Simian-specific gene SAGE1 “upgrades” the DNA damage repair network to safeguard genome stability in the male germline
Peer-Reviewed Publication
Updates every hour. Last Updated: 24-Oct-2026 12:17 ET (24-Oct-2026 16:17 GMT/UTC)
DNA damage poses a constant threat to genome integrity, especially in germ cells that transmit genetic information to offspring. While most DNA damage response (DDR) mechanisms are ancient and shared across vertebrates, the team discovered that simians (including humans, apes, Old World monkeys, and New World monkeys) possess a unique, recently evolved DDR regulator — SAGE1 — that provides an extra layer of protection to spermatogonia. Through its unique tandem exon repeats (SERs), SAGE1 coordinates multiple key repair complexes including MRN-CtIP, SOSS, and NuA4 to promote accurate homologous recombination (HR) repair while suppressing error-prone non-homologous end joining (NHEJ). This work reveals that simians have acquired an additional regulatory layer atop the conserved DDR machinery, offering new insights into the genetic basis of enhanced germline genome stability in the simian lineage.
Scientists have shown that genomics can help identify which wild populations are most vulnerable to climate change – offering practical guidance for the conservation of threatened species before declines become irreversible.
The study, led by researchers from Flinders University's Molecular Ecology Laboratory and published in the Journal of Heredity, examined the endangered southern pygmy perch across Australia's Murray-Darling Basin.
The International Society for Stem Cell Research (ISSCR) today announces that Lorenz Studer, M.D., founding director of the Center for Stem Cell Biology at Memorial Sloan Kettering Cancer Center, USA, has started his term as President of the Society.
Dr. Studer is known globally for his pioneering advances in stem cell biology, regenerative medicine, and the development of stem cell-based therapies for neurodegenerative disease. His research has established widely adopted methods for generating specialized neural cell types from human pluripotent stem cells, providing foundational tools for disease modeling, drug discovery, and regenerative medicine. Dr. Studer’s laboratory has also led efforts to translate these discoveries toward clinical applications, including stem cell-derived therapies for Parkinson's disease.
In the midwestern summer, humans and plants have to breathe through the heat and humidity. Researchers hope that a retooled crop plant—one with an improved ventilation system within its leaves—could thrive while avoiding drought stress by reducing “crop sweat”. Thanks to a next generation imaging technology powered by Argonne National Laboratory’s particle collider beamline, a team of scientists now has precise schematics of the leaf’s interior and can refine approaches to breeding hardier crop plants.
The research, published in Plant Physiology, was led by postdoctoral researcher James Fischer in the laboratory of Professor of Plant Biology and Crop Sciences Andrew Leakey at the University of Illinois Urbana-Champaign. Their work represents the first detailed look at how the pores on the leaf surfaces of sorghum, a highly productive and resilient grass crop, connect to the air pathways, photosynthetic centers, and veins beneath.
For decades, obesity medications produced only modest weight loss. But in recent years, Ozempic and related GLP-1 therapies have transformed the field, enabling sustained weight loss of 10 to 15% or more. Despite their success, however, scientists have not fully understood how these drugs work in the brain.
Now, in a new study, Yale researchers have identified an unexpected mechanism of action that challenges a long-held assumption about the brain’s hunger circuitry: that agouti-related peptide (AgRP) neurons, known as drivers of hunger, functioned solely to oppose weight loss. However, the new study shows that GLP-1 therapies like Ozempic instead recruit these neurons to help sustain fat loss.
“This completely changes how we think about the mechanism involved in these medications and provides new insight into the biology underlying their long-term effects, opening an avenue for the development of more efficient drugs,” said Mateus d’Ávila, a Ph.D. candidate in neuroscience working in Tamas Horvath’s lab in the Department of Comparative Medicine at Yale School of Medicine (YSM) and first author of the study.
Antisense oligonucleotides (ASOs) have been proposed as a therapeutic approach to shut down the production of faulty proteins in a wide variety of diseases, including cancer. In a study to be published August 11 in the Journal of Cell Biology (JCB), researchers at the Cancer Research UK Scotland Institute and the University of Glasgow identify a pathway by which ASOs enter cells and reach their targets, suggesting new ways to enhance the effectiveness of antisense therapy.