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

Meiosis I01:49

Meiosis I

193.5K
Meiosis is a carefully orchestrated set of cell divisions, the goal of which—in humans—is to produce haploid sperm or eggs, each containing half the number of chromosomes present in somatic cells elsewhere in the body. Meiosis I is the first such division, and involves several key steps, among them: condensation of replicated chromosomes in diploid cells; the pairing of homologous chromosomes and their exchange of information; and finally, the separation of homologous chromosomes by...
193.5K
Nondisjunction01:29

Nondisjunction

75.5K
During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
75.5K
Meiosis vs. Mitosis02:57

Meiosis vs. Mitosis

55.2K
Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is...
55.2K
Karyotyping01:17

Karyotyping

60.0K
Overview
60.0K

You might also read

Related Articles

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

Sort by
Same author

Verrucous and Erythrodermic Tinea Incognito Mimicking Epidermodysplasia Verruciformis.

Indian dermatology online journal·2026
Same author

Thick filament molecular interfaces play a critical role in the pathogenesis of hypertrophic cardiomyopathy.

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

Apelin analog treatment reverses severe pulmonary arterial hypertension and right ventricular heart failure.

JCI insight·2026
Same author

Targeting Inflammation by Pioglitazone and its R-Enantiomer Mitigates Pathological Myocardial Remodeling in Murine Hypertrophic Cardiomyopathy.

JACC. Basic to translational science·2026
Same author

Results in a 'Flash': Recognizing Misleading Clinical Photography.

Indian dermatology online journal·2026
Same author

Respiratory support and feeding-milestones in small-for-gestational-age, 34-36 weeks preterm infants.

Pediatric research·2026

Related Experiment Video

Updated: Jun 24, 2025

Generation of Induced Pluripotent Stem Cells from Turner Syndrome 45XO Fetal Cells for Downstream Modelling of Neurological Deficits Associated with the Syndrome
09:39

Generation of Induced Pluripotent Stem Cells from Turner Syndrome 45XO Fetal Cells for Downstream Modelling of Neurological Deficits Associated with the Syndrome

Published on: December 4, 2021

3.1K

Increased endothelial sclerostin caused by elevated DSCAM mediates multiple trisomy 21 phenotypes.

David M McKean1,2, Qi Zhang1, Priyanka Narayan1,3

  • 1Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA.

The Journal of Clinical Investigation
|June 3, 2024
PubMed
Summary

Trisomy 21 (T21) increases sclerostin, a Wnt inhibitor, by affecting DSCAM gene expression in heart cells. This may explain Down syndrome phenotypes and suggests anti-sclerostin therapies for T21-related conditions.

Keywords:
Bone developmentCardiologyCardiovascular diseaseGenetic diseasesGenetics

More Related Videos

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells
06:38

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

381
Combinational Treatment of Trichostatin A and Vitamin C Improves the Efficiency of Cloning Mice by Somatic Cell Nuclear Transfer
09:52

Combinational Treatment of Trichostatin A and Vitamin C Improves the Efficiency of Cloning Mice by Somatic Cell Nuclear Transfer

Published on: April 26, 2018

12.6K

Related Experiment Videos

Last Updated: Jun 24, 2025

Generation of Induced Pluripotent Stem Cells from Turner Syndrome 45XO Fetal Cells for Downstream Modelling of Neurological Deficits Associated with the Syndrome
09:39

Generation of Induced Pluripotent Stem Cells from Turner Syndrome 45XO Fetal Cells for Downstream Modelling of Neurological Deficits Associated with the Syndrome

Published on: December 4, 2021

3.1K
In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells
06:38

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

381
Combinational Treatment of Trichostatin A and Vitamin C Improves the Efficiency of Cloning Mice by Somatic Cell Nuclear Transfer
09:52

Combinational Treatment of Trichostatin A and Vitamin C Improves the Efficiency of Cloning Mice by Somatic Cell Nuclear Transfer

Published on: April 26, 2018

12.6K

Area of Science:

  • Genetics
  • Developmental Biology
  • Cardiology

Background:

  • Trisomy 21 (T21) causes congenital heart disease (CHD) and other phenotypes, but underlying mechanisms are unclear.
  • Understanding T21's developmental impact is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the molecular mechanisms by which T21 perturbs cardiac development.
  • To identify key genes and pathways dysregulated in T21-associated CHD.

Main Methods:

  • Comparative transcriptome analysis of CHD tissues from T21 and euploid (eCHD) patients.
  • Single-nucleus RNA sequencing and RNA in situ hybridization to resolve cell lineages.
  • Human induced pluripotent stem cell-derived endothelial cells were used to study gene deletion effects.

Main Results:

  • T21 tissues showed elevated chr21 gene expression, increased SOST (sclerostin) levels, and higher ZNF467 expression.
  • T21 cardiac endothelial cells exhibited significantly higher SOST expression and downregulated Wnt pathway genes.
  • DSCAM, within the chr21 CHD critical region, correlated with SOST and ZNF467; DSCAM deletion reduced sclerostin secretion.

Conclusions:

  • T21 leads to increased sclerostin, inappropriately inhibiting Wnt signaling crucial for heart development and other functions.
  • This mechanism likely contributes to Down syndrome phenotypes, suggesting therapeutic potential for anti-sclerostin antibodies in T21.