BAG1 modulates huntingtin toxicity, aggregation, degradation, and subcellular distribution

J Neurochem. 2009 Nov;111(3):801-7. doi: 10.1111/j.1471-4159.2009.06363.x. Epub 2009 Aug 27.

Abstract

Bcl-2-associated athanogene-1 (BAG1) is a multifunctional protein delivering chaperone-recognized unfolded substrates to the proteasome for degradation. It has been shown to be essential for proper CNS development in vivo, playing a crucial role in neuronal survival and differentiation. With regard to Huntington's disease, a sequestration of BAG1 into inclusion bodies and a neuroprotective effect in double transgenic mice have been reported. Here, we show that BAG1 reduces aggregation and accelerates degradation of mutant huntingtin (htt-mut). Moreover, it reduces nuclear levels of htt-mut. This effect can be overcome by over-expression of seven in absentia homolog 1, an E3 ligase negatively regulated by BAG1 and known to be involved in nuclear import of htt-mut. In vivo, BAG1 proved to be protective in a Drosophila melanogaster Huntington's disease model, preventing photoreceptor cell loss induced by htt-mut. In summary, we present BAG1 as a therapeutic tool modulating key steps in htt toxicity in vitro and ameliorating htt toxicity in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Cysteine Proteinase Inhibitors / pharmacology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Disease Models, Animal
  • Drosophila melanogaster
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / genetics
  • Green Fluorescent Proteins / genetics
  • Humans
  • Huntingtin Protein
  • Huntington Disease / genetics
  • Huntington Disease / metabolism*
  • Huntington Disease / pathology*
  • Leupeptins / pharmacology
  • Mice
  • Mutation
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Photoreceptor Cells / metabolism
  • Photoreceptor Cells / pathology
  • Proteins / metabolism
  • Subcellular Fractions / drug effects
  • Subcellular Fractions / metabolism*
  • Subcellular Fractions / pathology
  • Transcription Factors / genetics
  • Transcription Factors / physiology*
  • Ubiquitin-Protein Ligases

Substances

  • BCL2-associated athanogene 1 protein
  • Cysteine Proteinase Inhibitors
  • DNA-Binding Proteins
  • HTT protein, human
  • Huntingtin Protein
  • Leupeptins
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Proteins
  • Transcription Factors
  • enhanced green fluorescent protein
  • Green Fluorescent Proteins
  • Siah1a protein, mouse
  • Ubiquitin-Protein Ligases
  • benzyloxycarbonylleucyl-leucyl-leucine aldehyde