Katie Walzer Headshot

Name: Katelyn Walzer

Title: Assistant Professor

Department: Biological Sciences

Email: kwalzer@clemson.edu

LinkedIn: https://www.linkedin.com/in/katelyn-walzer/

Biosketch:
For over fifteen years, I have studied the genetics and genomics of apicomplexan parasites, including Toxoplasma gondii, Plasmodium falciparum, and Cryptosporidium parvum. As an undergraduate at the University of Pittsburgh, I worked with Dr. Jon Boyle on the comparative genomics of T. gondii and its closest relative, nonpathogenic Hammondia hammondi. After earning my Bachelor of Science as a dual major in Biological Sciences and English Writing, I pursued a PhD in Genetics and Genomics at Duke University under the tutelage of Dr. Jen-Tsan Ashley Chi. My dissertation work focused on the development of single-cell approaches to study the transcriptional heterogeneity of P. falciparum parasites during their asexual and sexual cycles. Of note, I identified genes expressed in either male or female parasites as early as mid-stage sexual development, providing more robust markers for P. falciparum sex-specific differentiation. I performed my postdoctoral research under the guidance of Dr. Boris Striepen at the University of Pennsylvania School of Veterinary Medicine, where I studied the transcriptional regulation of the C. parvum life cycle. I developed the C. parvum single-cell atlas and identified the transcription factor Myb-M as the earliest determinant of male fate. I joined the Department of Biological Sciences and the Eukaryotic Pathogens Innovation Center at Clemson University in 2025 as an assistant professor.

 

Research Summary:
I am determined to understand what makes apicomplexan parasites tick and was drawn to Cryptosporidium and its single-host model. Cryptosporidium is transmitted via the fecal-oral route and invades the epithelial cells of the small intestine, ultimately causing diarrheal disease. It propagates via a programmed countdown to sex, with three asexual cycles followed by the production of male and female gametes. This makes both asexual and sexual replication essential for continuous infection and transmission.

During my postdoctoral fellowship, I determined the complete life cycle transcriptome of C. parvum through single-cell RNA sequencing (scRNA-seq) of 9,098 individual parasites. This single-cell atlas provides a roadmap of gene expression across parasite development and has enabled us to pinpoint the timing of important regulators of cell cycle progression and fate. These regulators include AP2 and Myb transcription factors. My lab will define the regulatory networks of these transcription factors, with an initial focus on those expressed in males: Myb-M, AP2-M1, and AP2-M. I discovered that Myb-M alone is necessary and sufficient to drive male fate. Now, my lab will identify the targets of Myb-M and unravel the transcriptional switch that leads to male. We will prioritize the study of male-specific RNA-binding proteins as they share a similar expression profile to Myb-M and may coordinate its expression. We will also define the largely uncharacterized machinery involved in male egress, motility, attachment, and fusion. This will enable us to figure out how a male traverses the harsh conditions of the gut to find and fertilize a female. As there is no vaccine and only limited treatment for cryptosporidiosis, our work will directly contribute to new and better therapeutics as the ability to disrupt Cryptosporidium sexual reproduction will stop continuous infection and transmission.

 

Selected Publications:
Walzer KA, Tandel J, Byerly JH, Daniels AM, Gullicksrud JA, Whelan EC, Carro SD, Krespan E, Beiting DP, and Striepen B. (2024). Transcriptional control of the Cryptosporidium life cycle. Nature. 630, 174-180.

Pardy RD, Walzer KA, Wallbank BA, Byerly JH, O’Dea KM, Cohn IS, Haskins BE, Roncaioli JL, Smith EJ, Buenconsejo GY, Striepen B, and Hunter CA. (2024). Analysis of intestinal epithelial cell responses to Cryptosporidium highlights the temporal effects of IFN-γ on parasite restriction. PLoS Pathogens. 20(5): e1011820.

Tandel J, Walzer KA, Byerly JH, Pinkston B, Beiting DP, and Striepen B. (2023). Genetic ablation of a female-specific Apetala 2 transcription factor blocks oocyst shedding in Cryptosporidium parvum. mBio. 14(2):e0326122.

Walzer KA, Fradin H, Emerson LY, Corcoran DL, and Chi JT. (2019). Latent transcriptional variations of individual Plasmodium falciparum uncovered by single-cell RNA-seq and fluorescence imaging. PLoS Genetics. 15(12): e1008506.

Yang WH, Doss JF, Walzer KA, McNulty SM, Wu J, Roback JD, and Chi JT. (2019). Angiogenin-mediated tRNA cleavage as a novel feature of stored red blood cells. British Journal of Haematology. 185: 752-806.

Walzer KA, Kubicki DM, Tang X, and Chi JT. (2018). Single-Cell Analysis Reveals Distinct Gene Expression and Heterogeneity in Male and Female Plasmodium falciparum Gametocytes. mSphere. 3:e00130-18.

Walzer KA and Chi JT. (2017). Trans-kingdom small RNA transfer during host-pathogen interactions: The case of P. falciparum and erythrocytes. RNA Biology. 14(4): 442-449.

Park HS, Rinehart MT, Walzer KA, Chi JT, and Wax A. (2016). Automated Detection of P. falciparum Using Machine Learning Algorithms with Quantitative Phase Images of Unstained Cells. PLoS ONE. 11(9): e0163045.

Rinehart MT, Park HS, Walzer KA, Chi JT, and Wax A. (2016). Hemoglobin consumption by P. falciparum in individual erythrocytes imaged via quantitative phase spectroscopy. Scientific Reports. 6: 24461.

Healy JA, Nugent A, Rempel RE, Moffitt AB, Davis NS, Jiang X, Shingleton JR, Zhang J, Love C, Datta J, McKinney ME, Tzeng TJ, Wettschureck N, Offermanns S, Walzer KA, Chi JT, Rasheed SAK, Casey PJ, Lossos IS, and Dave SS. (2016). GNA13 loss in germinal center B cells leads to impaired apoptosis and GC B cell persistence and promotes lymphoma in vivo. Blood. 127(22): 2723-31.

LaMonte G, Walzer KA, Lacsina JR, Nicchitta CV, and Chi JT. (2015). Methods to investigate the regulatory role of small RNAs and ribosomal occupancy of Plasmodium falciparum. Journal of Visualized Experiments. (106), e53214.

Walzer KA, Wier GM, Dam RA, Srinivasan AR, Borges AL, English ED, Herrmann DC, Schares G, Dubey JP, and Boyle JP. (2014). Hammondia hammondi harbors functional orthologs of the host-modulating effectors GRA15 and ROP16 but is distinguished from Toxoplasma gondii by a unique transcriptional profile. Eukaryotic Cell. 13(12): 1507-18.

Walzer KA, Adomako-Ankomah Y, Dam RA, Herrmann DC, Schares G, Dubey JP, and Boyle JP. (2013). Hammondia hammondi, an avirulent relative of Toxoplasma gondii, has functional orthologs of known T. gondii virulence genes. Proceedings of the National Academy of Sciences of the U.S.A. 110(18): 7446-51.

Walzer KA and Boyle JP. (2012). A single chromosome unexpectedly links highly divergent isolates of Toxoplasma gondii. mBio. 3(1):e00284-11.