Event Title

The Effects of DIO2 and DIO3 Expression on Seasonal Reproduction in a Seasonally Breeding Animal

Location

CSU Ballroom

Start Date

11-4-2017 10:00 AM

End Date

11-4-2017 11:30 AM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

Rachel Cohen

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Description

Thyroid hormone (TH) is critical for testes development and a decrease in TH can cause hypogonadism, which decreases gonadal function. Deiodinase is responsible for the activation and inactivation of TH from the precursor, thyroxin (T4). Type 2 deiodinase (DIO2) produces the biologically active thyroid hormone, triiodothyronine (T3), while type 3 deiodinase (DIO3) produces an inactive isoform, reverse triiodothyronine (rT3). In developing testis, DIO3 expression is upregulated and DIO3 deficiency results in low T3, causing a drastic reduction in testis size. In seasonally breeding animals, testicular morphology and function are altered in the breeding (BS) compared to non-breeding season (NBS), such that they go through periods where the gonads are inactive (hypogonadism). Studying a seasonally breeding Green anole lizard, Anolis carolinensis, will allow us to examine natural changes in DIO2 and 3 expression patterns that might mediate these changes. Male green anole testes grow and produce steroid hormones and sperm during the BS, while they regress and the lizards no longer reproduce during the NBS. We are using quantitative polymerase chain reaction (qPCR) to measure how DIO2 and DIO3 mRNA expression in the testes differs between the BS and NBS. Since the presence of T3 is important for testicular maturity and development, we expect to find that testes from breeding lizards will have upregulated DIO2 and downregulated DIO3 compared to NBS testes. This will support the idea that TH is critical for regulating seasonal testicular changes, which may help us to understand how TH is involved in hypogonadism.

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

The Effects of DIO2 and DIO3 Expression on Seasonal Reproduction in a Seasonally Breeding Animal

CSU Ballroom

Thyroid hormone (TH) is critical for testes development and a decrease in TH can cause hypogonadism, which decreases gonadal function. Deiodinase is responsible for the activation and inactivation of TH from the precursor, thyroxin (T4). Type 2 deiodinase (DIO2) produces the biologically active thyroid hormone, triiodothyronine (T3), while type 3 deiodinase (DIO3) produces an inactive isoform, reverse triiodothyronine (rT3). In developing testis, DIO3 expression is upregulated and DIO3 deficiency results in low T3, causing a drastic reduction in testis size. In seasonally breeding animals, testicular morphology and function are altered in the breeding (BS) compared to non-breeding season (NBS), such that they go through periods where the gonads are inactive (hypogonadism). Studying a seasonally breeding Green anole lizard, Anolis carolinensis, will allow us to examine natural changes in DIO2 and 3 expression patterns that might mediate these changes. Male green anole testes grow and produce steroid hormones and sperm during the BS, while they regress and the lizards no longer reproduce during the NBS. We are using quantitative polymerase chain reaction (qPCR) to measure how DIO2 and DIO3 mRNA expression in the testes differs between the BS and NBS. Since the presence of T3 is important for testicular maturity and development, we expect to find that testes from breeding lizards will have upregulated DIO2 and downregulated DIO3 compared to NBS testes. This will support the idea that TH is critical for regulating seasonal testicular changes, which may help us to understand how TH is involved in hypogonadism.

Recommended Citation

Kang, Hyejoo. "The Effects of DIO2 and DIO3 Expression on Seasonal Reproduction in a Seasonally Breeding Animal." Undergraduate Research Symposium, Mankato, MN, April 11, 2017.
http://cornerstone.lib.mnsu.edu/urs/2017/poster-session-A/14