Cadmium (Cd) contamination is a growing threat to food safety, and rice is one of the most vulnerable crops. Because rice plants can accumulate cadmium from contaminated soils more readily than many other staples, Cd can become a major dietary exposure route for large parts of the world’s population. Yet attempts to lower cadmium often create trade-offs—reducing uptake of essential nutrients or weakening plant performance.

A new study from Okayama University, Japan, and collaborating researchers in China reports a precision-editing strategy designed to avoid those trade-offs. The team focused on the rice metal transporter gene OsNramp5, which is known to move metals such as manganese and cadmium, and used base-editing to search for a beneficial point mutation within the gene rather than disabling it.

Using adenine and cytosine base editors, the researchers generated more than 1,600 genome-edited rice lines and screened them for reduced cadmium accumulation. Their saturation mutagenesis approach targeted OsNramp5 to identify variants that kept normal plant physiology while limiting Cd buildup in grain.

The key breakthrough was the I441T substitution: changing isoleucine to threonine at amino acid position 441. This single change reduced cadmium levels in both shoots and brown rice without altering gene expression, protein abundance, or the subcellular localization of the transporter.

Importantly, the mutation did not come at the cost of micronutrients. Field trials on cadmium-contaminated soil showed a 48% decrease in cadmium concentration in brown rice, from 0.14 mg/kg in wild type to 0.07 mg/kg in the edited plants, while iron, manganese, and zinc levels remained essentially unchanged.

The researchers then explored the mechanism behind the selective effect. Although OsNramp5 transports multiple metals, the I441T mutation shifted its selectivity—enhancing zinc transport preference. Increased zinc accumulation in root cells promoted competitive inhibition against cadmium during root-to-shoot movement.

Instead of completely blocking cadmium uptake, the edited transporter selectively limited cadmium translocation, reducing grain contamination while preserving essential mineral delivery. The team supported these conclusions with physiological assessments, gene and protein analyses, yeast transport assays, and agronomic evaluation.

Overall, the work demonstrates how precision genome editing can address a long-standing breeding challenge: lowering toxic metal accumulation without disrupting nutrient homeostasis. The researchers propose that the OsNramp5^I441T allele could accelerate development of safer rice varieties for mildly contaminated regions.

Subject of Research: Not applicable
Article Title: Genome-edited rice variety with low-cadmium accumulation in the grain
News Publication Date: 18-Jun-2026
Web References: http://dx.doi.org/10.1073/pnas.2610609123
References: DOI: 10.1073/pnas.2610609123 (Proceedings of the National Academy of Sciences)
Image Credits: Credit: Professor Jian Feng Ma from Okayama University, Japan

Keywords: cadmium, rice, OsNramp5, base editing, genome editing, metal transporters, food safety, micronutrients, zinc competition, plant breeding

I’m sick of “opt-out” toggles for automatically enabled generative AI features. It’s past time to make “opt in” the default setting for sensitive features.

I’m sick of “opt-out” toggles for automatically enabled generative AI features. It’s past time to make “opt in” the default setting for sensitive features.

No, there weren't "2,700 heatwave deaths due to climate change", says Ben Pile – a figure conjured by Met Office and Imperial College modelling. But nobody must be allowed to remember the warm days of 2026 fondly.

The post No, There Weren’t “2,700 Heatwave Deaths Due to Climate Change” appeared first on The Daily Sceptic.

The end of the FIFA Men’s World Cup is nigh. Here’s how to watch the final games and the first ever World Cup halftime show.

Pig executions helped medieval communities punish negligence, display power and restore a threatened social order.

If you want to stream local media, this free and open source media server is just as good as Plex. But if you rely on remote access or live TV, prepare to tinker.

Did you know that the space shuttle once launched the Statue of Liberty into space?

In fact, there were two "Lady Liberties" on board Discovery when it lifted off on its fourth flight in April 1985. To be fair, each statue was only 15 inches tall (38.1 centimeters), but they were also each made of copper that was removed from the full-size statue during its then-still-ongoing restoration.

