Lice as Models for Studying Mitochondrial Disorders

A set of genes that in humans would indicate late-stage neurodegenerative diseases like Parkinson’s or Alzheimer’s are present in lice throughout their entire lives. This raises the question: how do lice survive with a genome structure that would cause serious neurological disorders in humans and many other animals?

According to Purdue University Entomology Professor Stephen Cameron, “we are a long way from connecting those dots.” Parkinson’s and Alzheimer’s are mitochondrial diseases associated with aging and are caused by dysfunctional mitochondria, which generate cellular energy.

“If animals develop a neurological disorder too early in life, they are not going to have offspring. Lice seem to have it from when they hatch. They are clearly handling it and have handled it for 50 million years,” Cameron explained.

Over the past decade, there has been a dramatic increase in mitochondrial genomics data for lice and other insects. This information not only helps in identifying and categorizing insect species but also supports the development of insecticides targeting mitochondria. Additionally, lice provide a model to study how evolution influences neurodegenerative illnesses.

Between 2014 and now, the number of insect mitochondrial genomes sequenced has grown by 876%, while the total number of insect species studied has increased by 790%. Cameron’s recent study, published in the Annual Review of Entomology, builds on his earlier research in 2014, highlighting genomic fragmentation and control region duplication as key areas for further study.

Natural selection influences how organisms process food and oxygen through mitochondria. Yet, as Cameron noted, “we have stunningly few examples of studies that actually take that into account.”

Cameron shared how advances in sequencing technology have revolutionized genomic research. “In 2002, sequencing a genome cost $4,000 and took six months of daily lab work. For that money, I could now do hundreds. Genetic-scale sequencing these days is just ludicrously efficient,” he said.

In his recent review, Cameron explored genomic fragmentation in lice, a rare phenomenon where mitochondrial DNA is broken into smaller pieces. This process may help small, inbred populations, like lice, eliminate harmful mitochondrial variations. He questioned, “Why is this constraint against fragmented genomes being released in the case of lice?”

Cameron also studies control region duplication in thrips, a winged insect species that can cause significant agricultural damage. Thrips are challenging to identify due to variations in their mitochondrial genome, but molecular diagnostics can help.

“We are trying to work up some better methods that allow us to more reliably use DNA-based species delimitation, which can then be used for quarantine services to keep pests out of America or other areas,” Cameron said. Such studies could also inform pest management strategies by targeting insect metabolism.

Most pesticides are neurotoxins that do not directly affect mitochondria, but mitochondrial DNA analysis has become a critical tool for identifying and controlling pests. Cameron compared this approach to how understanding coronaviruses after the SARS outbreak helped researchers respond to the COVID-19 pandemic.

Research into insect genomes also explores how harsh environments, like deserts or high altitudes, affect insect populations. This knowledge can inform strategies for controlling pests and preserving beneficial insects.

“It is good to know what their biology would allow them to evolve toward, to understand the escape hatches that evolution provides for them. And, with climate change, those aspects contribute to our understanding of how beneficial insects might respond to changing environments,” Cameron concluded.