E. Anne Hatmaker, Ph.D.

I am a biologist interested in the evolution of pathogenicity in fungi. Fungal infections impact millions of humans per year, and yet fungal pathogens are understudied. Many plant pathogens are also fungi, impacting crop yield and contaminating harvests with toxins. I explore the genomes of human and plant pathogens to better understand how they are able to infect a diverse array of hosts. My main projects are highlighted below. For more in-depth information regarding the publications resulting from these projects, see my Google Scholar page.

How do transposable elements impact host specificity in species causing Fusarium head blight?

Several species of Fusarium can cause Fusarium head blight (FHB), leading to major crop losses in cereal crops like wheat and barley. The main culprit is Fusarium graminearum, but related species can also cause FHB. Research shows recent shifts in species prevalence, influenced by both abiotic and biotic factors, emphasizing the need to understand the drivers of host specificity to protect cereal crops.

This project combines my background in plant pathology with my bioinformatics skillset. I use genomics to study the distribution and role of Starship transposable elements in Fusarium graminearum and related species. Thanks to collaborators in the USDA, I have access to isolates from crops and wild grasses and will explore the different genes associated with Starship elements in both the pathogenic isolates from crops and the endophytic isolates of wild grasses to better understand the genetic drivers of pathogenicity. This project was started in 2025 and is funded through my USDA-NIFA Postdoctoral Fellowship.

Do pathogenic fungi share transcriptional architecture?

Many fungi are capable of producing toxins which are harmful to humans and other animals. These compounds are known as mycotoxins (myco = fungal). Some mycotoxins are known to impact virulence. I am examining the transcriptional architecture of pathogens within the Pezizomycotina (Ascomycota) group of fungi. This work uses publicly available transcriptomic data from hundreds of experiments to generate gene-regulatory networks using machine learning. In parallel, I am also exploring the evolution of regulatory genes within the genomes of these fungi to determine whether orthologous transcription factors are regulating orthologous pathways and genes. This chapter of my postdoctoral research was funded through the USDA-ARS SCINet Postdoctoral Fellows program.

Are clinical isolates of Aspergillus flavus differentiated from environmental isolates?

Put another way, do clinical isolates of a human pathogenic fungus share genetic characteristics, or are they infecting at random? A. flavus is an opportunistic human pathogen responsible for eye and respiratory infections, among other diseases. Since there is no human-to-human transmission, human infections are an evolutionary dead-end for the fungus. Instead infections stem from patient contact with the fungus in the environment under the perfect conditions to encourage growth–sometimes with devastating consequences. Patients with Aspergillus respiratory infections are often immunocompromised, such as people with certain viral infections, those undergoing cancer treatment, or transplant patients. However, Aspergillus eye infections impact both immunocompromised and immunocompetent people.

My dissertation research used population genomics and phylogenetics to explore how isolates of A. flavus from patients and from the environment are related. I found evidence of a link between pathogenicity and genetics, as one group had a higher proportion and overall more clinical isolates than the others. Working with collaborators, I identified genes unique to the clinical group through examining the pan-genome of the species. To find out more about this work, keep an eye out for our upcoming publication in the journal Nature Communications, which will be available in the coming months. This project was funded by the NIH National Research Service Award Predoctoral Fellowship (F31) through the National Eye Institute.