2026 Speakers

Keith Slotkin holds a joint position at the University of Missouri and Danforth Plant Science Center, where he is the Vice President of Commercialization. He has studied mobile ‘jumping gene’ Transposable Elements for 25+ years, focused on understanding how they reshape plant genomes as natural genome engineers. His research began at The University of Arizona, then he received his Ph.D. in Plant Genetics from the University of California-Berkeley. Keith performed his postdoctoral research as an NIH-funded fellow at Cold Spring Harbor Laboratory before starting his own lab as an Assistant Professor at The Ohio State University in 2009. In 2018 he was attracted to the St. Louis Ag BioTech ecosystem and moved his laboratory to the Donald Danforth Plant Science Center. His lab has investigated how plant cells control the activity of harmful transposable elements, and through this work the Slotkin lab has learned enough to switch this question around to now ask how can we control the activity of transposable elements for genome engineering in plant cells.

Transposable elements are fragments of DNA that duplicate and move from one region of a genome to another. They are found in all eukaryotes genomes and are considered by most biologists as unwanted mutagens or ‘junk DNA’ to be avoided in their experiments. But transposable elements have a creative side and act over evolutionary timescales to move regulatory elements and create new genes. The Slotkin lab has been working for 16 years to understand how transposable elements are regulated in plant genomes. We have now learned enough to engineer transposable elements and take advantage of their unique ability to cut, copy and paste DNA sequences in plant genomes. We have combined the natural copy & paste ability of transposable elements with cutting of CRISPR-Cas to control the transposition process. We have created a system called TAHITI (Transposon-Assisted Homology-Independent Targeted Insertion) to perform custom gene insertions, replacements and large scale genome engineering, which we have working in Arabidopsis and soybean, with more crops on the way. 

Dr. Kranthi Mandadi is a Professor in the Department of Plant Pathology and Microbiology at the Texas
A&M AgriLife Research & Extension Center in Weslaco. Dr. Mandadi’s program focuses on translational
and applied research on agricultural biothreats and environmental stresses that impact Texas agriculture
and beyond. He has over 16 years of expertise in plant pathology, molecular biology, and biotechnology.
Dr. Mandadi has published over 75 peer-reviewed articles, holds 10 patents, and has delivered 40
invited talks at national and international meetings. Dr. Mandadi directed or co-directed large
interdisciplinary research grant projects totaling more than $54 million, including an active $7 million
multi-state USDA-NIFA Coordinated Agricultural Project and Center of Excellence at Weslaco. The goal
of this multi-state consortium is to discover and commercialize antimicrobial therapies for citrus
greening. He serves as senior editor and editorial board member for multiple scientific journals,
including Phytopathology, Frontiers in Microbiology, and Frontiers in Plant Sciences. Dr. Mandadi
received multiple honors and awards, including the 2024 American Phytopathological Society Syngenta
Award, the 2022 Texas A&M AgriLife Research Scientist of the Year, and the 2017 Foundation for Food
and Agricultural Research (FFAR) New Innovator Award.

Endemic and emerging pathogens, such as the Candidatus Liberibacter spp. associated with citrus
greening disease, and the potato zebra chip poses immense agricultural threats and causes billions of
economic losses. Unfortunately, studies of these pathogens are hindered by the fastidious
(unculturable), obligate lifestyle of Candidatus Liberibacter spp., and the recalcitrance of host crops to
conventional genetic evaluation technologies. To overcome these bottlenecks, we developed a novel
high-throughput hairy root-based efficacy-testing system that enabled 4-6X faster evaluation of
antimicrobials and gene-editing targets. Leveraging this platform and interdisciplinary collaborations, we
are leading the discovery of new strategies to control Candidatus Liberibacter spp. in citrus, potato, and
tomato. Lastly, through partnerships with the private sector, we are pursuing federal regulatory
approvals to deploy and commercialize the new antimicrobials as crop disease management solutions.

Natalia Rivera‑Torres, Ph.D. is the Associate Director of Pre-Clinical Development at the ChristianaCare Gene Editing Institute. Her research advances the understanding of DNA repair mechanisms in human cells, including Single-Strand Template Repair (SSTR/ExACT). With over a decade of experience in CRISPR/Cas systems, she focuses on developing gene editing therapies for solid tumors, particularly head and neck cancers. She leads preclinical programs advancing candidates toward IND status, serves as R&D lead to CorriXR Therapeutics, and supports clinical translation through advisory roles in clinical trial development.

Stephen Dolan is an Assistant Professor at Clemson University, where he studies the mechanistic basis of
fungal–bacterial interactions during human infection. His research focuses on how microbial physiology is
altered within complex communities, using clinically relevant models of respiratory infection to understand how
co-infecting organisms such as Aspergillus fumigatus and Pseudomonas aeruginosa influence one another.
Prior to this, he was a Cystic Fibrosis Foundation postdoctoral fellow in Dr. Marvin Whiteley’s laboratory at
Georgia Tech and the Emory-Children’s Cystic Fibrosis Center. He previously held a Herchel Smith
Postdoctoral Research Fellowship at the University of Cambridge, hosted in the Welch laboratory, where he
examined the physiology of Pseudomonas aeruginosa both in isolation and in polymicrobial interactions.
Stephen completed his PhD at Maynooth University, Ireland, under the supervision of Dr. Sean Doyle, where
he used comparative ‘omics and reverse genetics to study toxin regulation in A. fumigatus.

Polymicrobial infections involving the opportunistic fungal pathogen Aspergillus fumigatus and the bacterium
Pseudomonas aeruginosa are increasingly recognized as important contributors to disease progression in
cystic fibrosis and other chronic lung disorders. Within these environments, both organisms produce a diverse
arsenal of secondary metabolites, signaling molecules, and nutrient acquisition systems that shape microbial
community structure and influence pathogen fitness. Fungal metabolites, including gliotoxin and related natural
products, can profoundly alter bacterial physiology, while bacterial-derived compounds such as phenazines
and quorum sensing molecules impact fungal growth, metabolism, and stress responses.
Recent advances in CRISPR-based genome engineering have transformed our ability to dissect the genetic
networks that govern fungal adaptation to these complex interkingdom interactions. Using CRISPR-enabled
gene deletion, transcriptional regulation, and functional genomics approaches, we are uncovering the
regulatory pathways that allow A. fumigatus to detect bacterial competitors, respond to bacterial-derived
stresses, and remodel its physiology during polymicrobial growth. These studies have revealed previously
uncharacterized transcription factors, signaling pathways, and metabolic adaptations that contribute to fungal
persistence and survival in mixed-species communities.
By defining the molecular mechanisms that enable fungal adaptation within polymicrobial biofilms, these
studies provide new insight into the biology of chronic infections and identify potential therapeutic targets for
disrupting pathogenic interactions.