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Mcl-1 deficiency results in peri-implantation embryonic lethality.

We disrupted the Mcl-1 locus in murine ES cells to determine the developmental roles of this Bcl-2 family member. Deletion of Mcl-1 resulted in peri-implantation embryonic lethality. Mcl-1(-/-) embryos do not implant in utero, but could be recovered at E3.5-4.0. Null blastocysts failed to hatch or attach in vitro, indicating a trophectoderm defect, although the inner cell mass could grow in culture. Of note, Mcl-1(-/-) blastocysts showed no evidence of increased apoptosis, but exhibited a delay in maturation beyond the precompaction stage. This model indicates that Mcl-1 is essential for preimplantation development and implantation, and suggests that it has a function beyond regulating apoptosis.

Pubmed ID: 10640272


  • Rinkenberger JL
  • Horning S
  • Klocke B
  • Roth K
  • Korsmeyer SJ


Genes & development

Publication Data

January 1, 2000

Associated Grants

  • Agency: NCI NIH HHS, Id: CA49712-10

Mesh Terms

  • Animals
  • Apoptosis
  • Crosses, Genetic
  • Embryo Implantation
  • Female
  • Fetal Death
  • Humans
  • In Situ Hybridization
  • In Situ Nick-End Labeling
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Neoplasm Proteins
  • Polymerase Chain Reaction
  • Proto-Oncogene Proteins c-bcl-2