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Category: genetics

Shrink, remove and modify: Team successfully ‘trims’ wheat chromosomes

For the first time, a research team at the Leibniz Institute of Plant Genetics and Crop Plant Research (IPK) has succeeded in reducing the size of, or even completely removing, chromosomes in plants with large genomes, such as wheat. They achieved this by using the CRISPR/Cas gene-editing tool to target highly repetitive sections of DNA. The results of the study, published today in the journal Plant Communications, could significantly accelerate breeding processes.

While the targeted manipulation of entire chromosomes is well established in model organisms such as Arabidopsis thaliana, it has posed a significant challenge in crops with large genomes, such as wheat. The IPK research team has now set out to determine whether highly repetitive DNA sequences known as satellite DNA are suitable targets for the CRISPR gene-editing system. The idea was that cutting many of these identical sequences simultaneously could affect the entire chromosome. The team introduced CRISPR components into the plants using a virus-based system. This approach bypasses lengthy traditional transformation processes and enables highly efficient chromosomal modifications.

“In our study, we were actually able to demonstrate for the first time that chromosomes can be efficiently reduced in size by making targeted cuts in satellite DNA,” says Dr. Jianyong Chen, the study’s first author. This is a significant breakthrough, as such changes had previously only occurred by chance. You can think of it like a rope. If you cut a rope in several places at once, it becomes unstable and eventually snaps. The same thing happens to chromosomes when many cuts are made simultaneously.

Metal Ion-Mediated Regulation of Cell Fate: A Novel Strategy for Synergy with Radiotherapy and Immunotherapy

Metal ions are indispensable for living organisms, participating in essential physiological processes. However, their dysregulated accumulation can trigger cell death and metal overload. The recent discovery of novel regulated cell death modalities, such as cuproptosis and ferroptosis, has significantly advanced the understanding of metal ions in cell fate and immune regulation. This review systematically elucidates the molecular mechanisms underlying metal ion-induced cell death, encompassing oxidative stress, mitochondrial dysfunction, DNA damage, and epigenetic modifications. It further classifies and discusses the hallmarks of various programmed and non-programmed cell death pathways, emphasizing the pivotal role of metal ions in anti-tumor immunity.

Beyond Cell Death: The Hidden Drivers of Stem Cell Aging

As we age, our ability to maintain healthy blood and a strong immune system gradually declines, largely because hematopoietic stem cells (HSCs), the cells responsible for producing all blood cell types, begin to lose their effectiveness. Normally, HSCs can both self-renew and generate a balanced mix of blood cells, but over time they produce fewer new cells, favor certain cells such as myeloid cells over lymphoid cells, and struggle to support a robust immune response. Accumulated cellular damage, shifts in gene activity, ongoing low-level inflammation, and changes in the bone marrow environment, all appear to contribute to this decline. However, the precise mechanisms by which these diverse stresses converge to weaken HSCs have remained unclear.

Researchers from The University of Tokyo, Japan, and St. Jude Children’s Research Hospital, USA, sought to uncover a mechanism explaining how age-related stresses drive HSC functional deterioration, focusing on the receptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase like (MLKL) signaling axis—a pathway traditionally associated with necroptosis, or programmed cell death. The study was led by Dr. Masayuki Yamashita, an Assistant Member at St. Jude Children’s Research Hospital, who, at the time of the investigation, was an Assistant Professor at The Institute of Medical Science, The University of Tokyo. The other co-authors include Dr. Atsushi Iwama from The Institute of Medical Science, The University of Tokyo, and Dr. Yuta Yamada from St. Jude Children’s Research Hospital, who was a graduate student at The Institute of Medical Science, The University of Tokyo.

Explaining the motivation behind the study, Dr. Yamashita says, “We discovered an unexpected phenotype in HSCs of MLKL-knockout mice repeatedly treated with 5-fluorouracil, where aging-associated functional changes were markedly attenuated despite no detectable difference in HSC death, prompting us to investigate whether this pathway might induce functional changes beyond cell death.” This observation shifted the research focus toward a non-lethal role of MLKL—a concept later highlighted in their study, published in Volume 17 of the journal Nature Communications on April 6, 2026.

To investigate this, the team employed a combination of genetic mouse models, stress treatments, and functional assays. They used wild-type, MLKL-deficient, and RIPK3-deficient mice, along with specialized reporter mice capable of detecting MLKL activation through a Förster resonance energy transfer-based biosensor. Mice were exposed to stressors mimicking aging, including inflammation, replication stress, and oncogenic stress. HSC function was then assessed primarily through bone marrow transplantation, which measures the ability of stem cells to regenerate the blood system. Complementary analyses included flow cytometry, ex vivo expansion, RNA-seq, assay for transposase-accessible chromatin-seq, high-resolution microscopy, metabolic assays, and mitochondrial analyses, enabling a detailed understanding of how non-lethal MLKL activation impairs HSC function at molecular, cellular, and organelle levels.

Abstract: Nature Communications.

Non-necroptotic MLKL function damages mitochondria and promotes hematopoietic stem cell aging.

https://www.nature.com/articles/s41467-026-71060-4

Continue reading “Beyond Cell Death: The Hidden Drivers of Stem Cell Aging” | >

Fat-producing enzyme may amplify damage in Parkinson’s disease

As the flies aged, they developed Parkinson’s-like symptoms – including impaired movement and loss of brain cells – mirroring key aspects of disease progression seen in humans.

Using large-scale genetic screening made possible by the fruit fly model, the researchers systematically identified genes involved in α-synuclein-induced toxicity. Among these, the gene mino stood out for its strong effects on disease-related symptoms, leading the team to investigate its role further. This gene codes for the enzyme glycerol-3-phosphate acyltransferase (GPAT) and plays a key role in regulating fat metabolism in cells.

