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Developmental Biology

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David Gilmour

  • Professor of Molecular and Cell Biology and
  • Graduate Education Co-Director

Transcriptional regulation of the hsp70 heat shock gene in Drosophila

465A North Frear Laboratory
dsg11@psu.edu

(814) 863-8905


Wendy Hanna-Rose

  • Interim Department Head, Biochemistry and Molecular Biology
  • Associate Professor of Biochemistry and Molecular Biology
  • Department of Biochemistry and Molecular Biology

Molecular Genetics of Metabolism and Development in C. elegans

104D Life Sciences Building
wxh21@psu.edu

(814) 865-7904


Teh-hui Kao

  • Distinguished Professor of Biochemistry and Molecular Biology

Biochemical and molecular bases of self/non-self recognition during plant reproduction

333 South Frear Laboratory
txk3@psu.edu

(814) 863-1042


Kenneth Keiler

  • Professor of Biochemistry and Molecular Biology

Protein quality control and new antibiotics.

401 Althouse Laboratory
kkeiler@psu.edu

(814) 863-0787


Zhi-Chun Lai

  • Professor of Biology and
  • Professor of Biochemistry and Molecular Biology

Growth control and cancer genetics

127 Life Sciences Building
zcl1@psu.edu

(814) 863-0479


Bernhard Lüscher

  • Professor of Biology
  • Professor of Biochemistry and Molecular Biology

Molecular and cellular mechanisms and neural circuit changes underlying neuropsychiatric disorders. Molecular and cellular mechanisms underlying successful antidepressant drug treatment    Research Summary We are working to improve our understanding of the role and function of GABAergic transmission in health and disease. GABA (gamma-aminobutyric acid) is the principal inhibitory neurotransmitter in the brain and known to exert most of its function by activation of so-called GABA(A) receptors. These receptors are GABA-gated chloride channels and they serve as the targets of several classes of clinically and therapeutically important psychoactive drugs, most notably the benzodiazepines (Valium, Xanax, Versed, etc). Based on knowledge derived from these drugs, GABA(A) receptors are known to modulate virtually every higher-order brain function (learning, memory, cognition, emotion, pain, motivation, muscle tension, etc). A first line of research uses mouse genetics to model and investigate the molecular mechanisms underlying neuropsychiatric disorders. In particular, we are interested in the etiology of Major Depressive Disorder (MDD), a leading cause of total disability affecting about 17 percent of the human population at least once in their lives. Recent clinical evidence points to functional impairment of certain GABA-releasing interneurons and reduced brain concentrations of GABA as a likely cause of MDD. Using targeted mutagenesis in mice, we have shown that modest deficits in GABAergic transmission are sufficient to reproduce behavioral, cognitive, cellular, endocrine, and pharmacological alterations expected of a mouse model of depression. These mice, therefore, provide strong evidence that GABA deficits are not just an epiphenomenon of MDD, but that they can, in fact, be causal for MDD (reviewed in Luscher et al 2011, Mol. Psychiatry). Using these mice we have shown that defects in GABergic transmission can be causal for defects in the function of glutamate, the primary excitatory neurotransmitter in the brain, and that the defects in both GABA and glutamate can be reversed with the rapid-acting antidepressant, ketamine (Ren et al 2016)   As part of a second line of research, we are elucidating the mechanisms of antidepressant drug action. It is becoming increasingly clear that antidepressants act to ultimately increase and normalize GABAergic synaptic transmission even if they are designed to enhance the function of other neurotransmitters (serotonin, norepinephrine, glutamate, and their receptors. Therefore, we asked whether genetically enhancing the function of certain GABA-releasing interneurons would be sufficient to mimic the effects of above antidepressant drug treatments. We succeeded in showing that genetically increasing the excitability of GABA-producing interneurons known as somatostatin cells reproduced both biochemical and behavioral consequences of antidepressant drug treatment (Fuchs et al 2017).  Ongoing research seeks to better understand the molecular and cellular changes underlying MDD and antidepressant drug action, with the aim to design novel antidepressant drug treatments.          

209 Life Sciences Building
bxl25@psu.edu

(814) 865-5549


Tim Miyashiro

  • Assistant Professor of Biochemistry and Molecular Biology

Bacterial gene expression within natural host environments;  Host-microbe symbioses

410 South Frear Laboratory
tim14@psu.edu

(814) 865-1916


Melissa Rolls

  • Associate Professor of Biochemistry and Molecular Biology
  • Chair of the Molecular, Cellular and Integrative Biosciences Graduate Program

Subcellular compartmentalization of neurons

118 Life Sciences Building
mur22@psu.edu

(814) 867-1395


Claire Thomas

  • Associate Professor of Biology
  • and Biochemistry and Molecular Biology

Roles of the cytoskeleton in Drosophila development: molecular and genetic approaches

617 Mueller Lab (mailbox 208 Mueller)
ClaireT@psu.edu

(814) 863-0716


Yanming Wang

  • Associate Professor of Biochemistry and Molecular Biology

Epigenetic histone modifications in cell differentiation and cancer

454 North Frear Laboratory
yuw12@psu.edu

(814) 865-3775

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