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3D map of rice development charts gene activity across plant’s entire life cycle

Rice is one of the world’s most familiar staple foods, but how does a single cell develop into a rice plant with specialized tissues and organs? A new study offers a detailed look at this process through a three-dimensional (3D) spatiotemporal atlas covering 10 organs and 61 developmental stages across the rice life cycle, from seed to seed.

The study, published in Cell, was conducted by a research team led by professor Yang Weicai from the Institute of Genetics and Developmental Biology (IGDB) of the Chinese Academy of Sciences, in collaboration with several other research teams.

The plant life cycle alternates between a haploid phase, which produces sperm and egg cells, and a diploid phase, which develops following fertilization. In plants, the diploid zygote develops into a multicellular organism through coordinated cell divisions and cell fate specification. Understanding how these processes are regulated across different tissues and developmental stages is a fundamental goal of developmental biology.

Genetic Risk for Anorexia May Begin Outside the Brain

While the investigators emphasize that PLIN4 variants were identified in a selected clinical subpopulation and require replication across larger, multi-ancestry cohorts, the identification of a peripheral fat-storage defect opens immediate avenues for drug discovery.

“Discovering genes that underlie this disease isn’t going to fix the disease,” Robison concluded. “But what it can do is teach us what’s causing the disease in lots of people, and we can use that information to design new treatments.”

The research team plans to analyze primary adipocyte tissue from anorexia patients carrying PLIN4 mutations to observe lipid droplet morphology and metabolic signaling directly, working toward therapies that can target peripheral lipid regulation alongside psychological rehabilitation.

Blocking a protein may reduce buildup of harmful aging cells

A team led by Cedars-Sinai Health Sciences University investigators has identified a protein that may hide aging cells from the body’s immune system, allowing them to build up and contribute to age-related health problems.

The findings, published in Cell Metabolism, suggest that the protein, called PD-L2, could serve as a target for treatments designed to remove harmful aging cells or as a blood marker that helps researchers track them.

“Our findings suggest that PD-L2 may help aging cells stay in the body when they would normally be removed by the immune system,” said Selim Chaib, Ph.D., research assistant professor of medicine at Cedars-Sinai and first and co-corresponding author of the study.

Age-Based Testing Misses Most With Inherited Cancer Risk

Restricting germline genetic testing to patients diagnosed with cancer before age 50 may miss the large majority of all those with inherited pathogenic variants, a new study suggested.

The research, based on germline sequencing of 39,184 unselected patients with solid tumors, found that the age-50 cutoff would miss 72% of all patients harboring a pathogenic variant. That included 68% of those with moderate-or high-penetrance variants, which confer substantially elevated lifetime cancer risks.

“Hereditary cancer can occur at any age, and we should move toward a new standard in which genetic testing is considered for every patient diagnosed with cancer, regardless of age,” said lead study author Zsofia K. Stadler, MD, of Memorial Sloan Kettering (MSK) Cancer Center in New York City.

Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases

Synaptic dysfunction and intracellular accumulation of pathological tau are convergent hallmarks of Alzheimer’s disease (AD) and related tauopathies, yet the molecular mechanisms coupling these events to widespread neurodegeneration remain incompletely understood. The Src family kinase Fyn has emerged as a critical signaling hub that integrates upstream pathogenic triggers, such as amyloid-β (Aβ), with downstream neurotoxic cascades. Here, we review the multifaceted roles of Fyn in orchestrating synaptic failure, highlighting how Fyn recruitment by mislocalized tau promotes N-methyl-D-aspartate receptor hyperactivation and calcium dysregulation. We examine the biophysical basis of Fyn–tau interactions, particularly the role of liquid–liquid phase separation in stabilizing toxic signaling complexes. We also discuss how aberrant Fyn signaling in microglia and astrocytes amplifies neuroinflammation. Finally, we evaluate the potential of Fyn as a therapeutic target, emphasizing the necessity of strategies that selectively uncouple pathological signaling from physiological functions to effectively halt disease progression.

Prevalence and characteristics of patients with coronary heart disease and blood pressure below target: the INTERASPIRE study

Background Despite treatment, many hypertensive patients with coronary heart disease (CHD) have blood pressure (BP) that remains above guideline targets. However, less is known about patients in whom on-treatment BP is below target and major European guidelines differ substantially in their recommendations for such patients. Specifically, 2023 European Society of Hypertension (ESH) guidelines provide a Class 3 recommendation to proactively avoid BP below target whereas 2024 European Society of Cardiology (ESC) guidelines do not.

