Geometry shapes life
Peer-Reviewed Publication
Updates every hour. Last Updated: 8-Jun-2026 14:16 ET (8-Jun-2026 18:16 GMT/UTC)
Life begins with a single fertilized cell that gradually transforms into a multicellular organism. This process requires precise coordination; otherwise, the embryo could develop serious complications. Scientists at ISTA have now demonstrated that the zebrafish eggs, in particular their curvature, might be the instruction manual that keeps cell division on schedule and activates the appropriate genes in a patterned manner to direct correct cell fate acquisition. These insights, published in Nature Physics, could help improve the accuracy of embryo assessments in IVF.
Researchers at the Technion–Israel Institute of Technology have uncovered a surprising mechanism that may help explain how Alzheimer’s disease spreads through the brain. A cellular system designed to protect neurons by removing toxic proteins may, under certain conditions, actually facilitate the spread of those proteins to neighboring cells—accelerating disease progression.
The study, published in PNAS, was led by Prof. Michael Glickman, Dean of the Technion’s Faculty of Biology, together with Dr. Ajay Wagh. The researchers focused on UBB+1, a defective and toxic form of ubiquitin—a protein normally responsible for marking damaged proteins for degradation.
In healthy cells, toxic proteins are typically broken down internally. However, the team discovered that brain cells sometimes export UBB+1 outside the cell instead of destroying it. This process is mediated by p62, a protein involved in autophagy, the cell’s self-cleaning system. While p62 can direct toxic proteins to the cell’s recycling center (the lysosome), it can also package them into vesicles that are secreted into the extracellular brain fluid.
Once outside the cell, fragments of UBB+1 can leak into neighboring neurons, potentially spreading toxic protein aggregates across brain tissue. This finding may help explain how Alzheimer’s, which can begin in isolated neurons, gradually affects large regions of the brain.
“We all want someone to take out the trash,” says Prof. Glickman, “but in this case, the cells are dumping their trash on their neighbors.”
The discovery could pave the way for earlier diagnosis of Alzheimer’s through fluid biomarkers and for the development of targeted, personalized treatments.
The study was supported by the Israel Science Foundation (ISF) and the European Research Council (ERC).
Ovarian cancer often forms secondary tumors, especially in a certain tissue in the abdominal cavity known as the omentum. Researchers from the University of Basel and University Hospital Basel have investigated what happens when the cancer “hijacks” this organ. It is hoped their findings will lead to more successful treatments.
This study reveals how lipid metabolism dysregulation promotes colorectal cancer liver metastasis (CRLM) through a novel YTHDF3-mediated mechanism involving m6A RNA modification and liquid-liquid phase separation.
Though it has long been recognized that the liver exhibits remarkable immune tolerance, the underlying mechanisms driving this phenomenon remain poorly understood. Here, we explore the liver’s unique immune tolerance—a critical feature that enables it to process gut- and diet-derived inflammogens without eliciting excessive inflammation. We propose that entero-pancreatic peptide hormones (e.g., GLP-1, GIP, CCK, glucagon, VIP, amylin) and postprandially reabsorbed bile acids (BAs), delivered at high concentrations via the portal vein, activate G protein-coupled receptors and trigger cAMP signalling pathways that ultimately promote anti-inflammatory responses through mechanisms such as PKA–CREB and Epac activation. These pathways have been implicated in suppressing inflammation, and fostering a tolerogenic phenotype in resident immune cells.
Lymphatic malformations (LMs) are congenital vascular anomalies characterized by abnormal lymphatic development, leading to disfigurement and severe clinical complications. However, the immunopathological mechanisms underlying LMs remain poorly defined. Here, we provide a comprehensive single-cell immune landscape of LMs by integrating single-cell RNA, T-cell receptor, and B-cell receptor sequencing (scRNA-seq, scTCR-seq, and scBCR-seq) on peripheral blood and pleural effusion samples, uncovering profound immune dysregulation and chronic inflammation.
The intestinal epithelium undergoes rapid renewal every 3–5 days, a process driven by intestinal stem cells (ISCs) located at the base of crypts. While ISCs play an essential role in epithelial regeneration following injury, such as that induced by chemotherapy or radiation, the underlying regulatory mechanisms remain incompletely understood.
In recent decades, scientists have debated whether a seven-million-year-old fossil was bipedal—a trait that would make it the oldest human ancestor. A new analysis by a team of anthropologists offers powerful evidence that Sahelanthropus tchadensis—a species discovered in the early 2000s—was indeed bipedal by uncovering a feature found only in bipedal hominins.