Dr. Brittany Belin

Bio:
Dr.Brittany Belin is a graduate of Notre Dame (B.S., biochemistry & philosophy) and the University of California San Francisco (Ph.D., bBiophysics), where she studied the actin cytoskeleton using quantitative microscopy, cell biology and computational analysis. For her postdoc work, she transitioned to studying plant-bacteria symbiosis at Caltech, and she opened her own lab studying lipid biophysics in plant-bacteria symbiosis at the Carnegie Institution for Science in 2020. She is interested in symbiosis and microbial cell biology in all of its forms, and she loves learning and teaching about emerging models for studying these topics.

Abstract:
Life is powered by fixed carbon and nitrogen, and the exchange of these elements is a common basis for bacteria-eukaryote symbioses. The Bradyrhizobia are a globally dominant soil bacteria that form nitrogen-carbon exchange symbioses with peanuts, soybeans and other legumes, and work in our lab and others has shown that these symbioses require cholesterol-like bacterial lipids known as hopanoids. 

The mechanisms through which hopanoids participate in symbiosis are not clear, but our preliminary data suggest that hopanoids:

1. Participate in the early stages of the B. diazoefficiens-legume interaction by promoting bacterial motility and signal secretion.
2. Regulate bacterial membrane biophysics in a manner similar to that of cholesterol in animal cells. 

These findings suggest a fundamental connection between bacterial membrane biophysics and successful host-microbe interactions that likely is mediated by diverse, membrane-rigidifying “secondary lipids” throughout the bacterial domain of life.

Dr. Brittany Belin

Bio:
Dr.Brittany Belin is a graduate of Notre Dame (B.S., biochemistry & philosophy) and the University of California San Francisco (Ph.D., bBiophysics), where she studied the actin cytoskeleton using quantitative microscopy, cell biology and computational analysis. For her postdoc work, she transitioned to studying plant-bacteria symbiosis at Caltech, and she opened her own lab studying lipid biophysics in plant-bacteria symbiosis at the Carnegie Institution for Science in 2020. She is interested in symbiosis and microbial cell biology in all of its forms, and she loves learning and teaching about emerging models for studying these topics.

Abstract:
Life is powered by fixed carbon and nitrogen, and the exchange of these elements is a common basis for bacteria-eukaryote symbioses. The Bradyrhizobia are a globally dominant soil bacteria that form nitrogen-carbon exchange symbioses with peanuts, soybeans and other legumes, and work in our lab and others has shown that these symbioses require cholesterol-like bacterial lipids known as hopanoids. 

The mechanisms through which hopanoids participate in symbiosis are not clear, but our preliminary data suggest that hopanoids:

1. Participate in the early stages of the B. diazoefficiens-legume interaction by promoting bacterial motility and signal secretion.
2. Regulate bacterial membrane biophysics in a manner similar to that of cholesterol in animal cells. 

These findings suggest a fundamental connection between bacterial membrane biophysics and successful host-microbe interactions that likely is mediated by diverse, membrane-rigidifying “secondary lipids” throughout the bacterial domain of life.

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. 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 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!