Paul H. Taghert | |
---|---|
Born | January 13, 1953 Alexandria, Egypt | (age 71)
Nationality |
Egyptian American |
Alma mater |
Reed College University of Washington |
Scientific career | |
Fields |
Neurobiology Chronobiology |
Institutions | Washington University in St. Louis |
Paul H. Taghert (born January 13, 1953) is an American chronobiologist known for pioneering research on the roles and regulation of neuropeptide signaling in the brain using Drosophila melanogaster as a model. [1] He is a professor of neuroscience in the Department of Neuroscience at Washington University in St. Louis. [2]
Taghert was born on January 13, 1953, in Alexandria, Egypt and grew up in Montclair, New Jersey. He attended Reed College from 1971 to 1975 and went on to pursue a PhD in zoology at the University of Washington in Seattle with Jim Truman. He did a postdoc under Corey Goodman at Stanford University from 1981 to 1984. As of 2016, he is a professor of neuroscience at Washington University in St. Louis and the Lab Head at the Taghert Lab at Washington University School of Medicine. [2] [1]
Taghert and colleagues have identified the ~150 circadian clock neurons in the adult Drosophila melanogaster brain. [3] Two distinct regions, the small and large ventral lateral neurons (LNv), express the neuropeptide pigment dispersing factor ( PDF) and contribute to circadian locomotor activity rhythms. [4] Taghert's group has made several contributions including the identification of mutants for the PDF neuropeptide gene - this revealed a specific behavioral syndrome indicating important contributions by this neuropeptide to normal circadian control of locomotor activity. [3] This was the first genetic study identifying secreted substances (and not just clock elements) as critical proteins for circadian neurophysiology. [4] This led the way to many studies by many laboratories that now evaluate how neuronal properties interweave and interact with cell intrinsic clock properties. [4]
Taghert's work involves employing the GAL4 activation and GAL80 inhibition of PDF to study PDF's necessity as a circadian pacemaker. [4] Experiments with the LNvs found that ablation of PDF via GAL80 inhibition only affected some aspects of behavioral rhythms, suggesting the presence of other regulators controlling circadian behavior. [4] To further examine the peptidergic pathways regulating PDF, Taghert and his group discovered the PDF receptor (PDFR), a class B1 G protein coupled receptor. Null mutations of PDFR suggests that it is also required for circadian rhythms in Drosophila melanogaster. [5]
The Taghert group also demonstrated that PDF signaling influences pacemaker cell synchronicity through PER regulation, identified the PDF receptor, and identified critical PDF receptor signaling components. [6] They have shown that PDF receptor signals differently in different pacemaker groups, and that PDF receptor signaling interact with signals from Cryptochrome (CRY) to help sustain clock rhythmicity. [7]
Taghert's work on DIMM addresses the genetic programs underlying neuron diversification. [8] Through a developmental studies approach, his work explores how peptidergic neurons in Drosophila use transcriptional control mechanisms to acquire properties like the selection of a unique neuropeptide phenotype. [9] The bHLH protein DIMM is an example of a transcriptional control mechanism that operates in neurosecretory neurons and is responsible for the cells’ ability to accumulate, process, and package large amounts of secretory peptides. [8]
DIMM confers a specific peptidergic phenotype to neurons, referred to as LEAP cells (Large cells that Episodically release Amidated Peptides). [9] To map DIMM expression in Drosophila peptidergic systems, a large panel of peptide antibodies and gene reporters were used. [8] It was found that there is a substantial correlation of DIMM expression with peptidergic phenotypes. At a molecular level, DIMM concerns secretory peptides that are amidated, and at a cellular level, DIMM concerns peptidergic neurons which are neurosecretory. [9] Current research involves molecular pathways by which DIMM levels are induced in response to environmental challenges. [2]
Paul H. Taghert | |
---|---|
Born | January 13, 1953 Alexandria, Egypt | (age 71)
Nationality |
Egyptian American |
Alma mater |
Reed College University of Washington |
Scientific career | |
Fields |
Neurobiology Chronobiology |
Institutions | Washington University in St. Louis |
Paul H. Taghert (born January 13, 1953) is an American chronobiologist known for pioneering research on the roles and regulation of neuropeptide signaling in the brain using Drosophila melanogaster as a model. [1] He is a professor of neuroscience in the Department of Neuroscience at Washington University in St. Louis. [2]
Taghert was born on January 13, 1953, in Alexandria, Egypt and grew up in Montclair, New Jersey. He attended Reed College from 1971 to 1975 and went on to pursue a PhD in zoology at the University of Washington in Seattle with Jim Truman. He did a postdoc under Corey Goodman at Stanford University from 1981 to 1984. As of 2016, he is a professor of neuroscience at Washington University in St. Louis and the Lab Head at the Taghert Lab at Washington University School of Medicine. [2] [1]
Taghert and colleagues have identified the ~150 circadian clock neurons in the adult Drosophila melanogaster brain. [3] Two distinct regions, the small and large ventral lateral neurons (LNv), express the neuropeptide pigment dispersing factor ( PDF) and contribute to circadian locomotor activity rhythms. [4] Taghert's group has made several contributions including the identification of mutants for the PDF neuropeptide gene - this revealed a specific behavioral syndrome indicating important contributions by this neuropeptide to normal circadian control of locomotor activity. [3] This was the first genetic study identifying secreted substances (and not just clock elements) as critical proteins for circadian neurophysiology. [4] This led the way to many studies by many laboratories that now evaluate how neuronal properties interweave and interact with cell intrinsic clock properties. [4]
Taghert's work involves employing the GAL4 activation and GAL80 inhibition of PDF to study PDF's necessity as a circadian pacemaker. [4] Experiments with the LNvs found that ablation of PDF via GAL80 inhibition only affected some aspects of behavioral rhythms, suggesting the presence of other regulators controlling circadian behavior. [4] To further examine the peptidergic pathways regulating PDF, Taghert and his group discovered the PDF receptor (PDFR), a class B1 G protein coupled receptor. Null mutations of PDFR suggests that it is also required for circadian rhythms in Drosophila melanogaster. [5]
The Taghert group also demonstrated that PDF signaling influences pacemaker cell synchronicity through PER regulation, identified the PDF receptor, and identified critical PDF receptor signaling components. [6] They have shown that PDF receptor signals differently in different pacemaker groups, and that PDF receptor signaling interact with signals from Cryptochrome (CRY) to help sustain clock rhythmicity. [7]
Taghert's work on DIMM addresses the genetic programs underlying neuron diversification. [8] Through a developmental studies approach, his work explores how peptidergic neurons in Drosophila use transcriptional control mechanisms to acquire properties like the selection of a unique neuropeptide phenotype. [9] The bHLH protein DIMM is an example of a transcriptional control mechanism that operates in neurosecretory neurons and is responsible for the cells’ ability to accumulate, process, and package large amounts of secretory peptides. [8]
DIMM confers a specific peptidergic phenotype to neurons, referred to as LEAP cells (Large cells that Episodically release Amidated Peptides). [9] To map DIMM expression in Drosophila peptidergic systems, a large panel of peptide antibodies and gene reporters were used. [8] It was found that there is a substantial correlation of DIMM expression with peptidergic phenotypes. At a molecular level, DIMM concerns secretory peptides that are amidated, and at a cellular level, DIMM concerns peptidergic neurons which are neurosecretory. [9] Current research involves molecular pathways by which DIMM levels are induced in response to environmental challenges. [2]