Dr. Stefan Katharios-Lanwermeyer

Bio:
Dr. Stefan Katharios-Lanwermeyer is a postdoctoral researcher at the National Institutes of Health where he supported a PRAT postdoctoral Fellowship. He received his PhD in Microbiology from Dartmouth College where he studied the maintenance of bacterial biofilm under his mentor, Dr. George O’Toole. Currently, Katharios studies bacterial multicellularity in polymicrobial environments under his postdoctoral mentor Dr. Anupama Khare. His goal is to develop a model system to characterize how interspecies interactions result in multicellularity among cohabitating bacteria.

Abstract:
Microorganisms commonly exist in polymicrobial communities, where they can respond to interspecies secreted molecules by altering behaviors and physiology. However, the underlying mechanisms remain underexplored. I have investigated interactions between Stenotrophomonas maltophilia and Pseudomonas aeruginosa, co-infecting bacterial species pathogens found in pneumonia and chronic lung infections, such as in cystic fibrosis. We found that S. maltophilia forms large protective multicellular aggregates upon exposure to P. aeruginosa secreted factors. E

Experimental evolution for lack of aggregation selected for fimbrial mutations, and we found that fimbriae are required on both interacting S. maltophilia cells for aggregation. Untargeted metabolomics and targeted validations revealed that the quorum sensing molecule Pseudomonas quinolone signal (PQS) directly induced S. maltophilia aggregation, and co-localized with the aggregates. Further, in co-culture with P. aeruginosa, wild-type S. maltophilia formed aggregates, resulting in up to 75-fold increased survival from P. aeruginosa competition compared to fimbrial mutants. 

Finally, multiple other bacterial species similarly aggregated upon exposure to P. aeruginosa PQS, indicating a more general response. Collectively, our work identifies a novel multispecies interaction where a quorum sensing molecule from a co-infecting pathogen is sensed as a ‘danger’ signal, thereby inducing a protective multicellular response. This work provides a basis to expand to a three-species model system in which I aim to investigate bacterial multicellularity and interspecies interactions as bacteria respond to secreted factors produced by cohabitating microbes.

Dr. Stefan Katharios-Lanwermeyer

Bio:
Dr. Stefan Katharios-Lanwermeyer is a postdoctoral researcher at the National Institutes of Health where he supported a PRAT postdoctoral Fellowship. He received his PhD in Microbiology from Dartmouth College where he studied the maintenance of bacterial biofilm under his mentor, Dr. George O’Toole. Currently, Katharios studies bacterial multicellularity in polymicrobial environments under his postdoctoral mentor Dr. Anupama Khare. His goal is to develop a model system to characterize how interspecies interactions result in multicellularity among cohabitating bacteria.

Abstract:
Microorganisms commonly exist in polymicrobial communities, where they can respond to interspecies secreted molecules by altering behaviors and physiology. However, the underlying mechanisms remain underexplored. I have investigated interactions between Stenotrophomonas maltophilia and Pseudomonas aeruginosa, co-infecting bacterial species pathogens found in pneumonia and chronic lung infections, such as in cystic fibrosis. We found that S. maltophilia forms large protective multicellular aggregates upon exposure to P. aeruginosa secreted factors. E

Experimental evolution for lack of aggregation selected for fimbrial mutations, and we found that fimbriae are required on both interacting S. maltophilia cells for aggregation. Untargeted metabolomics and targeted validations revealed that the quorum sensing molecule Pseudomonas quinolone signal (PQS) directly induced S. maltophilia aggregation, and co-localized with the aggregates. Further, in co-culture with P. aeruginosa, wild-type S. maltophilia formed aggregates, resulting in up to 75-fold increased survival from P. aeruginosa competition compared to fimbrial mutants. 

Finally, multiple other bacterial species similarly aggregated upon exposure to P. aeruginosa PQS, indicating a more general response. Collectively, our work identifies a novel multispecies interaction where a quorum sensing molecule from a co-infecting pathogen is sensed as a ‘danger’ signal, thereby inducing a protective multicellular response. This work provides a basis to expand to a three-species model system in which I aim to investigate bacterial multicellularity and interspecies interactions as bacteria respond to secreted factors produced by cohabitating microbes.

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. David Katz | Katz Lab

View Katz's biosketch here!
 

Abstract:
The Katz lab is interested in the heritability of histone modifications and how this heritability contributes to traits and disease. We demonstrated in C. elegans how histone modifications can be trans-generationally maintained and lead to heritable phenotypes, ranging from sterility and longevity to behavior. 

