Bardet-Biedl Syndrome (BBS) is a pleiotropic ciliopathy characterized by a unique phenotype including obesity and type II diabetes, which has drawn attention to the disease as a way to discover new biochemical and developmental pathways related to the disease’s phenotypic manifestations. BBS2 knockout resulted in low insulin levels, disregulation of glucose homeostasis, and a unique phenotype of atypically short primary cilia in pancreatic islet cells. BBS2 knockdown in vitro showed downregulation of the canonical wnt signaling pathway, s-phase cell cycle arrest, and supported the finding that BBS2 depletion leads to low insulin levels. Both the in vivo and in vitro experiments pointed to the importance of BBS2 for normal glucose homeostasis and provided a new model for diabetes research.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Harris, Lauren Elisabeth

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-042513-143822

Advisor

• Adams, David S.

Year

• 2013

Sponsor

• Agata Jurczyk
• 'Project center: University of Massachusetts Medical Center.

Date created

• 2013-04-25

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright