TY - JOUR
T1 - Impaired mitotic progression and preimplantation lethality in mice lacking OMCG1, a new evolutionarily conserved nuclear protein.
AU - Artus, Jérôme
AU - Vandormael-Pournin, Sandrine
AU - Frödin, Morten
AU - Nacerddine, Karim
AU - Babinet, Charles
AU - Cohen-Tannoudji, Michel
N1 - Keywords: Amino Acid Sequence; Animals; Blastocyst; Cell Cycle Proteins; Conserved Sequence; Embryonic Development; Evolution; Female; Gene Expression; Genes, Lethal; Histones; Mice; Mitosis; Mitotic Spindle Apparatus; Molecular Sequence Data; Mutation; Nuclear Proteins; Pregnancy; Protein Processing, Post-Translational; Zinc Fingers
PY - 2005
Y1 - 2005
N2 - While highly conserved through evolution, the cell cycle has been extensively modified to adapt to new developmental programs. Recently, analyses of mouse mutants revealed that several important cell cycle regulators are either dispensable for development or have a tissue- or cell-type-specific function, indicating that many aspects of cell cycle regulation during mammalian embryo development remain to be elucidated. Here, we report on the characterization of a new gene, Omcg1, which codes for a nuclear zinc finger protein. Embryos lacking Omcg1 die by the end of preimplantation development. In vitro cultured Omcg1-null blastocysts exhibit a dramatic reduction in the total cell number, a high mitotic index, and the presence of abnormal mitotic figures. Importantly, we found that Omcg1 disruption results in the lengthening of M phase rather than in a mitotic block. We show that the mitotic delay in Omcg1-/- embryos is associated with neither a dysfunction of the spindle checkpoint nor abnormal global histone modifications. Taken together, these results suggest that Omcg1 is an important regulator of the cell cycle in the preimplantation embryo.
AB - While highly conserved through evolution, the cell cycle has been extensively modified to adapt to new developmental programs. Recently, analyses of mouse mutants revealed that several important cell cycle regulators are either dispensable for development or have a tissue- or cell-type-specific function, indicating that many aspects of cell cycle regulation during mammalian embryo development remain to be elucidated. Here, we report on the characterization of a new gene, Omcg1, which codes for a nuclear zinc finger protein. Embryos lacking Omcg1 die by the end of preimplantation development. In vitro cultured Omcg1-null blastocysts exhibit a dramatic reduction in the total cell number, a high mitotic index, and the presence of abnormal mitotic figures. Importantly, we found that Omcg1 disruption results in the lengthening of M phase rather than in a mitotic block. We show that the mitotic delay in Omcg1-/- embryos is associated with neither a dysfunction of the spindle checkpoint nor abnormal global histone modifications. Taken together, these results suggest that Omcg1 is an important regulator of the cell cycle in the preimplantation embryo.
U2 - 10.1128/MCB.25.14.6289-6302.2005
DO - 10.1128/MCB.25.14.6289-6302.2005
M3 - Journal article
C2 - 15988037
SN - 0270-7306
VL - 25
SP - 6289
EP - 6302
JO - Molecular and Cellular Biology
JF - Molecular and Cellular Biology
IS - 14
ER -