Recent headlines highlight the alarming rate at which species are being forced into extinction, and amphibians are particularly vulnerable. Up to 41% of frog, toad, newt, salamander, caecilian, and other amphibian species are listed as Vulnerable, Endangered, or Critically Endangered, and although habitat loss and other factors play a role in these extinctions and near-extinctions, it is now clear that a pathogenic fungus is responsible for the threatened state of many amphibian species. Batrachochytrium dendrobatidis, often called chytrid fungus or Bd, causes chytridiomycosis, a disease that strikes entire populations, causing widespread declines that can eventually lead to extinction.
But the Bd picture is far from complete. We know that Bd causes an electrolyte imbalance in amphibian bodies, and that it may suppress the immune system to some extent, but we have little understanding of its pathogenicity on a molecular level.
John Abramyan and Jason Stajich of UC Riverside examined the genomes of two Bd isolates to find clues about its pathogenicity, reasoning that since Bd is the only known amphibian pathogen in its phylum, its genome must bear the marks of restructuring to adapt to its new environmental niche and exploit its amphibian hosts. Other fungal lineages that evolved into pathogens or adapted to new host types have gained or lost genes and often showed signs of lineage-specific expansions of certain gene families and domains within a gene. Does Bd have telltale genome differences like these that could give away how the fungus causes disease?
Abramyan and Stajich say "yes". Compared with its fellow phylum members, Bd genomes have an expanded number of genes in the Carbohydrate-Binding Module Family 18 (CBM18), a family of proteins linked to pathogenicity in other fungal species. The expansions have been limited to three categories of genes, each of which has been implicated in host-pathogen interactions in the past.
This expansion in CBM18 could well mean it plays a role in the mode of pathogenicity of Bd an offers clues for future work to elucidate the why and how of chytrid disease in amphibians.
The results may also lead to a better understanding of the ecology of Bd and how it might be controlled. The authors predict that one of the categories of genes affected, lectin-like genes, function as lectins, possibly binding chitin in the way other lectin-like genes do in other fungal species. In other fungi, chitin-binding molecules protect the fungus from attack by plant chitin-targeting enzymes, and could protect Bd from amphibian chitinases. Or Bd may use its ability to bind chitin to attach itself to chitin-containing structures outside the host. This may mean Bd can attach and survive in ponds and wet places amphibians live, a crucial piece of knowledge that, if true, could have serious implications for amphibian conservation and eradication of the fungus.