Methods Between 2020 and 2023, adults hospitalised in the previous 6–24 months with incident or recurrent CHD were sampled in 14 countries from all six WHO regions and invited for a standardised interview and examination as part of the International Action on Secondary and Primary Prevention by Intervention to Reduce Events (INTERASPIRE) study. We measured seated BP twice using an automated oscillometric device after 5 min of rest. We defined participants as having BP above target (BP ≥130/80 mm Hg), at target (BP 120–129/70–79 mm Hg) or below target (120÷70 mm Hg); according to both 2023 ESH and 2024 ESC guidelines.

Results Among 4,548 participants (21.1% female), the mean age (±SD) was 60.0 (±10.3) years. At a median (IQR) of 1.05 (0.76–1.45) years after index CHD hospitalisation, 10.3% of patients had BP readings within the target range of 120–129/70–79 mm Hg, with 53.9% above target and 35.7% below target. Patients with below-target BP were more likely to have heart failure (13.6% vs 10.0%, p=0.041) and estimated glomerular filtration rate 60 mL/min/1.73 m² (18.9% vs 10.7%, p0.001), when compared with those at target. They were also statistically more likely to be severely frail (p=0.030). The median number of BP-lowering medications did not differ significantly between the 3 BP target groups. Cumulative dosing of BP-lowering medications in the below-target group was also not more intensive than that in the at-target group.

Nanoparticle injection reprograms NK immune cells to fight cancer and autoimmune disorders

MIT engineers have developed a new way to program natural killer (NK) immune cells to target cancerous T cells or T cells that have become autoreactive, leading to diseases such as lymphoma and autoimmune hepatitis.

Using their new technique, the researchers can reprogram NK cells to target diseased T cells without ever removing the NK cells from the patient’s body. Instead, they use lipid nanoparticles to deliver messenger RNA directly to NK cells. These mRNA molecules encode proteins that allow the NK cells to seek and destroy the dysfunctional T cells.

Known as CAR NK cells, these cells could be deployed against a variety of diseases. The MIT team’s new approach could bypass one of the major obstacles to using these cells, which is the time and expense of manufacturing them outside the body.

A high-resolution protein-RNA binding atlas for structure-aware interaction prediction and post-transcriptional regulatory modeling

The Goodarzi lab is on fire!

RNA-binding proteins (RBPs) recognize RNA by sequence and shape, but which matters varies by site. Introducing Pythia, an interpretable AI model trained on a new high-resolution atlas of 67 RBPs—a collaboration between Genophoria, Chan Zuckerberg Biohub, UCSF, Calico, & Vector Institute.

What if an AI could look at a strand of RNA, predict how it folds in 3D, and instantly tell you which proteins will attach to it? A groundbreaking new dataset and neural network are doing just that—bringing high-resolution clarity to the invisible mechanics of gene regulation.

Decoding how proteins shape our RNA: a new atlas and AI tool for cellular control.

Inside our cells, DNA serves as the master blueprint, but RNA acts as the working copy that delivers instructions to build proteins. Once RNA is made, it is heavily managed by a special class of molecules called RNA-binding proteins (RBPs). These proteins dictate how long an RNA molecule lasts, where it travels inside the cell, and how efficiently it is translated into functional proteins.

Despite their importance, scientists have lacked high-resolution, uniform maps showing exactly where these proteins bind across the entire human genome.

To bridge this gap, a team of researchers has developed a powerful suite of new experimental and computational tools to decode how proteins and RNA interact.

Key Breakthroughs of the Study.

Tie1 cleavage is dispensable for angiogenic responses but critical for inflammatory vascular responses

European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

2German Cancer Research Center, Heidelberg, Germany.

3Helmholtz Institute for Translational AngioCardioScience, Max Delbrück Center, Heidelberg University, Heidelberg, Germany.

AI tool reveals what attracts immune cells to tumors and what keeps them away

Researchers at The University of Texas MD Anderson Cancer Center and collaborating institutions in Texas developed an artificial intelligence (AI) model that helps explain how immune cells find their way to specific locations in the body and why they avoid others. The findings could help scientists better understand cancer, autoimmune diseases and treatment response.

The study, published in Nature Biomedical Engineering, was co-led by Tao Wang, Ph.D., associate professor of bioinformatics and computational biology, and Linghua Wang, M.D., Ph.D., professor of genomic medicine, executive director and head of the Center for Cellular Language Intelligence, associate member of the James P. Allison Institute and focus area co-lead with the Institute for Data Science in Oncology.

“While spatial technologies can show where immune cells are located, this new tool helps us investigate why they gather in certain areas and how they reach and recognize tumor cells,” Tao Wang said. “By identifying local signals that attract immune cells as well as potential barriers that may keep them out, we may be able to identify biomarkers and therapeutic targets that could be used to improve patient outcomes.”