Synaptic E3 ligase SCRAPPER in contextual fear conditioning: Extensive behavioral phenotyping of Scrapper heterozygote and overexpressing mutant mice

Ikuko Yao, Keizo Takao, Tsuyoshi Miyakawa, Seiji Ito, Mitsutoshi Setou

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

SCRAPPER, an F-box protein coded by FBXL20, is a subunit of SCF type E3 ubiquitin ligase. SCRAPPER localizes synapses and directly binds to Rab3-interacting molecule 1 (RIM1), an essential factor for synaptic vesicle release, thus it regulates neural transmission via RIM1 degradation. A defect in SCRAPPER leads to neurotransmission abnormalities, which could subsequently result in neurodegenerative phenotypes. Because it is likely that the alteration of neural transmission in Scrapper mutant mice affect their systemic condition, we have analyzed the behavioral phenotypes of mice with decreased or increased the amount of SCRAPPER. We carried out a series of behavioral test batteries for Scrapper mutant mice. Scrapper transgenic mice overexpressing SCRAPPER in the hippocampus did not show any significant difference in every test argued in this manuscript by comparison with wild-type mice. On the other hand, heterozygotes of Scrapper knockout [SCR (+/-)] mice showed significant difference in the contextual but not cued fear conditioning test. In addition, SCR (+/-) mice altered in some tests reflecting anxiety, which implies the loss of functions of SCRAPPER in the hippocampus. The behavioral phenotypes of Scrapper mutant mice suggest that molecular degradation conferred by SCRAPPER play important roles in hippocampal-dependent fear memory formation.

Original languageEnglish
Article numbere17317
JournalPloS one
Volume6
Issue number2
DOIs
Publication statusPublished - 04-03-2011

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Ubiquitin-Protein Ligases
conditioned behavior
Heterozygote
fearfulness
Thyristors
ligases
Fear
heterozygosity
F-Box Proteins
phenotype
Degradation
mutants
Molecules
mice
Synaptic Transmission
Phenotype
Data storage equipment
Defects
synaptic transmission
Hippocampus

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

Cite this

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title = "Synaptic E3 ligase SCRAPPER in contextual fear conditioning: Extensive behavioral phenotyping of Scrapper heterozygote and overexpressing mutant mice",
abstract = "SCRAPPER, an F-box protein coded by FBXL20, is a subunit of SCF type E3 ubiquitin ligase. SCRAPPER localizes synapses and directly binds to Rab3-interacting molecule 1 (RIM1), an essential factor for synaptic vesicle release, thus it regulates neural transmission via RIM1 degradation. A defect in SCRAPPER leads to neurotransmission abnormalities, which could subsequently result in neurodegenerative phenotypes. Because it is likely that the alteration of neural transmission in Scrapper mutant mice affect their systemic condition, we have analyzed the behavioral phenotypes of mice with decreased or increased the amount of SCRAPPER. We carried out a series of behavioral test batteries for Scrapper mutant mice. Scrapper transgenic mice overexpressing SCRAPPER in the hippocampus did not show any significant difference in every test argued in this manuscript by comparison with wild-type mice. On the other hand, heterozygotes of Scrapper knockout [SCR (+/-)] mice showed significant difference in the contextual but not cued fear conditioning test. In addition, SCR (+/-) mice altered in some tests reflecting anxiety, which implies the loss of functions of SCRAPPER in the hippocampus. The behavioral phenotypes of Scrapper mutant mice suggest that molecular degradation conferred by SCRAPPER play important roles in hippocampal-dependent fear memory formation.",
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Synaptic E3 ligase SCRAPPER in contextual fear conditioning : Extensive behavioral phenotyping of Scrapper heterozygote and overexpressing mutant mice. / Yao, Ikuko; Takao, Keizo; Miyakawa, Tsuyoshi; Ito, Seiji; Setou, Mitsutoshi.

In: PloS one, Vol. 6, No. 2, e17317, 04.03.2011.

Research output: Contribution to journalArticle

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