Related Experiment Video

Updated: Dec 8, 2025

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

9.0K

PIG-1 MELK-dependent phosphorylation of nonmuscle myosin II promotes apoptosis through CES-1 Snail partitioning

Hai Wei1, Eric J Lambie1,2, Daniel S Osório3

  • 1Department Biology II, Faculty of Biology, Ludwig-Maximilians-University Munich, Großhadener, Planegg-Martinsried, Germany.

Plos Genetics
|September 18, 2020
PubMed

Insights

The kinase MELK (Maternally expressed gene 3) promotes cancer by controlling cell death. Its C. elegans counterpart, PIG-1, ensures cell death by regulating protein partitioning during cell division.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Cancer Research

Background:

  • The role of mammalian kinase MELK (Maternally expressed gene 3) in promoting tumorigenesis remains unclear.
  • Apoptosis, or programmed cell death, is crucial for development and preventing cancer.
  • Asymmetric cell division is a fundamental process generating cellular diversity and tissue development.

Purpose of the Study:

  • To elucidate the conserved mechanism by which MELK family kinases regulate cell fate.
  • To investigate the function of the C. elegans MELK orthologue, PIG-1, in apoptosis.
  • To understand the regulation of CES-1 Snail partitioning and its role in neuroblast cell death.

Main Methods:

  • Utilized the nematode C. elegans as a model organism.
  • Investigated the role of PIG-1 (MELK orthologue) in NSM neuroblast asymmetric division.
  • Analyzed the partitioning of CES-1 Snail protein and its regulation by PIG-1 and PAR-4.

Main Results:

  • PIG-1 MELK is essential for the asymmetric partitioning of the anti-apoptotic factor CES-1 Snail in C. elegans neuroblasts.
  • PIG-1 MELK acts downstream of CES-1 Snail and PAR-4 LKB1 pathways, potentially via myosin II regulation.
  • CES-1 Snail forms a gradient, auto-regulating its own activity and promoting the apoptotic fate of the smaller daughter cell.

Conclusions:

  • PIG-1 MELK-induced actomyosin contractility is conserved in regulating the apoptotic fate during asymmetric cell division.
  • The study reveals a novel mechanism for controlling cell death through protein partitioning regulated by a kinase.
  • A CES-1 Snail auto-regulatory loop contributes to precise control over cell fate decisions.

More Related Videos

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

744
Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

2.9K

Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
13.3K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.8K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.0K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
4.5K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
13.3K