Jenna Collins
Pronouns: She/Her/Hers
Research Mentor(s): Megan Killian
Co-Presenter:
Research Mentor School/College/Department: Orthopaedic Surgery / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 3 – 1:40pm – 2:30 pm
Room: League Ballroom
Authors: Jenna Collins, Syeda Lamia, Megan Killian
Presenter: 81
Abstract
The Killian Lab aims to study the key regulators affecting musculoskeletal growth at a cellular and tissue level using transgenic mice in order to act advantageously upon both pediatric and young adult orthopedic disorders through the development of mechanobiological mechanisms. Specifically, identifying the requirement of Transcription Factor A: Mitochondrial (Tfam), a major regulator of mitochondrial DNA, in musculoskeletal function and repair will allow for potential mechanobiological interventions for promoting tissue recovery following injury. It is hypothesized that Tfam is efficiently deleted in such transgenic mice, allowing for further research in the induced effects to muscle function as a result of this deletion. This research primarily involves the multifaceted use of transgenic mice (e.g., Cre-lox) to visualize changes in skeletal muscle in the absence of Tfam gene expression, using both brightfield and fluorescent imaging, as well as genetic expression analysis (e.g., quantitative real-time polymerase chain reaction; qRT-PCR) to quantify the level of Tfam expression in the hindlimb gastrocnemius and soleus muscles of transgenic mice. Thus far, RNA has been isolated from mouse skeletal muscle in wildtype and Tfam-flox/flox; Acta1-Cre-tet-O mice. It has been shown that use of tetracycline-inducible Acta1-Cre-tet-O (i.e., skeletal muscle-specific) in adult mice leads to poor knockdown of Tfam after 3 weeks of doxycycline treatment. Currently, this research focuses on investigating the efficiency of Tfam knockdown in muscle and other tissues (e.g., in tendon using Scx-Cre) to determine if and how Tfam is deleted using cre-recombination. This work is essential to defining a genetic basis for muscle dysfunction in order to extrapolate beyond such preliminary findings to develop hypotheses as to how to approach musculoskeletal rehabilitation upon injury.
Biomedical Sciences
