62-10 Sat Jan 2 Chytrid fungi transcriptomic signatures indicate different infection strategies in newts Torres-Sánchez, M*; McGrath-Blaser, S; Villate, J; Longo, AV; University of Florida, Department of Biology, Gainesville, FL 326011; University of Florida, Department of Biology, Gainesville, FL 326011; University of Florida, Department of Biology, Gainesville, FL 326011 mtorressanchez@ufl.edu
The chytrid fungi Batrachochytrium dendrobatidis (Bd) and Batrachochytrium salamandrivorans (Bsal) are two of the most relevant pathogens in vertebrates due to their broad host range and their devastating effects on amphibians. However, we know little about the functional processes driving the invasion dynamics and disease outcome across hosts, and much less between single pathogen infections and coinfections. Here, we used publicly available RNA-seq data to find evidence of different infection strategies. We analyzed the transcripts from the skin of two species of newts (Notophthalmus viridescens and Tylototriton wenxianensis) singly infected with one or the other fungal pathogen, the transcripts from the skin of N. viridescens coinfected with both fungi, and performed four differential gene expression analyses: (i) Bd and (ii) Bsal expression between N. viridescens and T. wenxianensis, and (iii) Bd and (iv) Bsal expression between single and co-infection in N. viridescens. Overall, we uncovered distinct invasion strategies with significant changes in the fungal genetic machinery that is used to infect hosts. We also documented variation in the patterns of gene expression in coinfections that might be related to ecological competition between fungi. Many differentially expressed genes were related to DNA replication and synthesis/modification of proteins. Our findings showed that Bd chitin-related genes, which can modify the structural composition of the fungus, shifted their expression levels in coinfections. Finally, we detected expression changes in several genes encoding heat shock proteins, which could reflect hormesis processes (i.e. inhibition, toxicity) as a result of Bd–Bsal and host-pathogen interactions.