A question that remains unanswered is con cerned with the nature of the transcriptional networks in which maternal effect genes operate. This knowledge would further our understanding of the molecular identity of a developmentally competent egg and would allow to investi gate how this identity is modified during the switch to an embryonic control of development. Oct4 is one of the 27 maternal effect genes reported so far whose transcripts inherited by the zygote are necessary for development beyond the 2 cell stage. Most of our knowledge on Oct4 functions comes from studies that describe its key role in the control of tran scriptional regulatory circuits that maintain pluripotency in the inner cell mass of Inhibitors,Modulators,Libraries the blastocyst and in embryonic stem cells.

Furthermore, OCT4 is recognised for its capacity, when ectopically expressed in combination with other transcription factors, to reprogram differentiated cells into pluripotent cells. Recent studies have also shown a role for OCT4 in the acquisition of the egg developmental competence. During oocyte growth the OCT4 protein is first detected at Inhibitors,Modulators,Libraries the time of follicle recruitment, only in one of two major classes of oocytes present in the mouse ovary, named surrounded nucleolus oocytes and recognisable for the presence of a ring of heterochromatin surrounding their nucleolus, on the contrary, OCT4 expression is comparativelly down regulated in NSN oocytes that lack of a ring of heterochromatin around the nucleolus. Entinostat This distinct pattern of expression is maintained throughout oocyte growth, in fully matured antral SN and NSN oocytes and in their derived MIISN and MIINSN oocytes, respectively.

The most strik ing difference between these Inhibitors,Modulators,Libraries two categories of oocytes is that only MIISN oocytes may develop beyond the 2 cell stage and reach full term development. OCT4 down regulation in MIINSN oocytes correlates with the down regulation of the maternal effect factor STELLA and with the up regulation of eighteen OCT4 regulated genes that are part of a gene expres sion network implicated in mitochondrial dysfunction and apoptosis, explaining the developmental block encountered by 2 cell embryos obtained from MIINSN oocytes. This data indicate that Oct4 is an important component of a maternal regulatory TN that influences positively or negatively the oocyte developmental competence.

The molecular identity and extension of this TN, as much as whether its pre sence is circumscribed to the egg or, after fertilisation, is maintained beyond the first mitotic division, remains to be understood. In the present study, by comparing the genome wide transcriptional profile Inhibitors,Modulators,Libraries of ovulated MII oocytes that express the OCT4 protein to that of MII oocytes in which OCT4 is comparativelly down regulated, we unveiled an expanded maternal Oct4 TN made of 182 genes.