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

Mice lacking HSP90beta fail to develop a placental labyrinth.

A K Voss1, T Thomas, P Gruss

  • 1Department of Molecular Cell Biology, Max Planck Institute of Biophysical Chemistry, Goettingen, Germany. avoss@gwdg.de

Development (Cambridge, England)
|February 2, 2000
PubMed
Summary
This summary is machine-generated.

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

MOF maintains transcriptional programs regulating cellular stress response.

Oncogene·2015
Same author

MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway.

Oncogene·2015
Same author

Pro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3.

Cell death and differentiation·2014
Same author

Consequences of the combined loss of BOK and BAK or BOK and BAX.

Cell death & disease·2013
Same author

Use of polymerase chain reaction (PCR) to detect homologous recombination in transfected cell lines.

Methods in molecular biology (Clifton, N.J.)·2011
Same author

Breaking an absolute species barrier: transgenic mice expressing the mink PrP gene are susceptible to transmissible mink encephalopathy.

Journal of virology·2005
Same journal

Expanding the C. elegans toolkit with gonad explants.

Development (Cambridge, England)·2026
Same journal

Nuclear Factor Y controls nutrient-adaptive epithelial growth by regulating mTOR in the Drosophila midgut.

Development (Cambridge, England)·2026
Same journal

Primordial germ cells differentially contribute to the germline in zebrafish.

Development (Cambridge, England)·2026
Same journal

Dissecting planar and vertical organiser signals in early chick neural development.

Development (Cambridge, England)·2026
Same journal

Real-time transcriptomic profiling of hPSC-derived cartilage during development identifies a key role for the extracellular matrix in homeostasis and protection.

Development (Cambridge, England)·2026
Same journal

In preprints - housekeeping the housekeeping genes.

Development (Cambridge, England)·2026
See all related articles

Heat-shock protein beta (HSP90beta) is crucial for placental development in mice. Its absence causes embryonic lethality by day 10.5 due to failed placental labyrinth formation, highlighting HSP90beta

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Genetics

Background:

  • Heat-shock proteins (HSP90s) are vital molecular chaperones involved in protein folding and conformational activation.
  • Vertebrates possess two ubiquitous cytosolic HSP90s: HSP90alpha and HSP90beta.

Purpose of the Study:

  • To investigate the specific role of HSP90beta in murine development, particularly in placental formation.
  • To determine if HSP90alpha can compensate for the loss of HSP90beta during embryogenesis.

Main Methods:

  • Generation of Hsp90beta-mutant mice using embryonic stem cells.
  • Analysis of heterozygous and homozygous mutant embryos for phenotypic abnormalities.
  • Construction and analysis of chimeric embryos to assess cell-autonomous and non-autonomous effects.

Related Experiment Videos

Main Results:

  • Homozygous Hsp90beta mutant embryos exhibit normal development until embryonic day 9.0/9.5, followed by placental abnormalities and embryonic lethality.
  • Mutant concepti fail to form a fetal placental labyrinth, with impaired trophoblast differentiation and vascularization.
  • HSP90alpha cannot compensate for the loss of HSP90beta in placenta development.
  • Chimeric analysis reveals the primary defect lies within the allantois, which fails to induce trophoblast differentiation.

Conclusions:

  • HSP90beta plays an indispensable, non-redundant role in murine placenta development.
  • The allantois requires functional HSP90beta to induce proper trophoblast differentiation for labyrinth formation.
  • HSP90beta is a critical component of the signaling pathway mediating allantois-induced trophoblast differentiation.