British ash woodland is evolving resistance to ash dieback
Peer-Reviewed Publication
Updates every hour. Last Updated: 26-Jun-2025 15:10 ET (26-Jun-2025 19:10 GMT/UTC)
Scientists at the Royal Botanic Gardens, Kew and Queen Mary University of London have discovered that a new generation of ash trees, growing naturally in woodland, exhibits greater resistance to the disease compared to older trees. They find that natural selection is acting upon thousands of locations within the ash tree DNA, driving the evolution of resistance. The study, published in Science, offers renewed hope for the future of ash trees in the British landscape and provides compelling evidence for a long-standing prediction of Darwinian theory.
“Sleeping on it,” especially dropping deeper than a doze, might help people gain insight into certain kinds of tasks, according to a study published June 26th in the open-access journal PLOS Biology by Anika Löwe, Marit Petzka, Maria Tzegka and Nicolas Schuck from the Universität Hamburg, Germany, and colleagues.
By flipping an evolutionarily disabled genetic switch involved in Vitamin A metabolism, researchers have enabled ear tissue regeneration in mice. Unlike some animals such as fish and salamanders, mammals have limited capacity to regenerate damaged tissues or organs fully. A variety of strategies have been explored to trigger regeneration in mammals, such as stem cell therapies, gene editing, and electrical stimulation. While these approaches have shown promise, none have fully restored organ function. This is likely due to the biological complexity of mammals and a limited understanding of the genetic factors that govern regenerative abilities. Some mammals, including rabbits, goats, and African spiny mice, can regenerate complex tissues like the ear pinna (the visible outer part of the ear), while others, including common rodents like mice and rats, cannot. Because the ear pinna is a uniquely mammalian structure and varies widely in its ability to regenerate across species, Weifeng Lin and colleagues argue that it makes an ideal model for studying how regenerative capacity has evolved in mammals.
Here, Lin et al. performed a side-by-side comparison between mammal species that can regenerate ear tissue and those that cannot and found that failure of regeneration in nonregenerative species is not due to an inability to form or proliferate the early wound-healing structure known as the blastema. Instead, the key difference lies in how certain wound-induced fibroblasts (WIFs) respond after injury. According to the authors, single-cell RNA sequencing and spatial transcriptomic analyses show that regenerative species activate a gene called Aldh1a2, which is critical for producing Vitamin A or retinoic acid (RA), a signaling molecule essential for regeneration. In nonregenerative species, Aldh1a2 is insufficiently activated due to both reduced expression and enhanced breakdown of RA, which leads to regeneration failure. Notably, Lin et al. discovered that supplying RA externally, or activating Aldh1a2 using a gene enhancer from rabbits, was enough to restore regenerative ability in mice.
A new fossil discovery technique reveals that squids originated and rapidly became abundant, diverse, and dominant in the oceans 100 million years ago, reshaping our understanding of ancient marine ecosystems.
Increasing evidence supports the nutritional epigenetics model for autism and attention deficit/hyperactivity disorders that explains how unhealthy diet contributes to the epigenetic inheritance of these disorders. An unhealthy diet characterized by excessive intake of ultra-processed foods results in heavy metal exposures and deficits in zinc that may impact metallothionein gene function. Metallothionein gene malfunction may result in the bioaccumulation of mercury and/or lead in the blood depending on diet. Nutritional epigenetics education may be used as an intervention to reduce the intake of ultra-processed foods and heavy metals in expectant mothers and prevent the development of autism and attention deficit/hyperactivity disorders in children.