Event Title

Expression of a Potential Novel Deafness Gene

Location

CSU Ballroom

Start Date

20-4-2015 10:00 AM

End Date

20-4-2015 11:30 AM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

David Sharlin

Mentor's Email Address

david.sharlin@mnsu.edu

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Description

Over fifty percent of hearing loss is the result of genomic defects. Thyroid hormone plays a key role in developing the auditory organ, known as the cochlea, by regulating gene expression. A lack of this hormone during crucial periods of perinatal development leads to permanent hearing loss due to altered remodeling of the greater epithelial ridge, a transient structure that generates the tectorial membrane. However, the molecular mechanisms that the thyroid hormone regulates to direct the development of hearing are poorly understood. This project focuses on a novel potential thyroid hormone target gene, carbohydrate sulfotransferase 15 (chst15), which codes for an important enzyme involved in the sulfonation of glycoproteins in the tectorial membrane. The goal of this project is to determine the expression profile of chst15 during normal euthyroid cochlear development and determine how this expression changes in developmentally hypothyroid C57Bl/6 mice. Cochlea from control and hypothyroid mice were harvested at postnatal days 1, 5, 8, and 15, frozen, and cryosectioned. To locate the specific chst15 mRNAs within the cochlea, in situ hybridization, a process that uses anti-sense (complementary) labeled mRNA that can be detected with an enzyme-conjugated antibody for chromagen detection was used. Future studies will be aimed at detection Chst15 protein via immunohistochemistry (IHC). Together, these studies will demonstrate misregulation of Chst15 under hypothyroid conditions and document that mRNA molecules are translated into protein.

This document is currently not available here.

Share

COinS
 
Apr 20th, 10:00 AM Apr 20th, 11:30 AM

Expression of a Potential Novel Deafness Gene

CSU Ballroom

Over fifty percent of hearing loss is the result of genomic defects. Thyroid hormone plays a key role in developing the auditory organ, known as the cochlea, by regulating gene expression. A lack of this hormone during crucial periods of perinatal development leads to permanent hearing loss due to altered remodeling of the greater epithelial ridge, a transient structure that generates the tectorial membrane. However, the molecular mechanisms that the thyroid hormone regulates to direct the development of hearing are poorly understood. This project focuses on a novel potential thyroid hormone target gene, carbohydrate sulfotransferase 15 (chst15), which codes for an important enzyme involved in the sulfonation of glycoproteins in the tectorial membrane. The goal of this project is to determine the expression profile of chst15 during normal euthyroid cochlear development and determine how this expression changes in developmentally hypothyroid C57Bl/6 mice. Cochlea from control and hypothyroid mice were harvested at postnatal days 1, 5, 8, and 15, frozen, and cryosectioned. To locate the specific chst15 mRNAs within the cochlea, in situ hybridization, a process that uses anti-sense (complementary) labeled mRNA that can be detected with an enzyme-conjugated antibody for chromagen detection was used. Future studies will be aimed at detection Chst15 protein via immunohistochemistry (IHC). Together, these studies will demonstrate misregulation of Chst15 under hypothyroid conditions and document that mRNA molecules are translated into protein.

Recommended Citation

Verdon, Jonathan. "Expression of a Potential Novel Deafness Gene." Undergraduate Research Symposium, Mankato, MN, April 20, 2015.
http://cornerstone.lib.mnsu.edu/urs/2015/poster_session_A/23