After the weeklong STS-51D mission was over, one of the space-flown statues was placed on display, and the other was melted down to create copper seals, which were then sold to the public by the Statue of Liberty Ellis Island Centennial Commission.

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Schistosoma mansoni is a parasitic worm that infects millions of people worldwide, entering the body through the skin. Unlike bacterial infections that often cause pain and inflammation, S. mansoni usually slips in unnoticed, rarely causing discomfort. Scientists have long wondered why our skin’s defenses don’t react more strongly to this invader.

Researchers from the University of Pennsylvania and Tulane University explored whether a specialized group of pain-sensing neurons, called TRPV1+, plays a role in detecting and fighting off S. mansoni during its invasion. TRPV1+ neurons are nerve cells in the skin that respond to heat, spicy foods, and certain bacteria and fungi. When activated, they can trigger pain and release molecules that alert the immune system. Previous researchers have shown that these neurons help defend against bacterial and fungal skin infections, but their role in fighting off parasites was unclear. 

To examine how S. mansoni infects its hosts, the team conducted experiments using groups of 4 to 8 mice, matched for age and sex. They repeated each experiment 2 to 3 times to ensure their data was reproducible. They anesthetized the mice, exposed their ears to a solution containing 100 to 150 live S. mansoni larvae, and covered the area with vaseline to keep the solution in place. After 20 to 30 minutes, they counted the number of larvae remaining in the mice’s ears to assess how many had successfully penetrated their skin. 

Next, the team measured pain sensitivity in the mice exposed to the parasite by placing them in chambers and applying an infrared heat source to their paws. They recorded how long it took each mouse to withdraw its paw as a sign of pain. They repeated this test 3 times per paw on each mouse, waited at least 5 minutes between each measurement, and calculated an average withdrawal time. They found that mice infected with S. mansoni were approximately half as sensitive to heat-induced pain as an uninfected control group, suggesting that the parasite could be suppressing the mice’s TRPV1+ neurons.

To investigate this further, the team isolated nerve cells that transmit sensory signals from the mice’s skin, known as dorsal root ganglia, and grew them in the lab. They stimulated these neurons by adding a spicy compound in chili peppers, known as capsaicin. Then they measured calcium influx, a sign the neurons were active, using a special dye that glows differently under a microscope depending on calcium levels. This allowed them to see how active the neurons were and how many molecules they released in response to infection and stimulation. They found that 68% of neurons from uninfected mice responded to capsaicin, but only 26% of neurons from infected mice did so, confirming that the parasite dampened their sensory neuron responses.

To test whether restoring the mice’s neuron activity could help their bodies resist parasite invasion, the researchers genetically engineered the mice to produce a light-sensitive protein in their TRPV1+ neurons, called channelrhodopsin. They “turned on” these neurons by stimulating them with blue light for 30 minutes every day for 5 days before infecting the mice with parasites. Six days later, they assessed the mice’s immune response by using a laser to count immune cells in samples of ear tissue. They also determined how far the parasites had spread by counting larvae in lung samples. They saw that mice with the artificially activated TRPV1+ neurons had nearly double the immune response, blocked roughly twice as many larvae at the skin, and had about 20% fewer parasites in their lungs.

Next, the researchers selectively destroyed TRPV1+ neurons in a new set of mice using a compound known as resiniferatoxin. Three weeks later, they confirmed the treatment had worked by testing the mice’s pain sensitivity using the same heat assay as before. After confirming the mice had lost their pain sensitivity, the team exposed the mice to the parasites. They found that the reinfected mice had 1% to 3% weaker skin immune responses and approximately 25% to 30% more parasites in their lungs than a control group, further confirming that TRPV1+ neurons play a protective role during early infection.

The team concluded that S. mansoni has evolved ways to silence pain-sensing neurons, like TRPV1+. Their discovery suggests that future scientists could boost skin immunity against parasites by targeting sensory neurons. For example, they could develop topical creams or therapies that activate these neurons to help our bodies fight off S. mansoni and similar parasitic invaders.

The post A parasite that numbs your pain appeared first on Sciworthy.