These phenotypes demonstrate the histone modifications can serve as heritable information across generations. Based on these data, we have engineered a new mouse model where maternal epigenetic reprograming activity of the H3K4me1/2 demethylase LSD1/KDM1A is compromised. 

These maternally compromised mice exhibit inherited phenotypes that manifest postnatally, including perinatal lethality, developmental delay, craniofacial defects and altered behavior. These phenotypes include all of those found in the corresponding Kabuki-Syndrome like human patients, raising the possibility that maternal defects may contribute to phenotypes in LSD1 patients and Kabuki syndrome. 

Finally, we made the surprising discovery that loss of LSD1 in adult mice leads to neurodegeneration. Following up on this result, we generated significant data suggesting that LSD1 functions specifically in the pathological tau pathway. Pathological tau is thought to be a critical driver of neurodegeneration in Alzheimer’s disease. Based on our data, we propose that pathological tau contributes to neuronal cell death in Alzheimer’s disease by sequestering LSD1 in the cytoplasm and interfering with the continuous requirement for LSD1 to epigenetically repress transcription associated with alternative cell fates. Thus, it may be possible to target LSD1 therapeutically to block tau-mediated neurodegeneration. 

Dr. Brandon Logeman

Bio:
Brandon L. Logeman, PhD is a new Assistant Professor in the Department of Molecular and Cellular Biochemistry, College of Medicine, University of Kentucky. After completing his Ph.D. at Duke University, he joined the lab of Catherine Dulac at Harvard University to study the molecular mechanisms through which changes in cell-type specific gene expression influence neural activity and animal behavior. After receiving a K99/R00 Career Transition Award he joined the University of Kentucky in August 2025. His new lab will utilize custom designed single-cell genomics technologies such as microfluidic, droplet based sequencing assays and imaging based spatial transcriptomics as well as de novo protein binder design across a panel of genetically diverse mouse strains to discover how genomic and environmental influences contribute to observable differences in animal behavior.

Abstract:
Parental care is composed of multiple infant-directed behaviors that promote offspring survival and is influenced by the sex and physiological state of the caregiver. Previous work in mice has identified the medial preoptic area of the hypothalamus as a key brain area implicated in parental behaviors. However, numerous naturalistic behaviors and homeostatic processes are controlled by this area, hindering mechanistic investigation of the circuits underlying parental care. To overcome this challenge, here I employ cell-type specific RNA- and ATAC-seq analysis, neural activity recording, and perturbation to gain access into molecular, biophysical, and circuit-based causality of behavioral control. I find that various neuronal types involved in parenting behavior are each distinctively influenced by the sex and physiological status of an individual and uncover how cell-type specific regulatory programs alter gene expression and neural activity underlying behavior control. These results demonstrate how cell-type specific transcriptional responses to internal physiological cues mediate circuit specific alterations to neural activity and ultimately influence animal behavior.

Dr. Brandon Logeman

Bio:
Brandon L. Logeman, PhD is a new Assistant Professor in the Department of Molecular and Cellular Biochemistry, College of Medicine, University of Kentucky. After completing his Ph.D. at Duke University, he joined the lab of Catherine Dulac at Harvard University to study the molecular mechanisms through which changes in cell-type specific gene expression influence neural activity and animal behavior. After receiving a K99/R00 Career Transition Award he joined the University of Kentucky in August 2025. His new lab will utilize custom designed single-cell genomics technologies such as microfluidic, droplet based sequencing assays and imaging based spatial transcriptomics as well as de novo protein binder design across a panel of genetically diverse mouse strains to discover how genomic and environmental influences contribute to observable differences in animal behavior.

Abstract:
Parental care is composed of multiple infant-directed behaviors that promote offspring survival and is influenced by the sex and physiological state of the caregiver. Previous work in mice has identified the medial preoptic area of the hypothalamus as a key brain area implicated in parental behaviors. However, numerous naturalistic behaviors and homeostatic processes are controlled by this area, hindering mechanistic investigation of the circuits underlying parental care. To overcome this challenge, here I employ cell-type specific RNA- and ATAC-seq analysis, neural activity recording, and perturbation to gain access into molecular, biophysical, and circuit-based causality of behavioral control. I find that various neuronal types involved in parenting behavior are each distinctively influenced by the sex and physiological status of an individual and uncover how cell-type specific regulatory programs alter gene expression and neural activity underlying behavior control. These results demonstrate how cell-type specific transcriptional responses to internal physiological cues mediate circuit specific alterations to neural activity and ultimately influence animal behavior.