Friday profile: Stem cells by the numbers

If stem cells were superheroes, their power would be indefinite self-replication – so says researcher Jessica Mar, talking about her ongoing study of stem cell biology at the University of Queensland.

Like all heroes, stem cells have their kryptonite – and one of the major weaknesses is the ageing process in humans. The crux of Mar’s research, which recently earned her a Metcalf Prize and $50,000 from the National Stem Cell Foundation, is how and why our stem cells decline as we age.

“We all know from experience that ageing is a heterogeneous process – people age in different ways, and at different rates,” she says. 

“By developing a clear understanding of how genes are affected in the decline of stem cell functioning in ageing, the hope is to then translate this knowledge into ways to improve the ageing process for everyone.”

Understandably, this research garners plenty of attention from funding bodies and the wider public. 

Mar’s interest in mathematics began at an early age. “How could you not be excited, when statistics is the key to everything?” she asks me, rhetorically. Her love of science hit later, during university.

“I am fascinated by how variability is an inherent part of our genome, and human stem cells have been a quirky example to explore this question more deeply.”

Mar completed her honours degree in genomics at UQ back in 2002 before heading overseas, where she worked at the European Bioinformatics Institute in the UK, undertook her PhD in Boston, and even started her own lab at the Albert Einstein College of Medicine in New York.

But Mar is quick to point out that her scientific evaluations are mostly data-related. “I’m a computational biologist, so rather than being in the field or in a wet-lab, my typical research day is usually spent at a desk, focusing on computer code and data.”

This expertise in digital analysis saw Mar lead a breakthrough study back in 2011, which used a range of nasal stem cells to show a link between genetic variability – also called ‘genetic noise’ – and the onset of Parkinson’s.

“My hypothesis was that increased amounts of variability in gene expression occurred in the disease state – for instance, when parts of a system are broken, intuitively we expect to see more entropy or noise,” she explains.

“But in actual fact, we discovered that variability is like a tuning parameter – for pathways relevant to stem cell functioning, we saw increased variability in Parkinson’s disease patients, but decreased variability in schizophrenia patients.

“This was the first time, to our knowledge, that variability in gene expression was studied in the context of human disease.”

In between running half-marathons (“Running is a valuable tool for building resilience, intuition, discipline, and patience – all qualities that I draw on as a scientist every single day.”), this researcher has earned a slew of scientific accolades, including a Future Fellowship from the Australian Research Council in 2017. 

But her true passion lies in studying disease and ageing, and her general love of innovation in scientific thinking.

“What keeps me up at night, in a good way, is what new discoveries we can make by modelling variability in disease, and asking questions that no-one else thought to pose of the data,” Mar says.

Better outcomes as we age? Sounds like superhero work, indeed.