The autophagic pathway is an evolutionarily conserved homeostatic process, responsible for degradation and recycling of long-term proteins and cytoplasmic organelles in eukaryotic cells. This process constitutively occurs at basal levels and is involved in cell survival. Increased autophagy is induced by environmental cues, such as starvation and many stress agents, while excessive levels of autophagy can lead to autophagic Programmed Cell Death, with features that differ from those of the apoptotic process. We recently demonstrated massive activation of autophagy in P. lividus embryos, in cadmium stress conditions, and the existence of a temporal relationship between induced autophagy end apoptosis. Although there are numerous studies on the role of autophagy during development of different organisms, only a few of them examine its role during oocyte maturation and early embryogenesis.Here we report our recent data about the occurrence of autophagy, from oogenesis to early stages of embryogenesis. By detection and quantification of autophagic markers i.e. acidic vesicular Organelles (AVOs) and LC3-II protein we observed that: i) oocytes and early developmental stages exhibit a peculiar localization of autophagic signals; ii) these signals greatly increase after fertilization until 32 blastomeres; iii) interestingly a short autophagic inhibition, after fertilization, strongly interferes with starting developmental program, causing evident and irreversible impairments of morphology, as well as induction of apoptosis at gastrula stage. These data lead to the hypothesis that autophagy could act: i) during oogenesis, for recycling of cellular components and for elimination of the germinal vesicle; ii) during early embryogenesis, for yolk digestion or for removal of obsolete proteins and organelles; iii) in the micromeres for some mechanism probably linked to the subsequent gastrulation. Altogether these considerations pave the way for further investigation on the role of autophagy during development.
|Number of pages||1|
|Publication status||Published - 2015|