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

Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
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...
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 reduction of the tissue.

You might also read

Related Articles

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

Sort by
Same author

Lzts1 controls both neuronal delamination and outer radial glial-like cell generation during mammalian cerebral development.

Nature communications·2019
Same author

High levels of DNA polymerase β mRNA corresponding with the high activity in Graves' thyroid tissue.

Journal of endocrinological investigation·2016
Same author

CD4+CD25high regulatory T cells are markedly decreased in blood of patients with pemphigus vulgaris.

Dermatology (Basel, Switzerland)·2007
Same author

Possible role of VEGF in the progression of kidney disease in streptozotocin (STZ)-induced diabetic rats: effects of an ACE inhibitor and an angiotensin II receptor antagonist.

Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme·2004
Same author

A stable prostacyclin analogue reduces high serum TNF-alpha levels in diabetic patients.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association·2004
Same author

Changes of endothelin in streptozotocin-induced diabetic rats: effects of an angiotensin converting enzyme inhibitor, enalapril maleate.

The Journal of endocrinology·2002
Same journal

A planar dimer of bovine ATP synthase.

Cell death and differentiation·2026
Same journal

GCN5 and TADA2B constitutively regulate XRCC1 function during DNA repair to maintain cell survival.

Cell death and differentiation·2026
Same journal

MEGF8 controls osteogenic differentiation through post-transcriptional regulation of BMP-SMAD signaling in craniosynostosis.

Cell death and differentiation·2026
Same journal

Macrophage-secreted brain-derived neurotrophic factor promotes tumor growth in triple-negative breast cancer by inducing axonogenesis.

Cell death and differentiation·2026
Same journal

Species-specific regulation of necroptosis by STK38-dependent RIPK1 phosphorylation.

Cell death and differentiation·2026
Same journal

Ssu72 phosphatase orchestrates obesogenic adipogenesis and metabolic homeostasis during nutrient excess.

Cell death and differentiation·2026
See all related articles

Related Experiment Video

Updated: Jun 18, 2026

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Apaf-1-independent programmed cell death in mouse development.

A Nagasaka1, K Kawane, H Yoshida

  • 1Department of Medical Chemistry, Kyoto University, Yoshida-Konoe, Sakyo-ku, Japan.

Cell Death and Differentiation
|December 5, 2009
PubMed
Summary
This summary is machine-generated.

Apoptotic cell engulfment in mouse development relies on Apaf-1 (Apoptotic protease activating factor 1). However, an Apaf-1-independent cell death system backs up this process, ensuring developmental cell death continues.

More Related Videos

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening
08:16

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening

Published on: October 6, 2022

Related Experiment Videos

Last Updated: Jun 18, 2026

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening
08:16

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening

Published on: October 6, 2022

Area of Science:

  • Developmental Biology
  • Cell Death Mechanisms
  • Immunology

Background:

  • Mammalian development involves significant cellular death, with macrophages engulfing apoptotic cells.
  • DNase II-deficient (DNase II(-/-)) embryos provide a model for studying programmed cell death, as undigested DNA accumulates in macrophages.

Purpose of the Study:

  • To investigate the role of Apaf-1 (Apoptotic protease activating factor 1) in programmed cell death and macrophage engulfment during mouse embryogenesis.
  • To identify alternative pathways for programmed cell death when the Apaf-1-dependent mechanism is absent.

Main Methods:

  • Analysis of Apaf-1-null mutations in DNase II(-/-) mouse embryos.
  • Assessment of DNA-containing macrophages at various embryonic stages (E11.5 and later).
  • Detection of processed caspase-3 and caspase-9 in embryonic tissues and fetal thymocytes.
  • Induction of apoptosis in fetal thymocytes using staurosporine and etoposide.

Main Results:

  • Apaf-1 deficiency significantly reduced DNA-containing macrophages at E11.5 but not at later embryonic stages, indicating Apaf-1-independent engulfment.
  • Non-apoptotic dead cells were observed in Apaf-1(-/-) embryos, suggesting an alternative cell death pathway.
  • While most tissues in Apaf-1(-/-) embryos lacked processed caspase-3, E14.5 thymocytes showed active caspase-3 and could undergo caspase-dependent apoptosis independently of Apaf-1.

Conclusions:

  • Programmed cell death during mouse development primarily utilizes an Apaf-1-dependent mechanism.
  • An Apaf-1-independent programmed cell death system exists and can compensate for the absence of Apaf-1, particularly in later developmental stages and specific tissues like the thymus.
  • This backup system ensures the efficient removal of dead cells, crucial for normal embryonic development.