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 Concept Videos

Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...

You might also read

Related Articles

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

Sort by
Same author

Fatty acid regulation of feeding in <i>Caenorhabditis</i> elegans reveals the potential ancestral origin of a GLP-1-like multiagonist signaling system.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

p38 MAPK orchestrates cross-tissue potassium homeostasis for survival.

Nature communications·2026
Same author

Multi-Omics Integration Identifies <i>TNFRSF1A</i> as a Causal Mediator of Immune Microenvironment Reprogramming in Diabetic Kidney Disease.

International journal of molecular sciences·2026
Same author

Krüppel-like factor 1 acts upstream of the SKN-1/Nrf transcription factors to modulate oxidative stress, lipid homeostasis and longevity.

bioRxiv : the preprint server for biology·2025
Same author

Belzutifan for patients with Von Hippel-Lindau (VHL) disease-associated heterogeneous tumors - a retrospective single center analysis.

BMC cancer·2025
Same author

Genome-wide CRISPR Screen Identifies Sec31A as a Key Regulator of Alpha Cell Survival.

Nature communications·2025

Related Experiment Video

Updated: May 8, 2026

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline
08:40

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

TORC2 signaling antagonizes SKN-1 to induce C. elegans mesendodermal embryonic development.

Vanessa Ruf1, Christina Holzem, Tobias Peyman

  • 1Department of Medicine, Renal Division, University Hospital Freiburg, D-79106 Freiburg, Germany.

Developmental Biology
|August 27, 2013
PubMed
Summary

The target of rapamycin complex 2 (TORC2) and SGK-1 kinase antagonize SKN-1 during embryonic development. Inactivating rict-1/Rictor rescued SKN-1-deficient embryos, restoring mesendodermal development.

Keywords:
C. elegansDevelopmentRICTORSGK-1SKN-1TOR signaling

More Related Videos

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Modeling Paracrine Noncanonical Wnt Signaling In Vitro
11:14

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

Related Experiment Videos

Last Updated: May 8, 2026

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline
08:40

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Modeling Paracrine Noncanonical Wnt Signaling In Vitro
11:14

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • The target of rapamycin (TOR) kinase is a conserved regulator of cell growth and metabolism.
  • TOR functions in two complexes, TORC1 and TORC2, with TORC2 and Rictor recently linked to aging and metabolism.
  • SKN-1 is a transcription factor crucial for mesendoderm development, cellular homeostasis, and longevity.

Purpose of the Study:

  • To investigate the role of rict-1/Rictor, a component of TORC2, in embryonic development.
  • To determine if TORC2 regulates the function of the transcription factor SKN-1 during embryogenesis.

Main Methods:

  • Genetic inactivation of rict-1 and other TOR components in C. elegans.
  • Analysis of mesendodermal specification in SKN-1 deficient embryos.
  • Investigating the downstream effects of rict-1/TORC2 using SGK-1 gain-of-function mutants.

Main Results:

  • Genetic inactivation of rict-1/Rictor suppressed lethality in SKN-1 deficient embryos.
  • This suppression was associated with restored mesendodermal precursor specification, leading to intestine and pharynx formation.
  • Inactivation of other TORC2 components, but not TORC1, also partially rescued SKN-1 embryonic lethality.
  • The SGK-1 kinase was identified as a downstream mediator of rict-1/TORC2 function.

Conclusions:

  • TORC2, acting through Rictor and SGK-1, antagonizes SKN-1 during C. elegans embryonic development.
  • This pathway is critical for proper mesendodermal specification and embryonic viability.
  • The findings reveal a novel regulatory interaction between TORC2 and SKN-1 in controlling developmental processes.