ASHLEY S. WILLIAMS
Ashley S. Williams, first-generation PhD candidate, researcher, and proponent of improving diversity in STEM, uses an interdisciplinary approach to understand the role mitochondria play in the onset of cellular senescence in the reproduction-longevity tradeoff.
OVERVIEW OF MY RESEARCH
Female reproductive success naturally declines with increasing age, however, whether the cost of reproduction reduces longevity of an individual is still a matter requiring greater investigation. Reproduction and lactation are highly energetically demanding processes likely sequestering energy from mitochondria. I investigate how mitochondria are affected by reproduction and how that ultimately influences longevity. To do this, I maintain a colony of Mus musculus in semi-natural enclosures and monitor the body temperatures for reproductive and non-reproductive female mice, and I test their mitochondrial respiratory capacity, physical fitness, and look for markers of oxidative damages, senescence markers, and the types of mutations present in the liver, brain, and skeletal muscle tissues. I also collect the same data from animals of different age groups in a more traditional laboratory setting to understand how ageing influences mitochondrial function and performance.
MITOCHONDRIAL PHYSIOLOGY VARIES WITH PARITY AND BODY MASS IN THE LABORATORY MOUSE (MUS MUSCULUS)
June 6, 2020
Here we investigated the influence of parity on mitochondrial respiratory performance and oxidative stress in the liver. We observed multiparous females with high body masses displayed higher liver mitochondrial respiratory capacity (measured by RCR). Multiparous females also showed reduced basal respiration (state 4) and mitochondrial density while displaying a higher incidence of oxidized proteins in the liver than females who allocated less towards reproduction.
AN ECOLOGIST’S GUIDE TO MITOCHONDRIAL DNA MUTATIONS AND SENESCENCE
June 5, 2019
This paper lays the foundation behind the theory of my dissertation research indicating mutations from replication error of mitochondrial DNA (mtDNA) over an individual's lifetime and not free radical damage might lead to cellular senescence, and that such a mechanism should be considered by Ecologists who tradeoffs between reproduction and longevity in the context of mitochondrial theory of ageing and the free radical theory of aging.