Zhexing Wen, John Hopkins University

*********************************
There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
*********************************

Event Details
  • Date/Time:
    • Thursday February 26, 2015 - Friday February 27, 2015
      3:00 pm - 2:59 pm
  • Location: Georgia Tech, Molecular Science and Engineering, Room G021
  • Phone: (404) 894-3700
  • URL:
  • Email:
  • Fee(s):
    N/A
  • Extras:
Contact

If you have questions about logistics or would like to set up an appointment with the speaker, please contact the School of Biology's administrative office at bio-admin@biology.gatech.edu.

Summaries

Summary Sentence: Zhexing Wen, John Hopkins University

Full Summary: Modeling mental disorders with patient-specific iPSCs Abstract
Severe psychiatric illnesses, such as schizophrenia and major depression, are chronic and complicated neurological diseases with a prominent genetic basis. However, the causes of these mental disorders are still poorly understood due to the lack of a representative model that accurately recapitulates the nature and distribution of the human pathology. Human induced-pluripotent stem cells (iPSCs), which carry the genetic information from patients, pave the way to study human development and to discover the molecular and cellular basis of human diseases in a more tractable experimental system. Here we generated iPSCs from four members of a family in which a frame-shift mutation of Disrupted-in-schizophrenia 1 (DISC1) co-segregated with psychiatric disorders. We further produced different isogenic iPSC lines with TALEN genome editing technique. We show that mutant DISC1 leads to deficits in presynaptic vesicle release in human forebrain neurons. Mechanistically, mutant DISC1 causes transcriptional dysregulation of many genes related to synapses and psychiatric disorders and depletes wild-type DISC1. Furthermore, mechanism-guided pharmacological inhibition of phosphodiesterases rescues synaptic defects in mutant neurons. Our studies directly support the synapse hypothesis for the etiopathology of psychiatric disorders and uncover a novel mechanism through which the disease-relevant mutation affects synaptic functions via transcriptional dysregulation.

Modeling mental disorders with patient-specific iPSCs

Additional Information

In Campus Calendar
No
Groups

School of Biological Sciences

Invited Audience
Undergraduate students, Faculty/Staff, Public, Graduate students
Categories
Seminar/Lecture/Colloquium
Keywords
Greg Gibson, School of Biology Seminar, Zhexing Wen
Status
  • Created By: Jasmine Martin
  • Workflow Status: Published
  • Created On: Feb 23, 2015 - 7:11am
  • Last Updated: Apr 13, 2017 - 5:19pm