Ameson portunus infection is associated with RK13 mitochondrial abnormalities

Abstract

Microsporidia are obligate intracellular parasites with an extremely broad host range from invertebrates to vertebrates. Although host mitochondria were proved to be critical for the intracellular survival and propagation, their precise morphological and functional variation during microsporidian infection remain largely unclear. In this study, we firstly developed a feasible approach to track microsporidia proliferation by using a live-cell fluorescent dye DiI in the Ameson portunus-RK13 model. DiI-labeled A. portunus was observed to be surround by host mitochondria at 6 hpi (hours post infection) and gradually induced mitochondrial fragmentation in RK13 cells at 8 dpi (days post infection). Ultrastructural observation further revealed some mitochondria exhibited distinct swelling, and dissolution and fragmentation of cristae. Then, RNA sequencing of A. portunus-infected and uninfected RK13 cells at 8 dpi was employed to uncover the possible mechanisms underlying these mitochondrial abnormities. GSEA analysis revealed 11 mitochondrial structure- and function-related process were upregulated upon the infection of A. portunus. The expression alteration of genes related to mitochondrial fusion and fission might contribute to mitochondrial fragmentation, and the upregulation of genes encoding the components of mitochondrial respiratory chain and ATP synthesis coupled proton transport implied the increase of ATP production upon microsporidian infection. Upregulated expression of genes associated with the maintenance of mitochondrial morphology was possibly associated with mitochondrial swelling, and cristae dissolution and fragmentation. The upregulation of genes involved in mitophagy and mitochondrial protein biosynthesis was suggested to be involved in the maintenance of mitochondrial homeostasis against the infection. Collectively, our findings provide further information on the host mitochondria-involved pathophysiological responses to this microsporidian infection.