Exogenous paternal mitochondria rescue hybrid incompatibility and the destiny of exogenous mitochondria

The mitochondria of most organisms follow strict maternal inheritance, and the mechanism of elimination of paternal mitochondria is unclear. Our previous studies showed that the paternal mtDNA presented in the embryo of hybrid Megalobrama Amblycephala (BSB,♀) ​× ​Carassius auratus red var(RCC,♂) (BR) and its reciprocal hybrid (RB), but its expression was quiescent. However, the microinjected mitochondria persisted in the embryo and its mtDNA expressed throughout embryonic development. In addition, the chromosome number of RCC (2n ​= ​100) is much larger than that of BSB (2n ​= ​48). All BR embryos were severely abnormal and ultimately died, while the RB embryos could survive and grow up into adult. It implied that the nuclear-cytoplasm incompatibility may be an important cause of BR abnormality. In this study, exogenous parental mitochondria were microinjected into BR embryos, and it was found that paternal mitochondrial DNA persisted and expressed throughout embryonic development. Meanwhile, the study also found that microinjection of isolated paternal (RCC) mitochondria into BR embryos significantly improved the degree of early embryonic abnormality with some fry swimming normally, comparing to the control embryos. However, injection of maternal (BSB) mitochondria did not improve the development of BR embryos. We safely concluded exogenous mitochondria escape the mechanism of elimination and its DNA persist and express throughout embryonic development. In addition, the expression of paternal mitochondrial genes largely reduces the cyto-nuclear conflict, so that the early BR embryos exhibit less degree of abnormality and enhanced activity.