Fungi are a complex group with features ranging between plant and animal kingdom. A group of researchers have finally found some insight into a pathogenic fungi’s biological processes, which is known for causing devastating skin infection in frogs. The organism belongs to ‘chytrid’ group of fungi. Using the Batrachochytrium dendrobatidis (Bd)’s actin networks as a sample or an “evolutionary Rosetta Stone”, the researchers have revealed how the loss of cytoskeletal complexity happens in the fungus kingdom.
“Figuring out the basic biology of Bd will hopefully give insight into disease mitigation in the future,” said author Sarah Prostak.
Bd causes chytridiomycosis which destroys skins of frogs and other amphibians to the extent that they can die of heart failure. Frogs are important in maintaining ecological balance and the disease leads to loss of biodiversity. Dozens of species are presumed either extinct or threatened in the last five decades because of this disease.
“Fungi and animals seem so different, but they are actually pretty closely related. This work shows that during early fungal evolution, fungi probably had cells that looked something like our cells, and which could crawl around as our cells do,” said co-author, Lillian Fritz-Laylin of the University of Massachusetts Amherst (UMass Amherst).
Most fungi like yeast have lost features similar to animal cells during evolution. However, groups like Bd still share features with eukaryotes. This way, the evolution of actin cytoskeleton can be studied, the process of cells keeping their shape, organising, and their mobility. Even cell division and other vital functions are dependant on actin.
According to lead author Prostak, animal and fungal lineage can be tracked using Bd on account of its closeness to animal cells. Animal cells, including humans, have a much more complex actin network with a multitude of regulators. Whereas Bd has a comparatively simpler system which makes it easier to study.
They observed Bd’s two life-cycles. In the first one, flagellum and actins (similar to animal cells) help the zoospores swim. Then comes a reproductive stage where they become more similar to yeast as sporangia assemble actin shells and patches.
This actin is what aids the disease’s pathogenicity and propagation. Understanding this can help disease mitigation in the future, says Prostak.
Other authors of the paper include Margaret Titus, professor of genetics, cell biology and development at the University of Minnesota, and Kristyn Robinson, a UMass Amherst PhD candidate in Fritz-Laylin's lab.