Abstract
BackgroundThe decline in amphibian populations across the world is frequently linked to the infection of the chytrid fungus Batrachochytrium dendrobatidis (Bd). This is particularly perplexing because Bd was only recently discovered in 1999 and no chytrid fungus had previously been identified as a vertebrate pathogen.ResultsIn this study, we show that two large families of known virulence effector genes, crinkler (CRN) proteins and serine peptidases, were acquired by Bd from oomycete pathogens and bacteria, respectively. These two families have been duplicated after their acquisition by Bd. Additional selection analyses indicate that both families evolved under strong positive selection, suggesting that they are involved in the adaptation of Bd to its hosts.ConclusionsWe propose that the acquisition of virulence effectors, in combination with habitat disruption and climate change, may have driven the Bd epidemics and the decline in amphibian populations. This finding provides a starting point for biochemical investigations of chytridiomycosis.
Highlights
The decline in amphibian populations across the world is frequently linked to the infection of the chytrid fungus Batrachochytrium dendrobatidis (Bd)
Among the several factors often linked to the decline in amphibian populations is the chytrid fungus Batrachochytrium dendrobatidis (Bd), the causative agent of chytridiomycosis
Our data show that two large families of known virulence effector genes, CRN proteins and serine peptidases, were likely transferred to Bd from oomycete pathogens and bacteria, respectively
Summary
The decline in amphibian populations across the world is frequently linked to the infection of the chytrid fungus Batrachochytrium dendrobatidis (Bd). This is perplexing because Bd was only recently discovered in 1999 and no chytrid fungus had previously been identified as a vertebrate pathogen. Long-term population studies since the 1900’s had no records of mass mortalities until the late 1970’s when the first Bd epidemics were reported [8]. This leads to an interesting question about how pathogenesis suddenly evolved in this previously benign organism
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