Meet the Researcher - Michaela Vance

Breakout Room: 2

MichaelaVance_HeadshotResearcher Name: Michaela Vance
Co-Presenter: Nazka Nurbyek
Title of Research: Effect of phenylalanine, retinoic acid, retinal, and citral on proliferation of O9-1 mouse cranial neural crest cells
Division Representing: Biology
Institution: University of Central Oklahoma
Institution Location: Oklahoma
Home State: Oklahoma
District Number: 5
Advisor/Mentor: Nikki Seagraves

Research Experience:  
Michaela started working with Dr. Nikki Seagraves in her developmental biology lab in the summer of 2019, studying O9-1 mouse cranial neural crest cells. Michaela was awarded a SMaRT Grant. She has continued to work with Dr. Seagraves performing proliferation, differentiation, and apoptosis assays. She practiced mammalian cell culture, microdissection, histology, and fluorescent imaging techniques. During her time in the lab, Michaela was awarded the OK-INBRE Grant in the summer of 2020. She has been on the President's Honor Roll for the entirety of their time at the University of Central Oklahoma. She is an officer of the Tri-Beta Biological Honor Society as the Vice President. Her duties include organizing and planning meetings, inviting speakers, preparing presentations, and planning outreach events for members. Additionally, Michaela is a supplemental instructor for cell biology.

Presentation Experience: 
Michaela is well versed in presenting her research to academic audiences. She presented a poster at the Oklahoma Academy of Science (OAS) Technical Meeting in November 2019 to a panel of judges and the scientific community. The mission of OAS is to stimulate scientific research in Oklahoma through various facets of science including social sciences, physical sciences, and biological sciences among others. She also presented an oral presentation at OAS the following year. Michaela had a fulfilling opportunity to present a poster at the Society for Developmental Biology (SDB) 79th Annual Meeting in July 2020. The mission of SDB is to further the study of developmental biology, and it is a national conference allowing students and faculty to present their findings. Additionally, she has experience presenting to non-academic audiences. She presented her research at a Tri-Beta Biological Honor Society meeting to students and faculty in the biology department. 

Significance of Research:       
Maternal phenylketonuria [MPKU] is a syndrome that causes many different types of birth defects affecting growth and development of heart, brain, and bones of the face. The syndrome is caused by exposure to too much Phenylalanine [Phe], an amino acid found in proteins eaten by a mother with Phenylketonuria during pregnancy. It is not known why Phe causes abnormal development of embryos. Our lab has preliminary evidence that high levels of Phe could inhibit communication between cells mediated by Retinoic Acid [RA], which effects how cells divide, migrate, and specialize. Division of the neural crest cells are important in formation of components of the heart including the outflow tract (OFT) and aortic arch arteries (AAA). We hypothesize that Phe inhibits the rate that cells divide, which may be the cause of the birth defects seen in MPKU. We cultured O9-1 mouse neural crest cells and performed an experiment to determine the effect of Phe, RA, retinal, and citral exposure on how the cells divide. Images were analyzed with ImageJ and GraphPad Prism. Results suggest that Phe exposure causes a significant decrease in division of cells. It has been shown that RA and retinal increase cell division, and that citral decreases. Phe acted similar to citral, which suggests that it may act as an inhibitor of RA, which could cause the heart defects seen in MPKU. This work is significant because no one knows how Phe causes the types of defects observed in human MPKU.

Uniqueness of Research: 
To our knowledge, this is the first study to find a decrease in the proliferation of neural crest cells caused by phenylalanine. Our work eludes to a potential mechanism that phenylalanine could affect the retinoic acid pathway which may result in the defects observed in MPKU.


Main POH 2021 PAge MEET MORE ReseaRchers