Title

The Location and Timing of CHD7 and the Role of SOX9 on CHD7's Expression During Embryonic Mouse Development

School Name

South Carolina Governor's School for Science & Mathematics

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Abstract

Atrioventricular septal defects (AVSDs) are a congenital heart defect (CHD) that is often seen in patients with CHARGE Syndrome. Around 60% of CHARGE Syndrome cases are caused by mutations to the chromodomain-helicase-DNA-binding protein 7 (CHD7) gene. The second heart field (SHF) is an embryonic structure that gives rise to multiple structures of the heart. The transcription factor SRY-BOX 9 (Sox9) is important in the development of the SHF, and when Sox9 is removed from the SHF, an AVSD occurs. Previous research stated that CHD7 regulates Sox9's expression. The goal of this work was to observe the location and timing of CHD7 expression during embryonic development and the effects of the transcription factor Sox9 on CHD7's levels of expression. The hypothesis was that CHD7 is expressed in the SHF and that Sox9 lowers CHD7's level of expression. Mice embryos at 10.5, 12.5, and 16.5 days of development were sectioned and underwent antigen retrieval and immunohistochemical staining. Previous research stated that CHD7 stops being expressed after 11.5 days of development. However, the results of this experiment showed that CHD7 is expressed in various embryonic structures, like the SHF, from 10.5 to 16.5 days of development. Knocking out Sox9 in the SHF did not affect CHD7's level of expression. An understanding of the timing and location of CHD7 expression during development will allow for future research to work on CHD7 during these stages and uncover its role in the pathogenesis of AVSDs.

Location

Furman Hall 107

Start Date

3-28-2020 9:15 AM

Presentation Format

Oral Only

Group Project

No

COinS
 
Mar 28th, 9:15 AM

The Location and Timing of CHD7 and the Role of SOX9 on CHD7's Expression During Embryonic Mouse Development

Furman Hall 107

Atrioventricular septal defects (AVSDs) are a congenital heart defect (CHD) that is often seen in patients with CHARGE Syndrome. Around 60% of CHARGE Syndrome cases are caused by mutations to the chromodomain-helicase-DNA-binding protein 7 (CHD7) gene. The second heart field (SHF) is an embryonic structure that gives rise to multiple structures of the heart. The transcription factor SRY-BOX 9 (Sox9) is important in the development of the SHF, and when Sox9 is removed from the SHF, an AVSD occurs. Previous research stated that CHD7 regulates Sox9's expression. The goal of this work was to observe the location and timing of CHD7 expression during embryonic development and the effects of the transcription factor Sox9 on CHD7's levels of expression. The hypothesis was that CHD7 is expressed in the SHF and that Sox9 lowers CHD7's level of expression. Mice embryos at 10.5, 12.5, and 16.5 days of development were sectioned and underwent antigen retrieval and immunohistochemical staining. Previous research stated that CHD7 stops being expressed after 11.5 days of development. However, the results of this experiment showed that CHD7 is expressed in various embryonic structures, like the SHF, from 10.5 to 16.5 days of development. Knocking out Sox9 in the SHF did not affect CHD7's level of expression. An understanding of the timing and location of CHD7 expression during development will allow for future research to work on CHD7 during these stages and uncover its role in the pathogenesis of AVSDs.