#immunofluorescence

Seams Vital

Like the carefully stitched hem of a pleated skirt, the outer layer of the heart is fundamental to its entire shape and function. This epicardium is a regulator of development and regeneration, and supports vessel and muscle growth. To better understand the molecular mechanisms guiding its development, researchers investigated a protein called SRSF3, which helps process RNA messages (strands of genetic material). When it was removed from early mouse epicardial precursor cells, the epicardium failed to form normally (right, reduced green SRSF3 limiting outgrowth around explants cultured from embryonic hearts, compared to normal, left) so proper heart formation was prevented. Their experiments also showed cells that dodged SRSF3 deletion increased production to compensate, cautioning researchers that incomplete gene deletion can hide how important a gene really is in experiments. Understanding these growth controls could eventually help researchers tackle both congenital heart defects and the challenge of repairing broken hearts.

Written by Anthony Lewis

Image from work by Irina-Elena Lupu and Susann Bruche, and colleagues

Institute of Developmental and Regenerative Medicine, British Heart Foundation Centre of Research Excellence, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Development, March 2026

Variety Upon Variety

Titin, the largest protein produced in the body, is a giant spring-like protein found in muscle cells, including those of the heart (pictured). There are multiple versions of titin, and their production is regulated, at least in part, by splicing factor (cutting the RNA transcript to make different sized versions of the same protein) RBM20 (coloured blue). In the infant mammalian heart, for example, most titin is long and elastic, while in older mammals RBM20 activity leads to shorter stiffer versions of the protein. Aberrant production of RBM20 has been linked to certain cardiomyopathies, suggesting its inhibition in these disorders could be clinically beneficial. Interestingly, new research in rodent and human samples reveals RBM20 itself also has multiple versions, and their production is influenced by developmental stage and disease. The findings suggest regulation of heart muscle flexibility is much more complex than previously thought and that any therapies targeting RBM20 might need fine tuning to pinpoint specific versions of the factor.

Written by Ruth Williams

Image from work by Michael H. Radke, Victor Badillo Lisakowski and Stefan Meinke, and colleagues

Translational Cardiology and Functional Genomics, Max Delbrück Center for Molecular Medicine, Berlin, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, May 2026

Metal Liker Unforgiven

We need trace metals for healthy cell function but then so do all other organisms, handily we have a means of safeguarding the supply of certain metals which doubles as an anti-pathogen strategy. A protein in the mammalian gut lining cells called natural resistance-associated macrophage protein 2 (also known as SLC11A2) starves pathogenic microrganisms of iron and manganese – shown here using Salmonella enterica (in red) as a model in cow gut, with metals tracked using fluorescent sensors

Read the published research article here

Image from work by Emilia S. Norberg and colleagues

Department of Microbiology and Molecular Genetics, Robert Larner, M.D. College of Medicine, University of Vermont, Burlington, VT, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Proceedings of the National Academy of Science (PNAS), June 2026

Arbor Mastered

Assembling and growing in the lab the different cell types that make up a particular body tissue – cultures known as organoids – emulates physiology in many ways sufficiently to study cell and molecular interactions for example, but there's more to life. Here, using a defined chemical protocol, lung organoids have been coaxed to branch, mimicking the tree-like pattern seen in our lungs, upgrading to a more life-like means to study development and regeneration

Read the published research article here

Image from work by Mengjie Pan, Baomei Cai, Guanlie Li, Ruifang Zhang, Chuncao Deng, Huan Chen and colleagues

Guangzhou National Laboratory, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China

Image originally published with a Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0)

Published in Developmental Cell, June 2026

Unexpected Barrier Function

All eukaryotic organisms – that is, all animals, plants and fungi – contain a protein called cyclin dependent kinase 1 (CDK1), which is critical for driving cells through the process of division. This role in cell division has been known for about fifty years, but recent research reveals that CDK1 has another hitherto unknown function. Scientists studying mammalian kidney epithelial cells (pictured) discovered that the protein was located at intercellular connections (green) where it interacted with cell-to-cell cohesion factors and promoted epithelial barrier integrity. Indeed, inhibiting CDK1 activity led to perturbed cell contacts and caused areas of the barrier to become leaky (purple regions). Because of CDK1’s role in the cell cycle, the protein has been proposed as a potential target for cancer therapy. Investigations into such therapies, should thus keep in mind CDK1’s newly discovered function and the implications of its disruption.

Written by Ruth Williams

Image by from Margarida Dantas and Martijn Gloerich. Re: work by Margarida Dantas & Lisa Donker, and colleagues

Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, Netherlands

Image copyright held by the original authors

Research published in Science Signaling, June 2026

Deep Cell Pursuit

Tagging red blood cells and neutrophils ('first responder' cells of the immune system) with distinct optoacoustic signatures (using near-infrared dyes) allows real-time cell tracking in vessels deep in a live mouse's brain (cerebral vasculature represented left and flow velocity right). Clinical application of such principles in the future, for example after a stroke, could accelerate diagnosis and recovery

Read the published research article here

Still from video from work by Lin Tang and colleagues

Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Science Advances, June 2026

Loss of Flexibility

During infancy, the brain is exceptionally plastic, with sensory neuronal activity continuously shaping and refining the brain’s circuitry. By adolescence, however, this plasticity reduces and pathways become increasingly fixed. Astrocytes, like the one pictured, appear to be responsible for this restriction. Neuroscientists have discovered that the stress hormone cortisol acts on these cells during mouse development, prompting them to produce factors that promote maturation of the extracellular matrix around neurons, which in turn restrains the neurons from making new connections. Indeed, blocking cortisol’s action on astrocytes leads to increased brain plasticity in adult mice. In humans, aberrations in plasticity are thought to contribute to neurodevelopmental conditions including autism spectrum disorder and schizophrenia. Since the cortisol-astrocyte pathway seems to be conserved in humans too, the big question is, could modifying adult plasticity, via astrocyte manipulation, help treat such disorders?

Written by Ruth Williams

Image from work by Bruno Gegenhuber and colleagues, Greenberg Lab

Department of Neurobiology, Harvard Medical School, Boston, MA, USA

Image originally published with no restrictions – hence published here with as Creative Commons Attribution 4.0 International (CC BY 4.0)

Research published in Nature, May 2026

Danger Mouse

Keeping tabs on the living processes in the body is a struggle. Even when sensitive tests are available, spotting the early stages of issues across tissues is a huge challenge. Computer learning models – a form of artificial intelligence – can help. Here a fluorescence microscope takes high-definition scans of two mice, highlighting organs and tissues in different colours – the peripheral nerves (green), bones and other organs (red) and muscle (blue). There’s a lot going on, so researchers turn to new software called Mousemapper, which looks for changes between the healthy mouse (left) and the obese mouse (right). The software finds widespread inflammation in the obese mouse – but also an unexpected change to the trigeminal nerve in the face. With similar signs discovered in obese humans, Mousemapper might be crucial to spotting unexpected symptoms that may otherwise go unnoticed.

Written by John Ankers

Video by Doris Kaltenecker, Izabela Horvath, Rami Al-Maskari, Ying Chen, Zeynep Ilgin Kolabas, and colleagues

Institute for Intelligent Biotechnologies, Helmholtz Munich, German Research Center for Environmental Health, Neuherberg, Germany

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature, May 2026