Mary Lauren Benton, Ph.D.
Assistant Professor Baylor University
- Waco TX
Research focuses on the application of computer science methods to interpret how DNA sequences alter genome function and disease risk.
Media
Biography
Dr. Benton’s research focuses on the application of computer science methods to interpret how DNA sequences alter genome function and impact disease risk. Her current interests include the development of new approaches that integrate diverse datasets and advance our understanding of gene regulation.
The Benton Lab is particularly interested in developing new methods to interpret the impact of genetic variation on gene regulatory processes, and to understand the genetic and environmental risk factors of substance use.
Areas of Expertise
Accomplishments
Rising Star
Kern Entrepreneurial Engineering Network (KEEN)
2025
Outstanding Bioinformatics Senior
Baylor University School of Engineering and Computer Science
2015
Outstanding Computer Science Scholar
Baylor University School of Engineering and Computer Science
2015
Education
Baylor University
BSI
Bioinformatics
2015
Vanderbilt University
M.S.
Biomedical Informatics
2018
Vanderbilt University
Ph.D.
Biomedical Informatics
2020
Media Appearances
Cracking the Code
Baylor ECS Magazine online
2025-12-10
As a child, Mary Lauren Benton, B.S.I. ’15, Ph.D., was drawn to puzzles of all kinds: the more challenging, the better. Riddles, logic, crosswords and jigsaw puzzles all held the same allure, the opportunity to problem-solve. When dumping out a 1,000-piece jigsaw puzzle featuring an image of hundreds of postage stamps that all looked similar, Benton remembers thinking, “Oh, this will be hard,” with a feeling of delighted anticipation. Perhaps it’s this mindset — finding excitement instead of dread in difficult challenges — that has allowed Benton to flourish in the world of bioinformatics, even if she originally wandered into the field by accident.
Mary Lauren Benton: 2025 KEEN Rising Star
Engineering Unleashed online
2025-10-22
Congratulations to Mary Lauren Benton (Baylor University), recipient of the 2025 KEEN Rising Star award!
A KEEN Rising Star is a junior faculty member who has gone above and beyond to equip undergraduate engineers with an entrepreneurial mindset (EM). Awards are given annually.
Enjoy these excerpts from her interview
5 Ways Baylor Research is Impacting Public Health
Baylor Magazine online
2023-12-07
Embedded within the 3 billion letters that comprise a person’s DNA sequence are clues about the processes that make up human life, including the underlying genetics of disease. Mary Lauren Benton, B.S. ’15, Ph.D., assistant professor of bioinformatics, probes the secrets DNA sequences contain to improve human health and open the door to tailored treatments for individuals.
“The biggest mystery of all is how our DNA sequence encodes instructions for so many different processes,” Benton said.
Articles
Identifying deleterious noncoding variation through gain and loss of CTCF binding activity
The American Journal of Human Genetics2025
CCCTC binding factor (CTCF) regulates gene expression through DNA binding at thousands of genomic loci. Genetic variation in these CTCF binding sites (CBSs) is an important driver of phenotypic variation, yet extracting those that are likely to have functional consequences in whole-genome sequencing remains challenging. To address this, we develop a hypothesis-driven framework to identify and prioritize CBS variants in gnomAD. We synthesize CTCF's binding patterns at 1,063,878 genomic loci across 214 biological contexts into a summary of binding activity. We find that high binding activity significantly correlates with both conserved nucleotides (Pearson R = 0.35, p < 2.2 × 10−16) and sequences that contain high-quality CTCF binding motifs (Pearson R = 0.63, p = 2.9 × 10−12).
PANoptosis, a combination of inflammatory cell death mechanisms, induced by Ophiobolin A in breast cancer cell lines
bioRxiv2025
An unmet challenge in managing breast cancer is treatment failure due to resistance to apoptosis-inducing chemotherapies. Thus, it is important to identify novel non-apoptotic therapeutic agents. Several non-apoptotic programmed cell death pathways utilize specific cellular signaling events to trigger lytic and pro-inflammatory cell death. PANoptosis, which encompasses pyroptosis, apoptosis and necroptosis, is of paramount importance in the regulation of cell death and immune responses. Our study illustrates that ophiobolin A (OpA) is an anti-cancer agent that triggers lytic cell death in breast cancer cells, including triple-negative breast cancer (TNBC), via a mechanism dependent on RIPK1. This study reveals that OpA induces typical pyroptosis-like characteristics, including cellular swelling, plasma membrane rupture, GSDMD cleavage and release of cytokines in breast cancer cells.
Nanopore-based sequencing of active DNA replication reveals key principles of metazoan replication fork progression, origin and termination sites
bioRxiv2025
Balancing replication fork progression and origin usage is essential to maintain genome stability, but measuring replication fork progression rates and origin usage throughout the genome has been challenging. Here, we use nanopore sequencing combined with DNAscent to measure replication fork progression together with origin and termination site usage with single-molecule precision throughout the Drosophila genome with nearly full genome coverage. We find that replication fork progression rates are not uniform throughout the genome. Rather, fork progression is slowest in euchromatin, and this is not correlated with active transcription. Replication origins are also influenced by chromatin, but the exact position of initiation is highly variable and are often several kilobases away from ORC binding sites.
Ethanol consumption has minimal effects on cancellous bone architecture in femur and lumbar vertebra in two species of non-human primates
Bone2025
Alcohol abuse is a risk factor for atraumatic fractures. Our previous work using a non-human primate model of voluntary ethanol consumption showed that chronic ethanol intake for 6 months to 2.5 years decreased global bone turnover and tibial cortical porosity but did not result in changes in distal tibia cancellous architecture. However, bone remodeling varies among skeletal sites. Here, we extended this analysis to include 3 additional cancellous bone compartments (distal femur metaphysis, distal femur epiphysis, lumbar vertebra). Specifically, we applied a machine learning framework to data from 155 monkeys (100 ethanol and 55 controls) to identify the bone features associated with chronic ethanol use. In concordance with our prior findings, we did not find that ethanol consumption resulted in population-level changes in cancellous bone architecture.
Gasdermin D Cleavage and Cytokine Release, Indicative of Pyroptotic Cell Death, Induced by Ophiobolin A in Breast Cancer Cell Lines
International Journal of Molecular Sciences2026
An unmet challenge in managing breast cancer is treatment failure due to resistance to apoptosis-inducing chemotherapies. Thus, it is important to identify novel non-apoptotic therapeutic agents. Several non-apoptotic programmed cell death pathways utilize specific cellular signaling events to trigger lytic and pro-inflammatory cell death, examples of which are pyroptosis and necroptosis. Our study illustrates that ophiobolin A (OpA) is an anti-cancer agent that triggers lytic cell death in breast cancer cells, including triple-negative breast cancer (TNBC). This study reveals that OpA induces typical pyroptosis-like characteristics, including cellular swelling, plasma membrane rupture, GSDMD cleavage, and release of cytokines in breast cancer cells. However, the additional involvement of RIPK1 and induction of RIPK3 clustering in select cell lines suggest that multiple pathways may be triggered upon OpA treatment. T