When the scientists reduced the activity of the mino gene, the flies experienced less loss of brain cells, improved movement, and healthier activity patterns. In contrast, increasing the gene’s activity worsened the flies’ symptoms.

The researchers then explored whether blocking GPAT could help counter these toxic effects. They tested a compound called FSG67, which blocks the activity of GPAT and has previously been studied in laboratory settings for obesity-related and metabolic disorders.

When the flies were treated with FSG67, the harmful effects of α-synuclein – including protein clumping and fat damage – were reduced. The scientists observed similar protective effects in mouse brain cells grown in the laboratory.

Going forward, the scientists will focus on further validating these findings and exploring the possibility of developing GPAT inhibitors as a new class of drugs for Parkinson’s disease. ScienceMission sciencenewshighlights.

Continue reading “Fat-producing enzyme may amplify damage in Parkinson’s disease” | >

Abstract: Offering a topical strategy in skin cancer

https://doi.org/10.1172/JCI189044 Brian C. Capell & team identify the epigenetic regulator LSD1 as critical for epidermal development and find its inhibition suppresses tumors in two cutaneous squamous cell carcinoma mouse models by promoting immunosurveillance.

The image shows immunofluorescence from mice lacking LSD1 in the skin, revealing profound activation of cutaneous retinoid signaling (as measured by CRABP2 levels in green); keratin 14 (red); nuclei (blue).

1Department of Dermatology and.

2Penn Epigenetics Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.

3Division of Allergy and Immunology, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.

Marine sponge bacterium enzyme reveals a two-part route to make terpenoids

The molecular structure of an enzyme from a marine bacterium with potential industrial uses has been determined by RIKEN researchers. The insights they have gained could help make a range of useful compounds through genetic modification. The research is published in the journal Chemical Science.

The class of natural compounds known as terpenoids is nothing if not versatile, being used in a wide assortment of products, from perfumes and insect repellents to pesticides and drugs. More than 100,000 terpenoids have been identified so far. They are produced by an impressive range of organisms spanning animals, plants, fungi, bacteria, and viruses.

Recently, marine organisms such as corals, sponges, and marine bacteria have been found to produce terpenoids with complex structures that show promise for fighting infectious diseases.

Scientists Discover Game-Changing New Way To Treat High Cholesterol

Scientists are rethinking how to treat a widespread genetic cholesterol disorder by targeting particle production instead of removal.

Familial hypercholesterolemia (FH) disrupts one of the body’s most important cleanup systems. Normally, low-density lipoprotein (LDL), often called “bad” cholesterol, is removed from the bloodstream by LDL receptors (LDLR) in the liver. These receptors act like docking stations, pulling cholesterol into cells where it can be broken down. In people with FH, mutations in the LDLR gene weaken or disable this process.

As a result, cholesterol builds up in the blood for decades, often without obvious symptoms until it leads to heart attacks or other cardiovascular problems. About 1 in 200 adults carries this genetic change, making it one of the most common inherited disorders worldwide.

Human Gene Editing Has Begun | George Church

We are already gene editing humans. You just haven’t noticed.

George Church, Harvard geneticist and Human Genome Project pioneer, explains why CRISPR wasn’t the real breakthrough, how multiplex gene editing unlocked organ transplants and de-extinction, and why aging will likely require rewriting many genes at once.

Hosted by Mgoes → https://twitter.com/m_goes_distance
Brought to you by SuperHuman Fund → https://superhuman.fund/

0:00 — Gene Editing Mammals → Humans
8:36 — Germline vs Somatic
14:56 — Modified Humans Are Already Here
18:50 — Enhancing Healthy Humans
25:00 — Aging Therapies vs Cognitive Enhancement
30:20 — Embryo Selection
38:10 — Is US Losing To UAE?
42:33 — Biotech Failures
49:31 — Next Dire Wolf Moment
54:21 — AI x Science
1:02:07 — Synthetizing Entire Genomes.

The Accelerate Bio Podcast explores the future of humanity in the age of Artificial Intelligence. Subscribe for deep-dive conversations with founders, scientists, and investors shaping AI, biotechnology, and human progress.

This episode discusses George Church, gene editing, CRISPR, human enhancement, longevity, aging, embryo selection, synthetic biology, multiplex editing, AI biotech.

Continue reading “Human Gene Editing Has Begun | George Church” | >

Genetic atlas reveals how human liver cells divide their labor

If scientists could shrink themselves to microscopic size and take a journey through the human body—like the submarine crew in the 1966 science fiction classic “Fantastic Voyage”—one of their first stops would no doubt be the liver. The unique structure of our largest internal organ comprises small, hexagonal functional units called lobules, each carrying out more than 500 functions simultaneously. Studies from the 1970s and 1980s revealed that liver cells divide these many tasks among themselves according to their location within each subunit; however, the technology available at the time provided only a blurred picture of this division of labor.

In a new study published in Nature, scientists from the Weizmann Institute of Science, together with colleagues at Sheba Medical Center and the Mayo Clinic, present the first genetic atlas of a healthy human liver at a resolution of 2 microns. The findings show that the division of labor in the human liver differs from that of other mammals and is more extensive than previously recognized, helping explain why certain regions of the liver are particularly vulnerable to fatty liver disease.

In recent years, technological advances have made it possible to identify which genes are active in each individual cell while also mapping the cells’ precise spatial positions within the tissue. Still, a comprehensive map of functional division in the human liver remained elusive, largely due to the difficulty of obtaining tissue samples from healthy donors.

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