-1, and what cell-specific RTKs it may interact with in retinal tissue are not known.

Keywords: 417 gene/expression • 605 transcription factors • 528 proteins encoded by disease genes 
×
×

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.

×