A defect in cytosolic carboxypeptidase 1 (Nna1) causes autophagy in Purkinje cell degeneration mouse brain

Iryna Berezniuk, Lloyd D. Fricker

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Purkinje cell degeneration (pcd) is a mouse mutant which is characterized by postnatal degeneration of selective cell types. The pcd mutation was mapped to a gene encoding a cytosolic carboxypeptidase-like protein (CCP), named CCP1/Nna1. Many neurons in pcd mice show increased levels of autophagy, including cell types which do not undergo neurodegeneration. These brain regions have greatly elevated levels of many intracellular peptides, suggesting that CCP1/Nna1 functions in protein turnover by degrading peptides to amino acids. We propose that the lack of CCP1/Nna1 leads to decreases in cellular levels of amino acids, which leads to elevated autophagy as a protective response to cellular amino acid starvation.

Original languageEnglish (US)
Pages (from-to)558-559
Number of pages2
JournalAutophagy
Volume6
Issue number4
DOIs
StatePublished - May 16 2010

Keywords

  • Carboxypeptidase
  • Neurodegeneration
  • Peptidase
  • Peptides
  • Proteasome
  • Purkinje cells

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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