The interaction between volcanic eruptions and coral reefs are commonly reported to be detrimental to corals. However, recent laboratory experiments on cultured corals exposed to moderate concentrations of volcanic ash, reveal quite the opposite: ash-exposed corals exhibit surprising health improvements compared to the control counterparts.

Phosphorylation is a fundamental mechanism in eukaryotic cells that allows signals to propagate. Kinases orchestrate this process by phosphorylating proteins to modulate their activity. Our work reveals the architecture of the complex between two key players of the mitogen-activated protein kinase signaling pathway, p38α and MKK6, while also giving an idea of what happens when the two come together.

Natural selection is often thought to “perfect” an organism. Yet, real organisms show lots of diversity in their behaviours and morphology. We show that competition for resources can either maintain trait diversity at a constant high level, or lead to wild cycles in trait evolution. Continuous differences in resources like those found in nature are an important part of these outcomes.

Our quest is to control how molecules come together to form large assemblies. In our earlier studies we showed that we can stack saddle-shaped molecular chips into neat columns that then stick together laterally to form 2D sheets, but can we limit this process to form different morphologies? Here we show how blocking the sides of the columns equalizes the secondary interaction, yielding 1D fibers.

Establishing an appropriate immune response is essential to recover from viral diseases such as COVID-19.The thymus, an organ of the immune system, plays a vital role in producing new T-lymphocytes that help eliminate the virus that causes COVID-19. We recently discovered that a genetic trait determines the effectiveness of thymic activity in fighting this virus, and thus the clinical outcome.

DNA mutations causing cancer occur in cells through aging, environmental exposures, and cellular factors. By analysing thousands of cancer genomes, we found that tobacco smoking, APOBEC enzymes, and oxidative stress often introduce harmful “stop-gain” mutations that disable genes. This study highlights how some lifestyle choices and cellular processes can modify genes that protect us from cancer.