Dr. Keturah Adams

EDUCATION

2009 – B.S. Chemistry, Southwestern Oklahoma State University

2012 – M.S. Biological Chemistry, Texas A&M University

2016 – Ph.D. Biological Chemistry, Texas A&M University

2019 – Began teaching at SWOSU

RESEARCH

Exploring ELOVL4 Splice Variants in the Retina and Brain

Dr. Keturah A. Adams (Mentor)

Actively accepting research students for credit.

Background and Significance: There is currently no cure for macular dystrophy or neurodegenerative disorders, and the need for treatments is growing worldwide. Mutations in the ELOngation of Very Long chain fatty acids (ELOVL4) protein cause two distinct human diseases. Stargardt-like Macular Dystrophy (STGD3) results in early-onset vision loss, while Spinocerebellar Ataxia 34 (SCA34) leads to late-onset motor dysfunction. Interestingly, patients with STGD3 do not show motor deficits, and patients with SCA34 do not experience vision loss, suggesting that ELOVL4 mutations act differently in the retina versus the brain.

ELOVL4 is responsible for the synthesis of special fatty acids. In the retina, it predominantly produces very long-chain polyunsaturated fatty acids (VLC-PUFA), whereas in the brain it mainly generates very long-chain saturated fatty acids (VLC-SFA). These differences in fatty acid products may explain why ELOVL4 mutations lead to distinct diseases. However, the molecular mechanisms underlying this tissue specificity remain unknown, including whether splice variants of ELOVL4 maintain, reduce, or inhibit enzymatic activity. Understanding these functions is critical for the development of targeted therapies.

We hypothesize that tissue-specific factors, such as fatty acid precursor availability and alternative splice variants of ELOVL4, drive the differences in disease phenotypes caused by ELOVL4 mutations. Dr. Martin-Paul Agbaga originally discovered the role of ELOVL4 as a fatty acid elongase, and our work builds on this foundation to investigate how ELOVL4 contributes to the pathogenesis of STGD3 and SCA34.

Research Plan: Our research focuses on how splice variants of ELOVL4 influence fatty acid synthesis and disease outcomes. First, we test ELOVL4 splice variants in vitro using HEK293T mammalian cells transfected with recombinant adenoviral plasmids carrying six different ELOVL4 splice variants. We then measure the production of VLC-SFA and VLC-PUFA using gas chromatography–mass spectrometry (GC-MS). This approach will allow us to determine which variants preferentially synthesize VLC-SFA or VLC-PUFA and how these differences may explain the tissue-specific outcomes observed in human diseases.

CONTACT INFORMATION

Email:
keturah.adams@swosu.edu Office Number: CPP 202-B
Phone Number: 580-774-6027

TEACHING: BASIC COURSES

SCI 1513 Concepts of Physical Science
SCI 1501 Concepts of Physical Science Lab
CHEM 1004 Gen Chem
CHEM 1004L Gen Chem Lab
CHEM 1203 Gen Chem I
CHEM 1252 Gen Chem

TEACHING: BIOCHEMISTRY

CHEM 4124 Biochemistry
CHEM 4124L Biochemistry Lab
CHEM 4133 Pharmaceutical Biochemistry

OTHER ACTIVITIES

AUG 2020-PRESENT
Chemistry Tutoring Coordinator

RECENT PUBLICATIONS

Kurra Y, Odoi KA, Lee YJ, Yang Y, Lu T, Wheeler SE, Torres-Kolbus J, Deiters A, & Liu WR. (2014 Sep 17). Two rapid catalyst-free click reactions for in vivo protein labeling oy genetically encoded strained alkene/alkyne functionalities. Bioconjugate Chem, 25(9), 1730-1738.
PMID: 25158039
doi: 10.1021/bc500361d
*Contributed equally

Odoi KA, Huang Y, Rezenom YH, & Liu WR. (2013). Nonsense and sense suppression abilities of original and derivative Methanosarcina mazei pyrrolysyl-tRNA synthetase-tRNA(Pyl) pairs in the Escherichia coli BL21(DE3) cell strain. PLos One, 8(3), e57035.
PMID: 23520461
doi: 10.1371/journal.pone.0057035

O’Donoghue P, Prat L, Heinemann IU, Ling J, Odoi KA, Huang Y, Liu WR, & Söll D. (2012). Near-cognate suppression of amber, opal and quadruplet codons competes with aminoacyl-tRNAPyl for genetic code expansion. FEBS Letters, 586(21), 3931-3937.
PMID: 23036644
doi: 10.1016/j.febslet.2012.09.033