Early oocytes of nearly all animal species contain a transient organelle assemblage termed the Balbiani body. Structure and composition of this assemblage may vary even between closely related species. Despite this variability, the Balbiani body always comprises of numerous tightly clustered mitochondria and accumulations of nuage material. It has been suggested that the Balbiani body is an evolutionarily ancestral structure, which plays a role in various processes such as the localization of organelles and macromolecules to the germ plasm, lipidogenesis, as well as the selection/elimination of dysfunctional mitochondria from female germline cells. We suggest that the selection/elimination of mitochondria is a primary and evolutionarily ancestral function of Balbiani body, and that the other functions are secondary, evolutionarily derived additions. We propose a simple model explaining the role of the Balbiani body in the selection of mitochondria, i.e., in the mitochondrial DNA (mtDNA) bottleneck phenomenon.

The most important role of mitochondria is to supply cells with metabolic energy in the form of adenosine triphosphate (ATP). As synthesis of ATP molecules is accompanied by the generation of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) is highly vulnerable to impairment and, consequently, accumulation of deleterious mutations. In most animals, mitochondria are transmitted to the next generation maternally, i.e., exclusively from female germline cells (oocytes and eggs). It has been suggested, in this context, that a specialized mechanism must operate in the developing oocytes enabling escape from the impairment and subsequent transmission of accurate (devoid of mutations) mtDNA from one generation to the next. Literature survey suggest that two distinct and irreplaceable pathways of mitochondria transmission may be operational in various animal lineages. In some taxa, the mitochondria are apparently selected: functional mitochondria with high inner membrane potential are transferred to the cells of the embryo, whereas those with low membrane potential (overloaded with mutations in mtDNA) are eliminated by mitophagy. In other species, the respiratory activity of germline mitochondria is suppressed and ROS production alleviated leading to the same final effect, i.e., transmission of undamaged mitochondria to offspring, via an entirely different route.