Dr. Alice Accorsi | Accorsi Lab

Bio:
Alice Accorsi is an assistant professor in the Department of Molecular and Cellular Biology at the University of California, Davis. She is a developmental biologist whose research focuses on the development and regeneration of sensory organs. She earned her bachelor’s and master’s degrees, as well as her PhD, from the University of Modena and Reggio Emilia (Italy), where she conducted a comparative analysis of immune-neuron communication in invertebrates. She then moved to Kansas City to begin her postdoctoral training at the Stowers Institute for Medical Research in the laboratory of Alejandro Sánchez Alvarado. During her postdoctoral work, she established the freshwater apple snail, Pomacea canaliculata, as the first genetically tractable system for studying complete regeneration of vertebrate-like eyes. This work, published in Nature Communications, opened new avenues for investigating visual system regeneration. Her laboratory now focuses on uncovering the molecular and cellular mechanisms underlying the regeneration of the visual system.

Abstract:
The ability to regenerate complex sensory organs varies widely across the animal kingdom and remains poorly understood, particularly in systems capable of restoring highly organized, vertebrate-like eyes. While vertebrates exhibit limited regenerative capacity in the visual system, several invertebrates can regenerate entire sensory structures; however, these models often lack genetic tractability or fail to recapitulate key features of vertebrate eye organization. To address this gap, we established the freshwater apple snail, Pomacea canaliculata, as a novel and genetically tractable model for studying eye regeneration. Following complete amputation, P. canaliculata is able to fully regenerate its eyes. 

Through integrated morphological, cellular, and molecular analyses, we define the sequential stages of regeneration, revealing dynamic tissue remodeling, proliferative activation, and the re-establishment of organized visual architecture. Together, this work provides a powerful platform for dissecting the cellular and genetic basis of eye regeneration, advancing our understanding of how complex organs can be rebuilt, and informing future strategies to promote regeneration in systems with limited intrinsic capacity, including the human visual system.

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

Dr. David Katz | Katz Lab

View Katz's biosketch here.
 

Abstract:
The Katz lab is focused on 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. 

Watch the seminar here!

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.

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.