Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Presenilin function in Caenorhabditis elegans.

Agata Smialowska1, Ralf Baumeister

  • 1Bio3/Bioinformatics and Molecular Genetics, University of Freiburg, Freiburg, Germany.

Neuro-Degenerative Diseases
|October 19, 2006
PubMed
Summary

The study identifies novel suppressors of presenilin mutations in C. elegans, revealing a conserved pathway involving REST/NSRF, CoREST, and LSD1 that regulates presenilin gene expression and impacts neuronal development.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.

Research square·2026
Same author

Opposing roles of pseudokinases NRBP1 and NRBP2 in regulating L1 retrotransposition.

Nature communications·2025
Same author

Acute suppression of mitochondrial ATP production prevents apoptosis and provides an essential signal for NLRP3 inflammasome activation.

Immunity·2024
Same author

SGK-1 mediated inhibition of iron import is a determinant of lifespan in <i>C. elegans</i>.

microPublication biology·2023
Same author

Reprogramming of the transcriptome after heat stress mediates heat hormesis in Caenorhabditis elegans.

Nature communications·2023
Same author

Molecular Mechanisms of Lipid-Based Metabolic Adaptation Strategies in Response to Cold.

Cells·2023

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • The nematode C. elegans genome harbors homologs of human familial Alzheimer's disease genes, including presenilins (sel-12, hop-1) and amyloid precursor protein (apl-1).
  • Presenilin mutations in C. elegans disrupt Notch/lin-12 signaling, leading to cell specification and attachment defects, ultimately causing reduced egg-laying.

Purpose of the Study:

  • To identify genetic suppressors of presenilin loss-of-function mutations in C. elegans.
  • To elucidate the molecular mechanisms by which these suppressors counteract presenilin-related defects.

Main Methods:

  • Utilized genetic suppressor screens to identify mutations that rescue the egg-laying defect in presenilin/sel-12 mutants.
  • Characterized the identified suppressor genes (spr-1, spr-3, spr-4, spr-5) and their corresponding proteins.
  • Investigated the functional relationship between suppressors and presenilin genes at the molecular level.

Main Results:

  • Identified spr-1, spr-3, spr-4, and spr-5 as suppressors of the sel-12 loss-of-function phenotype.
  • These spr genes encode C. elegans homologs of human REST/NSRF, CoREST, and LSD1, key components of a transcriptional repressor complex.
  • Mutations in spr genes suppress the egg-laying defect by derepressing the expression of the hop-1 presenilin gene.

Conclusions:

  • Discovered a conserved regulatory pathway involving REST/NSRF, CoREST, and LSD1 that modulates presenilin gene expression in C. elegans.
  • This pathway plays a crucial role in neuronal development and can be targeted to rescue presenilin-related cellular defects.

Related Experiment Videos