Expression of Follistatin-Like 1 (Fstl1) in the Cochlea: A Potential Deafness Gene
Location
CSU Ballroom
Start Date
10-4-2018 10:00 AM
End Date
10-4-2018 11:30 AM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
David Sharlin
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
More than 360 million cases of auditory deficits world-wide are linked to hereditary genetic deafness. The 115 genes linked to hereditary genetic deafness, does not account for entirety of genetic deafness. Untreated congenital hypothyroidism results in permanent hearing loss. Thyroid hormone works by binding to a nuclear receptor that controls gene expression. It is proposed that deafness associated with lack of thyroid hormone in early development results from the mis-regulation of specific genes that drive development of hearing. Follistatin-like 1 (Fstl1) - a bone morphogenetic protein (BMP) 4 signaling antagonist important in the development of the brain, lung, and urinary system - is a potential thyroid hormone receptor target gene. However, whether Fstl1 is important in cochlea development is completely unknown. Therefore, this research aims to map the expression of Fstl1 in euthyroid and hypothyroid conditions during development. Using a postnatal day 3 total cochlear cDNA pool, we amplified a candidate Fstl1 cDNA using PCR. It was cloned into the pGEMT-easy vector and transfected into JM109 bacterial cells. Colonies are currently being screened for the proper Fstl1 containing plasmids. The animal experiments are generating euthyroid cochlear and hypothyroid cochlear tissues for in situ hybridization. We predict Fstll mRNA will be expressed in a cochlear region known as the greater epithelial region (GER) and be increased in the hypothyroid cochlear tissues compared to euthyroid control tissues. Ultimately, our study has the possibility to identify Fstl1 as a novel cochlear expressed gene and potentially a unique deafness gene.
Expression of Follistatin-Like 1 (Fstl1) in the Cochlea: A Potential Deafness Gene
CSU Ballroom
More than 360 million cases of auditory deficits world-wide are linked to hereditary genetic deafness. The 115 genes linked to hereditary genetic deafness, does not account for entirety of genetic deafness. Untreated congenital hypothyroidism results in permanent hearing loss. Thyroid hormone works by binding to a nuclear receptor that controls gene expression. It is proposed that deafness associated with lack of thyroid hormone in early development results from the mis-regulation of specific genes that drive development of hearing. Follistatin-like 1 (Fstl1) - a bone morphogenetic protein (BMP) 4 signaling antagonist important in the development of the brain, lung, and urinary system - is a potential thyroid hormone receptor target gene. However, whether Fstl1 is important in cochlea development is completely unknown. Therefore, this research aims to map the expression of Fstl1 in euthyroid and hypothyroid conditions during development. Using a postnatal day 3 total cochlear cDNA pool, we amplified a candidate Fstl1 cDNA using PCR. It was cloned into the pGEMT-easy vector and transfected into JM109 bacterial cells. Colonies are currently being screened for the proper Fstl1 containing plasmids. The animal experiments are generating euthyroid cochlear and hypothyroid cochlear tissues for in situ hybridization. We predict Fstll mRNA will be expressed in a cochlear region known as the greater epithelial region (GER) and be increased in the hypothyroid cochlear tissues compared to euthyroid control tissues. Ultimately, our study has the possibility to identify Fstl1 as a novel cochlear expressed gene and potentially a unique deafness gene.
Recommended Citation
Kim, Eunwon and Lauren Hesser. "Expression of Follistatin-Like 1 (Fstl1) in the Cochlea: A Potential Deafness Gene." Undergraduate Research Symposium, Mankato, MN, April 10, 2018.
https://cornerstone.lib.mnsu.edu/urs/2018/poster-session-A/9
