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Cse1l is essential for early embryonic growth and development

  1. Author:
    Bera, T. K.
    Bera, J.
    Brinkmann, U.
    Tessarollo, L.
    Pastan, I.

  2. Author Address

    NCI, Mol Biol Lab, NIH, Bldg 37, Room 4E16, 37 Convent Dr, MSC 4255, Bethesda, MD 20892 USA. NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, Mammalian Genet Lab, NIH, Frederick, MD 21702 USA. Pastan I NCI, Mol Biol Lab, NIH, Bldg 37, Room 4E16, 37 Convent Dr, MSC 4255, Bethesda, MD 20892 USA.
    1. Year: 2001
  2. Journal: Molecular and Cellular Biology
    1. 21
    2. 20
    3. Pages: 7020-7024
  4. Type of Article: Article
  1. Abstract:

    The CSE1L gene, the human homologue of the yeast chromosome segregation gene CSE1, is a nuclear transport factor that plays a role in proliferation as well as in apoptosis. CSE1 and CSE1L are essential genes in Saccharomyces cerevisiae and mammalian cells, as shown by conditional yeast mutants and mammalian cell culture experiments with antisense-mediated depletion of CSE1L. To analyze whether CSE IL is also essential in vivo and whether its absence can be compensated for by other genes or mechanisms, we have cloned the murine CSE1L gene (Cse1l) and analyzed its tissue- and development-specific expression: Csell was detected at embryonic day 7.0 (E7.0), E11.0, E15.0, and E17.0, and in adults, high expression was observed in proliferating tissues. Subsequently, we inactivated the Csell gene in embryonic stem cells to generate heterozygous and homozygous knockout mice. Mice heterozygous for Csell appear normal and are fertile. However, no homozygous pups were born after interbreeding of heterozygous mice. In 30 heterozygote interbreeding experiments, 50 Csell wild-type mice and 100 heterozygotes were born but no animal with both Csell alleles deleted was born. Embryo analyses showed that homozygous mutant embryos were already disorganized and degenerated by E5.5. This implicates with high significance (P < 0.0001, Pearson chi- square test) an embryonically lethal phenotype of homozygous murine CSE1 deficiency and suggests that Csell plays a critical role in early embryonic development.

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