UMass scientists fight a deadly fungus on a molecular level
Over the last several decades, hundreds of amphibian species around the world have become endangered or extinct. The cause? A unique type of fungus known as Batrachochytrium dendrobatidis (Bd). As the fungal infection grows, it makes it hard for amphibians to regulate their body temperature, release gases, and breathe; eventually, this leads to heart failure.
As anyone who has taken high school biology knows, changes in the composition of the animal kingdom have widespread impacts. With each extinction, the food chain is forced to adapt. On a global scale, the changes can be catastrophic. With increased frog deaths, for instance, mosquito populations are on the rise—spreading mosquito-borne diseases at higher rates. Fortunately, biologist Lillian Fritz-Laylin and her team of UMass researchers are studying Bd to understand how it operates and find ways to stop it in its tracks.
Fritz-Laylin’s research comes at the problem of Bd by focusing on actin—a group of proteins found in plant, animal, and fungal cells responsible for creating microfilaments that help them move and build internal structures. Actin has evolved to operate differently across species. “As a field, we have invested so much into understanding how yeast uses actin, and how animal cells use actin, but we don’t know how the actin structures in these different species relate to each other.”
Reverse-engineering a fungal threat could shield our ecosystem from catastrophe.
Our culprit fungus, Bd, belongs to the division of the fungi kingdom called chytrids, which branched off from the fungal lineage much earlier than ordinary mushrooms, or even yeast. They have cell structures that are, in some ways, more like animals. “I started studying chytrids because their genomes suggest that chytrids can do all these things that other fungi can’t,” explains Fritz-Laylin. “Understanding chytrid biology will help us integrate our knowledge of animal and yeast actin.”
By understanding how actin works in chytrids, scientists like Fritz-Laylin can learn to manipulate the actin-triggered processes happening within Bd cells and, eventually, help stop their spread among amphibians. “Using host molecules, we can trigger a switch between different stages in development, from the motile form that can swim through water to the stationary growth form,” she says. “Other labs are exploring using this trigger to make a trap of sorts. Because if you can make [Bd cells] nonmotile, then they can’t spread.”