Autophagy means “self-eating” and it is a major catabolic pathway within cells. A basal level of autophagy is required for survival of cells or organisms, but prolonged activation of autophagy may have an adverse effect. In mammalian systems, autophagy is stimulated by nutrient starvation or deprivation of growth factors. Ovariectomy on day 4 of pregnancy in mice to deprive blastocysts of estrogen induces “dormancy” in blastocysts and delay the process of implantation until estrogen is given. Dormant blastocysts maintain a state of low metabolism in utero and survive for many days without initiating implantation under the unfavorable condition of estrogen deficiency. We tested the hypothesis if an autophagic response is operative in dormant blastocysts for prolonged survival in utero during the delayed implantation. We observed that autophagy is highly activated in dormant blastocysts. Interestingly, autophagic activation is more prominent in trophectoderm than in inner cell mass. Activation of blastocysts by estrogen supplementation induces formation of multivesicular bodies and exosomes in the trophectoderm. Dormant blastocysts with longer period of autophagic activation show compromised development after implantation. Thus, autophagy may be a critical cellular mechanism to provide energy source during extended survival of dormant blastocysts. However, prolonged activation of autophagy may compromise developmental outcome of blastocysts with irreparable cellular damage.

• Hyunjung (Jade) Lim(Department of Veterinary Medicine, Konkuk University)