Around the world in Health this week

A ‘fitbit’ for plants?

Scientists have developed a tool called ‘Phenocart’ to capture essential plant health data. The ‘Phenocart’ measures a plant’s vital signs like growth rate and colour the same way a Fitbit monitors human health signals like blood pressure and physical activity. In a field experiment with thousands of plots, the ‘Phenocart’ is a quick way to evaluate plant health. It can also help plant breeders design larger experiments. Knowing what physical traits a plant has is called phenotyping. “Larger sample size gives you more power,” said Jesse Poland, assistant professor in the Departments of Plant Pathology and Agronomy at Kansas State University. “Measuring phenotypes is very labour-intensive, and really limits how big an experiment we can do.” The new tool will allow for faster measurements and accelerate the breeding process.

Self-organising soft materials

Researchers have created self-organising soft materials that mimic the spontaneous folding motion seen in the

Mimosa pudica plant. The technology could benefit numerous emerging technologies and commercial applications including wearable sensors, microfluidics, and artificial muscles. Many biological systems in nature adapt to their environments using self-assembly techniques; the crystallisation-driven formation of seashells is one example. Some self-assembling organisms exhibit spontaneous motion. The Mimosa pudica plant, for example, reacts to the slightest contact pressure, with a very rapid folding of its leaflets, triggered by a cascade of electrical potentials and osmotic pressure waves.

Signatures and cancer treatment

Researchers have found unique signatures in four different human breast cancer cell types that could be used to develop tailor-made cancer treatment. This will increase the efficacy of drug treatments for breast cancer patients as well as reduce side effects. Certain cancer-triggering genes, or oncogenes as they are called, drive solid tumour growth in some breast cancer patients but are just passenger genes in others, i.e. expressed but not essential for growth. As a result, tumours in different breast cancer patients may respond differently to the same treatment depending on which oncogenes are active and which are just along for the ride. Identifying the panel of active genes in a patient’s tumour — called the functional oncogene signature — could help an oncologist select therapies that target its growth, says the study published in

Oncotarget .

The ‘nice’ and ‘nasty’ genes

A mathematical model claims to shed light on why some individuals may be genetically programmed to be nice while others are nasty. Using colony-living microbes as inspiration to explore why some individuals are by nature generous and others less so, the researchers produced an innovative model of social evolution that allows them to understand how far this is likely to be influenced by conditioning or the surrounding environment. They found that the behaviour of individuals can often evolve to be determined by a set of inherited genetic tendencies that accurately predict social relationships, including their likely relatedness to other members of their community and their surroundings rather than in direct response to what they sense or experience.

Demystifying Science

What are Paternal Mitochondrial DNA?

Mitochondria are the power houses of cells. They are so important that they have their own DNA, which is stored outside the cell’s nucleus. While most cells get half their DNA from each parent, mitochondrial DNA can only be got from the mother. This insight is critical to tracing human lineages and broader evolutionary genealogy. It’s been a mystery as to what prevents paternal mitochondrial DNA from being passed on. This week scientists have a clue about what stymies paternal mDNA. They found that when paternal mitochondria persist for longer than they should during development, the embryo is at greater risk of lethality. Based on studies in roundworm, they found that shortly after a sperm penetrates an egg during fertilisation, the sperm’s mitochondria are degraded while the egg’s mitochondria persist. A gene, called cps-6, seemed to be responsible, as deleting it caused paternal mitochondria to linger longer in the embryo and cause higher rates of embryonic death.