Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

Dr. Horacio de la Iglesia | de la Iglesia Lab

Bio:
Horacio de la Iglesia finished his undergraduate studies in biology at the University of Buenos Aires, Argentina. He earned his Ph.D. in neuroscience and behavior at the University of Massachusetts, Amherst, where working with Eric Bittman he studied the neuroanatomical interactions between the master circadian clock of mammals and the brain centers that control reproduction. He then continued his research on the neural control of circadian rhythms as a post-doctoral fellow and as an instructor in the laboratory of William Schwartz at the University of Massachusetts Medical School. He was also an Instructor at Harvard University, where he taught a course on Stem Cells. De la Iglesia joined the University of Washington Department of Biology in 2003.

Abstract:
Throughout evolution and history, humans have progressively isolated themselves from natural cycles through built environments that isolate them from the external environment. Key to this isolation is our ability to manipulate artificial light and extend our activity into the nighttime. Recent studies from our laboratory suggest that moonlight not only had a similar effect on activity in ancestral times, but also that the phases of the moon continue to shape our daily sleep in highly urbanized communities. I will present data from human and nonhuman primates that provide evidence for the synchronization of sleep by lunar gravity, and for the mechanisms by which the moon may regulate sleep physiology.

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!