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

Expression and functional analysis of Uch-L3 during mouse development.

L J Kurihara1, E Semenova, J M Levorse

  • 1Howard Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.

Molecular and Cellular Biology
|March 14, 2000
PubMed
Summary

The s(1Acrg) mouse mutation causes embryonic lethality, but targeted deletion of the Uch-L3 gene did not replicate this phenotype. This suggests Uch-L3 is not the sole cause of the s(1Acrg) defect.

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

Alanine Scanning Mutagenesis of the MEDI4893 (Suvratoxumab) Epitope Reduces Alpha Toxin Lytic Activity <i>In Vitro</i> and Staphylococcus aureus Fitness in Infection Models.

Antimicrobial agents and chemotherapy·2018
Same author

Multimechanistic Monoclonal Antibodies (MAbs) Targeting Staphylococcus aureus Alpha-Toxin and Clumping Factor A: Activity and Efficacy Comparisons of a MAb Combination and an Engineered Bispecific Antibody Approach.

Antimicrobial agents and chemotherapy·2017
Same author

Ph-negative chronic myeloproliferative neoplasm (primary myelofibrosis) - as one of the reasons of the budd-Chiari syndrome.

Mediterranean journal of hematology and infectious diseases·2012
Same author

Controlled light-matter coupling for a single quantum dot embedded in a pillar microcavity using far-field optical lithography.

Physical review letters·2009
Same author

Lifetime of THz acoustic nanocavity modes.

Physical review letters·2009
Same author

Genomic imprinting of a placental lactogen gene in Peromyscus.

Development genes and evolution·2002

Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • The s(1Acrg) mutation in mice leads to embryonic lethality by embryonic day 8.5.
  • Positional cloning identified the mouse Uch-L3 (ubiquitin C-terminal hydrolase L3) gene within the s(1Acrg) minimal region.

Purpose of the Study:

  • To investigate the molecular basis of the s(1Acrg) embryonic lethal phenotype.
  • To determine the role of Uch-L3 in mouse development and its potential contribution to the s(1Acrg) phenotype.

Main Methods:

  • Positional cloning to identify genes within the s(1Acrg) minimal region.
  • Creation of a targeted mutation in the Uch-L3 gene (Uch-L3(Delta3-7)).
  • Analysis of Uch-L3(Delta3-7) homozygous mice for developmental, histological, fertility, and T-cell differentiation abnormalities.

Related Experiment Videos

Main Results:

  • Mice homozygous for the Uch-L3(Delta3-7) mutation were viable and showed no obvious developmental or histological abnormalities.
  • Uch-L3(Delta3-7) homozygotes were fertile, despite high Uch-L3 RNA levels in testes and thymus.
  • No defects in intrathymic T-cell differentiation were observed in Uch-L3 mutant mice.

Conclusions:

  • The Uch-L3 gene is likely not the sole cause of the s(1Acrg) embryonic lethal phenotype.
  • The s(1Acrg) phenotype may be complex, involving multiple genes, or caused by the loss of another gene in the region.
  • Uch-L3 might be functionally redundant with its homologue, Uch-L1, in mouse development.