Dr. Maria Antonietta Tosches | Tosches Lab

Abstract:

The cerebral cortex is arguably the brain area that underwent the most profound transformations in vertebrate brain evolution. The expansion of the cerebral cortex in mammals was accompanied by an explosion of neuronal diversity. To discover general principles underlying the evolution of neuron types and circuits, we study the simple cerebral cortices of non-mammalian vertebrates. Our recent work has focused on the Spanish newt Pleurodeles waltl, a species with a key phylogenetic position in the vertebrate tree. We are investigating the neuroanatomy, cell type composition, and function of the Pleurodeles brain using a combination of modern neuroscience tools.

Our work on amphibians and reptiles indicates that the cerebral cortex of ancestral tetrapods was layered, with two main classes of neurons with distinct laminar positions, molecular identities, and long-range projections. In salamanders, these two layers are generated sequentially from multipotent progenitors in an outside-in sequence. We propose that in mammals new types of pyramidal neurons evolved from these two ancestral classes by diversification, through the emergence of novel gene regulatory interactions during neuronal differentiation.

Watch the seminar here!

Dr. Maria Antonietta Tosches | Tosches Lab

Abstract:

The cerebral cortex is arguably the brain area that underwent the most profound transformations in vertebrate brain evolution. The expansion of the cerebral cortex in mammals was accompanied by an explosion of neuronal diversity. To discover general principles underlying the evolution of neuron types and circuits, we study the simple cerebral cortices of non-mammalian vertebrates. Our recent work has focused on the Spanish newt Pleurodeles waltl, a species with a key phylogenetic position in the vertebrate tree. We are investigating the neuroanatomy, cell type composition, and function of the Pleurodeles brain using a combination of modern neuroscience tools.

Our work on amphibians and reptiles indicates that the cerebral cortex of ancestral tetrapods was layered, with two main classes of neurons with distinct laminar positions, molecular identities, and long-range projections. In salamanders, these two layers are generated sequentially from multipotent progenitors in an outside-in sequence. We propose that in mammals new types of pyramidal neurons evolved from these two ancestral classes by diversification, through the emergence of novel gene regulatory interactions during neuronal differentiation.

Watch the seminar here!

Dr. Maria Antonietta Tosches | Tosches Lab

Abstract:

The cerebral cortex is arguably the brain area that underwent the most profound transformations in vertebrate brain evolution. The expansion of the cerebral cortex in mammals was accompanied by an explosion of neuronal diversity. To discover general principles underlying the evolution of neuron types and circuits, we study the simple cerebral cortices of non-mammalian vertebrates. Our recent work has focused on the Spanish newt Pleurodeles waltl, a species with a key phylogenetic position in the vertebrate tree. We are investigating the neuroanatomy, cell type composition, and function of the Pleurodeles brain using a combination of modern neuroscience tools.

Our work on amphibians and reptiles indicates that the cerebral cortex of ancestral tetrapods was layered, with two main classes of neurons with distinct laminar positions, molecular identities, and long-range projections. In salamanders, these two layers are generated sequentially from multipotent progenitors in an outside-in sequence. We propose that in mammals new types of pyramidal neurons evolved from these two ancestral classes by diversification, through the emergence of novel gene regulatory interactions during neuronal differentiation.

Watch the seminar here!

Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Samantha Brugmann | Brugmann Lab

Bio:

Dr. Samantha Brugmann is a developmental biologist studying craniofacial development and disease. Her longterm goal is to help children with craniofacial anomalies by generating tissue amenable for surgical repair. To achieve this goal, her lab specifically focuses on the role the primary cilium during craniofacial development and the craniofacial anomalies that arise when the cilium do not function properly. Projects in her lab utilize avian, murine and humaninduced pluripotent stem cells to gain a better understanding of the molecular mechanisms associated with craniofacial anomalies. In addition to using existing animal models to understand human craniofacial disorders, her lab also sequences patients and generates cell-based models to uncover novel genetic causes for craniofacial ciliopathies.



