162. FRIEND OR FOE? THE ROLES OF PAF AND p53 DURING EMBRYONIC DIAPAUSE
J. C. Fenelon A B , C. O’Neill C , G. Shaw A B and M. B. Renfree A BA ARC Centre of Excellence for Kangaroo Genomics, Australia.
B Zoology, University of Melbourne, Parkville, VIC, Australia.
C Royal North Shore Hospital, The University of Sydney, Sydney, NSW, Australia.
Reproduction, Fertility and Development 22(9) 80-80 https://doi.org/10.1071/SRB10Abs162
Published: 6 September 2010
Abstract
In the tammar wallaby, Macropus eugenii, the blastocyst normally remains in embryonic diapause for 11 months without cell division or apoptosis occurring. Progesterone regulates reactivation by inducing active secretion from the endometrium, but the molecular cross-talk between the endometrium and blastocyst is unknown. This process may involve the phospholipid paf. Paf is an embryotrophin that acts as a trophic/survival factor in the early embryo, partly by inactivating (via the PI3K/Akt pathway) the expression of p53, a cell cycle arrest factor (1,2). In vitro, paf production from the tammar endometrium increases after diapause (3). This study examined the expression of the paf receptor (pafr) and p53 in the tammar endometrium and embryo at entry into, during and reactivation from diapause. Both pafr and p53 mRNA were expressed in the endometrium at all stages. However there was no quantitative change in pafr expression. In the endometrium, pafr protein is present on the membrane of the glandular epithelium at all stages examined, but p53 was not expressed in the endometrial nuclei at any stage and hence does not appear to be active. Both pafr and p53 mRNA were also expressed in the embryo from the early cleavage stages, during diapause and in the reactivated blastocyst. Pafr protein was present in the embryo both before and after diapause, but levels were greatly reduced during diapause, indicating it may be necessary for active growth. Unexpectedly, the expression of p53 in the embryo does not appear to depend on the presence or absence of pafr. p53 was expressed in the nuclei of the cleavage stage embryonic cells before diapause, but not during or after diapause. These results suggest that paf and pafr may participate in the molecular control of embryonic diapause in the tammar independent of p53.
(1) Jin XL et al. (2009) Biology of Reproduction 80: 286–294.
(2) O’Neill C (2005) Human Reproduction Update 11(3): 215–228.
(3) Kojima T et al. (1993) Reproduction Fertility Development 5: 15–25.
