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Undergraduate Research Project Management System

Testing the role of ISWI in Xenopus Laevis development with a dominant negative ISWI mutant

Status Current
Seeking Researchers No
Start Date 09/01/2008
End Date 12/31/2011
Funding Source Undergraduate Research Grants
Funding Amount
Community Partner
Related Course
Last Updated 07/05/2008 01:25AM
Keywords

People

Faculty
  Jocelyn Krebs

Student Researchers
  Carly Craig

Abstract

Williams Syndrome is a genetic disorder that is characterized by visual and spatial processing dysfunction and growth deficiency. Individuals with the disease lack the Williams Syndrome Transcription Factor (WSTF) which forms the WICH complex in conjunction with ISWI. Imitation Switch (ISWI) is a chromatin remodeler that orchestrates gene activation or silencing in an organized process. Previous Xenopus laevis studies have shown that fatal neurological and visual impairment results from ISWI inhibition during embryonic development (Dirscherl et al. 2005). Additionally, depleted ISWI concentrations led to cataracts in embryos and may illuminate mechanisms responsible for congenital cataracts in humans. Transgenesis involving a dominant negative ISWI mutant will eliminate all function of the ISWI gene following induction of heat shock in vivo. This will determine if critical developmental periods demand a functional ISWI complex or if continuous expression is necessary for normal growth. Presently, it is not known if the late abnormal phenotypes (cataracts or brain defects) correspond to ISWI function at specific stages or a downstream effect of an early requirement during neurulation. The significance of this research is that it will increase our understanding of how an essential remodeling enzyme serves as a master regulator of brain and eye development.

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