Abstract:

The Brugmann Lab focuses on the understanding molecular and cellular processes important for craniofacial development and the onset of craniofacial anomalies (CFAs). CFAs represent approximately one third of all birth-defects. For the past decade, my research program has centered on treating these conditions by garnering a fundamental understanding of craniofacial development and pathological mechanisms associated with CFAs. We have specifically focused on a class of CFAs called ciliopathies, which are caused by disruptions to a cellular organelle called the primary cilium. Ciliopathies represent a fast-growing group of disorders, that can affect up to 1 in 800 people. My lab was the first to report that the craniofacial complex is the primary organ system affected in 30% of all ciliopathies, and thus coined the term craniofacial ciliopathies. My lab uses murine, avian and human model systems to understand molecular mechanisms associated with ciliopathies. Furthermore, we use these model systems to identify potential therapeutic avenues to treat this class of diseases. 

Dr. Carrie Adler | Adler Lab

Bio:

Carrie is currently an Assistant Professor in the Department of Molecular Medicine at Cornell University, where she started her lab in 2015. She attended college at Wesleyan University and afterwards worked as a technician with Bruce Mayer at Harvard Medical School, studying signal transduction pathways. For graduate school, Carrie enrolled in the Tetrad program at UCSF, joining Cori Bargmann's lab to study neural development in C. elegans. As a postdoc, Carrie trained with Alejandro Sánchez Alvarado at the University of Utah and the Stowers Institute for Medical Research.

Abstract:

Throughout our lives, we are constantly exposed to insults, including injuries, disease, and environmental toxins. Frequently referred to as a ‘fountain of youth’ given their potential for rejuvenation, stem cells have the capacity to restore damaged tissue. In most model organisms, regenerative capacity is limited and stem cells are scarce, which has made it difficult to pinpoint the mechanisms regulating their behavior. In addition, stem cell exhaustion occurs as we age, diminishing our ability to repair damaged tissues. Finally, while we have made significant progress in recapitulating organ growth in vitro, how might these tissues be used in humans to restore physiological function?

My research program has probed these questions in an emerging model organism, planarian flatworms. These animals have long been regarded as champion regenerators because they can rapidly replace any tissue that’s been damaged or lost, including the nervous system. The basis of this unlimited renewal lies in an abundant population of stem cells. My lab’s primary goals are to understand how these cells sense and respond to injury, and how they maintain genome integrity through repeated cell divisions that occur during regeneration.

Check out the seminar here!

Dr. Carrie Adler | Adler Lab

Bio:

Carrie is currently an Assistant Professor in the Department of Molecular Medicine at Cornell University, where she started her lab in 2015. She attended college at Wesleyan University and afterwards worked as a technician with Bruce Mayer at Harvard Medical School, studying signal transduction pathways. For graduate school, Carrie enrolled in the Tetrad program at UCSF, joining Cori Bargmann's lab to study neural development in C. elegans. As a postdoc, Carrie trained with Alejandro Sánchez Alvarado at the University of Utah and the Stowers Institute for Medical Research.

Abstract:

Throughout our lives, we are constantly exposed to insults, including injuries, disease, and environmental toxins. Frequently referred to as a ‘fountain of youth’ given their potential for rejuvenation, stem cells have the capacity to restore damaged tissue. In most model organisms, regenerative capacity is limited and stem cells are scarce, which has made it difficult to pinpoint the mechanisms regulating their behavior. In addition, stem cell exhaustion occurs as we age, diminishing our ability to repair damaged tissues. Finally, while we have made significant progress in recapitulating organ growth in vitro, how might these tissues be used in humans to restore physiological function?

My research program has probed these questions in an emerging model organism, planarian flatworms. These animals have long been regarded as champion regenerators because they can rapidly replace any tissue that’s been damaged or lost, including the nervous system. The basis of this unlimited renewal lies in an abundant population of stem cells. My lab’s primary goals are to understand how these cells sense and respond to injury, and how they maintain genome integrity through repeated cell divisions that occur during regeneration.

Check out the seminar here!