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

Midgestation lethality in mice deficient for the RecA-related gene, Rad51d/Rad51l3.

D L Pittman1, J C Schimenti

  • 1The Jackson Laboratory, Bar Harbor, Maine 04609, USA.

Genesis (New York, N.Y. : 2000)
|March 21, 2000
PubMed
Summary

Disrupting the Rad51d gene in mice leads to embryonic death due to developmental delays. This suggests Rad51d is crucial for DNA repair and embryonic development.

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

Germline genome protection: implications for gamete quality and germ cell tumorigenesis.

Andrology·2019
Same author

Role of DNA damage response pathways in preventing carcinogenesis caused by intrinsic replication stress.

Oncogene·2013
Same author

Mutagenesis-generated mouse models of human infertility with abnormal sperm.

Human reproduction (Oxford, England)·2006
Same author

Homologous recombinational repair proteins in mouse meiosis.

Cytogenetic and genome research·2004
Same author

New mouse genetic models for human contraceptive development.

Cytogenetic and genome research·2004
Same author

Reciprocal mouse and human limb phenotypes caused by gain- and loss-of-function mutations affecting Lmbr1.

Genetics·2001

Area of Science:

  • Genetics
  • Molecular Biology
  • Developmental Biology

Background:

  • Homologous recombination (HR) is vital for DNA repair, meiosis, and genetic diversity.
  • The RecA/RAD51 family, including seven mammalian members, plays critical roles in HR.
  • Rad51d (Rad51l3) is a mammalian gene involved in these processes.

Purpose of the Study:

  • To investigate the function of Rad51d by creating and analyzing Rad51d-deficient mice.
  • To understand the phenotypic consequences of Rad51d disruption during embryonic development.

Main Methods:

  • Gene disruption of Rad51d in mice.
  • Phenotypic analysis of Rad51d-deficient embryos and embryonic fibroblasts.
  • Blastocyst outgrowth experiments assessing sensitivity to DNA damaging agents (gamma radiation, methyl methanesulfonate).

Main Results:

  • Rad51d-deficient mice exhibit embryonic lethality between 8.5 and 11.5 days post-coitum (dpc).
  • Affected embryos show developmental delays, are smaller, and possess posterior truncations.
  • Mutant embryonic fibroblasts have limited propagation capacity.
  • Rad51d-deficient blastocysts do not show increased sensitivity to gamma radiation or MMS.

Conclusions:

  • Rad51d is essential for normal embryonic development in mice.
  • Defects suggest suboptimal DNA repair or cell cycle perturbation in Rad51d-deficient embryos.
  • Rad51d plays a critical, non-redundant role in embryonic development, likely through its function in DNA repair.

Related Experiment Videos