The Innate Immune System and Post-Fertilization Paternal Mitochondrial Autophagy in Caenorhabditis elegans
In many species the mitochondrial genome is maternally inherited despite the fact that paternal mitochondria enter the egg during fertilization. The model organism Caenorhabditis elegans is no exception to this phenomena. It has recently been shown that these paternal mitochondria are degraded in the egg through autophagy. However, it is not known what triggers this targeted autophagy. Curiously, the innate immune system has recently been shown to trigger the clearance of mitochondria in C. elegans. The Mitogen Activated Kinase p38MAPK is a key component in triggering the innate immune response in C. elegans as it activates the transcription factor ATF-7, which is responsible for the upregulation of many genes involved in the response. Through the use of an innate immune system deficient strain of C. elegans in mating experiments and Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) to assess mRNA levels, we explored the involvement of the innate immune system in the targeted autophagy of paternal mitochondria. qRT-PCR analysis revealed the activation of the innate immune system upon mating in wild-type worms, indicating the innate immune response does serve some function post-mating. Mating experiments between males harboring mitochondria stained with a vital dye, and unstained hermaphrodites were used to observe the progressive degradation of mitochondria in both wild-type worms and innate immune system deficient worms. It was found that innate immune system deficient worms contained significantly more paternal mitochondria at the 8 cell stage of the egg and had paternal mitochondria that persisted longer into development.