Project description:Amphibian populations around the world are threatened by an emerging infectious pathogen, the chytrid fungus Batrachochytrium dendrobatidis (Bd). How can a fungal skin infection kill such a broad range of amphibian hosts? And why are certain species particularly susceptible to the impacts of Bd? Here we use a genomics approach to understand the genetic response of multiple susceptible frog species to Bd infection. We characterize the transcriptomes of two closely-related endangered frog species (Rana muscosa and Rana sierrae) and analyze whole genome expression profiles from frogs in controlled Bd-infection experiments. We integrate the Rana results with a comparable dataset from a more distantly-related susceptible species (Silurana tropicalis). We demonstrate that Bd-infected frogs show massive disruption of skin function and show no evidence of a robust immune response. The genetic response to infection is shared across the focal susceptible species, suggesting a common effect of Bd on susceptible frogs.
Project description:Amphibian populations around the world are threatened by an emerging infectious pathogen, the chytrid fungus Batrachochytrium dendrobatidis (Bd). How can a fungal skin infection kill such a broad range of amphibian hosts? And why are certain species particularly susceptible to the impacts of Bd? Here we use a genomics approach to understand the genetic response of multiple susceptible frog species to Bd infection. We characterize the transcriptomes of two closely-related endangered frog species (Rana muscosa and Rana sierrae) and analyze whole genome expression profiles from frogs in controlled Bd-infection experiments. We integrate the Rana results with a comparable dataset from a more distantly-related susceptible species (Silurana tropicalis). We demonstrate that Bd-infected frogs show massive disruption of skin function and show no evidence of a robust immune response. The genetic response to infection is shared across the focal susceptible species, suggesting a common effect of Bd on susceptible frogs. A total of five (12-plex) chips were analyzed from 60 samples comprising 2 conditions (control and infected), 3 tissues (skin, liver and spleen) and 2 timepoints (early and late). Three biological replicates were used for each condition and tissue at each time point. Twentyfour arrays were analyzed for skin samples, 24 for liver, and 12 for spleen. The same dye, Cy5, was used for all samples.
Project description:Global amphibian declines and extinction events are currently occurring at an unprecedented rate. While various factors are influencing these declines, one factor that is readily identifiable is disease. Specifically, the fungal pathogen Batrachochytrium dendrobatidis is thought to play a major role in amphibian declines in tropical and neotropical regions of the globe. While the effects of this chytrid fungus have been shown to be devastating, certain individuals and relict populations have shown resistance. This resistance has been attributed in part to the cutaneous microbiome. Many identified bacterial species that make up the microbiome have shown anti-B. dendrobatidis activity in vitro. One bacteria that is commonly associated as being a member of the amphibian microbiome across amphibian species and shows such anti-B. dendrobatidis activity is Serratia marcescens. Here, we look at transcriptomic shifts in gene expression of S. marcescens (high homology to strain WW4) in response to both live and heat-killed B. dendrobatidis.
2016-07-11 | GSE84057 | GEO
Project description:Amphibian mast cells: barriers to deadly chytrid fungus infections
Project description:The fungal skin disease chytridiomycosis has caused the devastating decline and extinction of hundreds of amphibian species globally, yet the potential for evolving resistance, and the underlying pathophysiological mechanisms remain poorly understood. We exposed 406 naïve, captive-raised alpine tree frogs (Litoria verreauxii alpina) to the aetiological agent Batrachochytrium dendrobatidis in two concurrent and controlled infection experiments. We investigated (A) survival outcomes and clinical pathogen burdens between populations and clutches, and (B) individual host tissue responses to chytridiomycosis. Here we present multiple interrelated datasets associated with these exposure experiments, including animal signalment, survival and pathogen burden of 355 animals from Experiment A, and the following datasets related to 61 animals from Experiment B: animal signalment and pathogen burden; raw RNA-Seq reads from skin, liver and spleen tissues; de novo assembled transcriptomes for each tissue type; raw gene expression data; annotation data for each gene; and raw metabolite expression data from skin and liver tissues. These data provide an extensive baseline for future analyses.
Project description:Albinism results from defects in melanin synthesis and is associated with increased sensitivity to ultraviolet (UV) radiation. While the genetic basis of albinism is well studied, the systemic physiological consequences of melanin deficiency remain poorly understood, particularly in amphibians where the skin serves additional respiratory and osmoregulatory functions. Here we investigated the morphological, physiological and transcriptomic basis of the albino phenotype in the American bullfrog (Rana catesbeiana), a species that naturally experiences variable UVB exposure in its aquatic habitats. We compared albino and wild‑type bullfrogs using histology, a time‑course UVB irradiation experiment (1000 μW cm⁻² for 4 h with five recovery time points), and multi‑tissue transcriptomics of dorsal skin, liver and eyeball. Albino bullfrogs completely lacked melanin in skin and retina. Under basal conditions, they had markedly lower total antioxidant capacity (T‑AOC) and catalase (CAT) activity in skin and liver, and showed elevated protein carbonyl content, indicating chronic oxidative stress. After UVB exposure, wild‑type bullfrogs mounted a dynamic antioxidant response, whereas albino individuals failed to recover. Transcriptomic analysis identified 520, 1074 and 1355 differentially expressed genes in skin, liver and eye, respectively, with 51 genes shared across all three tissues. Unexpectedly, key melanogenic genes (TYR, TYRP1, MLANA, SLC24A5, OCA2) were significantly upregulated in albino skin and eye–a paradoxical finding given the absence of pigment. Pathway enrichment revealed direct photoxidative damage in the two light‑exposed organs (skin: downregulation of glutathione metabolism; eye: downregulation of cell cycle, p53 and DNA replication pathways) and secondary metabolic stress in the liver (downregulation of PPAR and glutathione pathways). qRT‑PCR validation of four representative genes (TYR, CHAC1, GADD45A, ARL5C) confirmed the RNA‑seq trends (Pearson’s R² = 0.91). These results demonstrate that albinism in the bullfrog is not merely a local pigmentation defect but a systemic condition involving direct photoxidative injury to skin and eye, secondary oxidative burden on the liver, and a paradoxical transcriptional activation of the melanogenic machinery. Our findings provide a multi‑tissue resource for understanding the physiological consequences of pigmentation loss in vertebrates and highlight the vulnerability of albino individuals to environmental UVB exposure.
Project description:Chytridiomycosis is an emerging infectious disease of amphibians caused by the chytrid Batrachochytrium dendrobatidis (Bd). The disease has been associated with global amphibian declines and is driving the species in the wild to extinction. Using DNA microarray technology we have analysed transcriptional changes in Xenopus tropicalis during the course (7 and 42 days) of infection by Bd under warm (26oC) and cold (18oC) temperatures.