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Architectural reorganization of the nuclei upon transfer into oocytes accompanies genome reprogramming
Author(s) -
Martin Catherine,
Brochard Vincent,
Migné Carole,
Zink Daniele,
Debey Pascale,
Beaujean Nathalie
Publication year - 2006
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20506
Subject(s) - biology , nucleolus , genetics , chromatin , reprogramming , heterochromatin , microbiology and biotechnology , somatic cell nuclear transfer , blastocyst , somatic cell , zygote , embryo , gene , embryogenesis , nucleus
The ability of cloned embryos to sustain full‐term development depends on the ability of the recipient ooplasm to reprogram the donor cell genome. As the nuclear architecture has recently emerged as a key‐factor in the regulation of gene expression, we questioned whether early embryos obtained from transfer of ES metaphasic chromosomes into mouse ooplasm would adopt the somatic or embryonic type of nuclear organization. We have particularly focused on the arrangement of chromosomal territories with respect to the nucleolar compartment, and the pericentric heterochromatin domains called chromocenters. We found that nuclear transfer triggers profound chromatin rearrangements including the dispersion of the donor cell chromocenters components. These rearrangements lead to a typical 1‐cell pronuclear organization, namely a radial arrangement of the chromosome territories with centromeres attached to the nucleoli, which adopt the compact fibrillar structure of nucleolar precursor bodies (NPBs). Subsequently, during the second cycle, the cloned embryos undergo further reorganization with the establishment of new chromocenters, clustered in one part of the nucleus, as during normal embryogenesis. We could also establish that the adequate distribution of chromosomal territories at the pronuclear stage seems important for the development until blastocyst. Mol. Reprod. Dev. 1102–1111, 2006. © 2006 Wiley‐Liss, Inc.