Plaks, V., Department of Biological Regulation of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel, Department of Anatomy, University of California, San Francisco, CA, United States
Gershon, E., Department of Biological Regulation of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel, Department of Ruminant Science, Volcani Center, Bet Dagan, Israel
Zeisel, A., Department of Physics of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel
Jacob-Hirsch, J., Sheba Cancer Research Center, Sheba Medical Center, Tel Hashomer, Israel
Neeman, M., Department of Biological Regulation of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel
Winterhager, E., Institute of Anatomy, University Hospital Duisburg-Essen, Essen, Germany
Rechavi, G., Sheba Cancer Research Center, Sheba Medical Center, Tel Hashomer, Israel
Domany, E., Department of Physics of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel
Dekel, N., Department of Biological Regulation of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel

Oocyte quality is a well-established determinant of embryonic fate. However, the molecular participants and biological markers that affect and may predict adequate embryonic development are largely elusive. Our aim was to identify the components of the oocyte molecular machinery that part take in the production of a healthy embryo. For this purpose, we used an animal model, generated by us previously, the oocytes of which do not express Cx43 (Cx43 del/del). In these mice, oogenesis appears normal, fertilisation does occur, early embryonic development is successful but implantation fails. We used magnetic resonance imaging analysis combined with histological examination to characterise the embryonic developmental incompetence. Reciprocal embryo transfer confirmed that the blastocyst evolved from the Cx43del/del oocyte is responsible for the implantation disorder. In order to unveil the genes, the impaired expression of which brings about the development of defective embryos, we carried out a genomic screening of both the oocytes and the resulting blastocysts. This microarray analysis revealed a low expression of Egr1, Rpl21 and Eif4a1 in Cx43del/del oocytes and downregulation of Rpl15 and Eif4g2 in the resulting blastocysts. We propose that global deficiencies in genes related to the expression of ribosomal proteins and translation initiation factors in apparently normal oocytes bring about accumulation of defects, which significantly compromise their developmental capacity. The blastocysts resulting from such oocytes, which grow within a confined space until implantation, may be unable to generate enough biological mass to allow their expansion. This information could be implicated to diagnosis and treatment of infertility, particularly to IVF.