Preventing polyglutamine-induced activation of c-Jun delays neuronal dysfunction in a mouse model of SCA7 retinopathy

Neurobiol Dis. 2007 Mar;25(3):571-81. doi: 10.1016/j.nbd.2006.11.002. Epub 2006 Dec 26.

Abstract

We have approached the role of cellular stress in neurodegenerative diseases caused by polyglutamine expansion (polyQ) in the context of Spinocerebellar ataxia type 7 (SCA7) that includes retinal degeneration. Using the R7E mouse, in which polyQ-ataxin-7 is specifically over-expressed in rod photoreceptors, we previously showed that rod dysfunction correlated to moderate and prolonged activation of the JNK/c-Jun stress pathway. SCA7 retinopathy was also associated with reduced expression of rod-specific genes, including the transcription factor Nrl, which is essential for rod differentiation and function. Here, we report that R7E retinopathy is improved upon breeding with the JunAA knock-in mice, in which JNK-mediated activation of c-Jun is compromised. Expression of Nrl and its downstream targets, which are involved in phototranduction, are partially restored in the JunAA-R7E mice. We further show that c-Jun can directly repress the transcription of Nrl. Our studies suggest that polyQ-induced cellular stress leads to repression of genes necessary for neuronal fate and function.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ataxin-7
  • Base Sequence
  • Basic-Leucine Zipper Transcription Factors / genetics
  • Basic-Leucine Zipper Transcription Factors / metabolism
  • Disease Models, Animal
  • Eye Proteins / genetics
  • Eye Proteins / metabolism
  • Female
  • JNK Mitogen-Activated Protein Kinases / genetics*
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Transgenic
  • Molecular Sequence Data
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism
  • Peptides / genetics*
  • Peptides / metabolism
  • Phosphorylation
  • Retinal Diseases / genetics*
  • Retinal Diseases / metabolism*
  • Retinal Diseases / pathology
  • Retinal Rod Photoreceptor Cells / pathology
  • Retinal Rod Photoreceptor Cells / physiology
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism
  • Transgenes / physiology
  • Up-Regulation / physiology

Substances

  • Ataxin-7
  • Atxn7 protein, mouse
  • Basic-Leucine Zipper Transcription Factors
  • Eye Proteins
  • Nerve Tissue Proteins
  • Nrl protein, mouse
  • Peptides
  • Transcription Factor AP-1
  • polyglutamine
  • JNK Mitogen-Activated Protein Kinases