Increased autophagy in transgenic mice with a G93A mutant SOD1 gene

Nobutoshi Morimoto, Makiko Nagai, Yasuyuki Ohta, Kazunori Miyazaki, Tomoko Kurata, Mizuki Morimoto, Tetsuro Murakami, Yasushi Takehisa, Yoshio Ikeda, Tatsushi Kamiya, Koji Abe

Research output: Contribution to journalArticlepeer-review

199 Citations (Scopus)


Autophagy, like the ubiquitin-proteasome system, is considered to play an important role in preventing the accumulation of abnormal proteins. Rat microtubule-associated protein 1 light chain 3 (LC3) is important for autophagy, and the conversion from LC3-I into LC3-II is accepted as a simple method for monitoring autophagy. We examined a SOD1G93A transgenic mouse model for amyotrophic lateral sclerosis (ALS) to consider a possible relationship between autophagy and ALS. In our study we analyzed LC3 and mammalian target of rapamycin (mTOR), a suppressor of autophagy, by immunoassays. The level of LC3-II, which is known to be correlated with the extent of autophagosome formation, was increased in SOD1G93A transgenic mice at symptomatic stage compared with non-transgenic or human wild-type SOD1 transgenic animals. Moreover, the ratio of phosphorylated mTOR/Ser2448 immunopositive motor neurons to total motor neurons was decreased in SOD1G93A-Tg mice. The present data show the possibility of increased autophagy in an animal model for ALS. And autophagy may be partially regulated by an mTOR signaling pathway in these animals.

Original languageEnglish
Pages (from-to)112-117
Number of pages6
JournalBrain Research
Issue number1
Publication statusPublished - Sept 5 2007
Externally publishedYes


  • ALS
  • Autophagy
  • G93A
  • LC3
  • Spinal cord
  • mTOR

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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