Sampling DNA in Seawater Can Reveal the Health of Dolphin Populations, in First for Conservation

SWNS

DNA floating in seawater is now enough to let scientists monitor the health of America’s dolphin populations.

Sampling DNA in seawater can show the local presence (or absence) of a species, but until now could give little information about those measures of biodiversity that are the most useful in conservation.

But, scientists in the US have now shown that mitochondrial DNA in water sampled near schools of dolphins contains enough information to measure their local effective population size—and monitor the health of these populations.

 

DNA is everywhere in the world’s oceans—not only inside cells from skin, scales, mucous, and feces, but also floating freely. Sequencing such ‘environmental DNA’ (eDNA) from open water has long been used as a cost-effective way of gauging the number and identity of species in a region, especially when they are rare and elusive or living at great depths.

But species richness is only the most basic biodiversity measure. Until now, eDNA-based methods could only give limited insight into the variables that are most relevant for conservation: the number of individuals, the evenness of the abundances of co-occurring species, or their within-species genetic diversity.

But that may be about to change, shows a new groundbreaking study in Frontiers in Marine Science.

“Here we show that repeated eDNA sampling can be used to estimate the genetic diversity of dolphins that occur in large schools and have very large populations,” said corresponding author Dr Frederick Archer from the NOAA/NMFS Southwest Fisheries Science Center in La Jolla, California.

“This is important because genetic diversity, its outcome measure, can be used as a measure of population size and how ready a population is to react to changes in its environment.”

Around Santa Catalina Island, located 47 km off Long Beach, California, the researchers followed 15 schools of dolphins with small boats in 2021. They focused on the four most common species locally: long-beaked common dolphins, short-beaked common dolphins, common bottlenose dolphins, and Risso’s dolphins.

Whenever they encountered a school, the researchers collected two-liter samples of seawater from the surface to compare the mitochondrial eDNA with that in public databases.

The scientists found 836 mitochondrial sequence variants in 126 water samples, of which 76% were from cetaceans and 60% from toothed whales. Overall, 29% were from the species of the school, which had been visually identified.

Long-beaked common dolphins had the greatest genetic diversity, followed by short-beaked common dolphins, while Risso’s and bottlenose dolphins proved much less diverse around Santa Catalina.

“Our study demonstrates the utility [of eDNA surveys] for efficiently assessing and comparing genetic diversity in social odontocetes,” concluded the authors.

Theory holds water

The authors are eager to put their methods to good use in conservation, now that they have been proven to work.

“It would be good to start eDNA monitoring programs as soon as possible that were not possible before. For example, we will be able to see how species composition in very small areas change over the course of a year – including rarer species that we don’t often detect on visual surveys,” said Archer.

“This can give us a lot of information on habitat use and will also allow us to potentially observe how environmental changes and anthropogenic effects such as pollution or underwater sound affect species distributions.” Sampling DNA in Seawater Can Reveal the Health of Dolphin Populations, in First for Conservation

Read More........→May 28, 2026

Chemical Shield Stops DNA Damage from Triggering Disease–’A Paradigm Shift’

Infographic by Linlin Zhao, University of California Riverside

A new chemical probe protects healthy cells from DNA damage, preserving them from one of the 8 hallmarks of aging.

The story of this potentially paradigmatic development begins where so much of human health begins: the mitochondria. These organelles are disrespectfully monikered as “the powerhouses” of the cell, but they do so much more than just provide cellular energy.

It’s so important, it even has its own DNA. Mitochondrial DNA (mtDNA) is separate from the DNA housed in a cell’s nucleus. While nuclear DNA contains the vast majority of the genetic code, mitochondria carry their own smaller genomes that are essential for cellular functions.

MtDNA exists in multiple copies per cell, but when damage occurs these copies are often degraded rather than repaired. If left unchecked, this degradation can set off a cascade of failures linked to heart conditions, neurodegeneration, and chronic inflammation.

Published in the German Chemical Society journal Angewandte Chemie International Edition, researchers at UC Riverside developed a chemical probe that binds to damaged sites in mitochondrial DNA and blocks the enzymatic processes that lead to its degradation.

“There are already pathways in cells that attempt repair,” said Linlin Zhao, UCR associate professor of chemistry, who led the project. “But degradation happens more frequently than repair due to the redundancy of mtDNA molecules in mitochondria. Our strategy is to stop the loss before it becomes a problem.”

The new molecule includes two key components: one that recognizes and attaches to damaged DNA, and another that ensures it is delivered specifically to mitochondria, leaving nuclear DNA unaffected.

In lab tests as well as studies using living cells, the probe significantly reduced mtDNA loss after lab-induced damage mimicking exposure to toxic chemicals such as nitrosamines, which are common environmental pollutants found in processed foods, water, and cigarette smoke.

In cells treated with the probe molecule, mtDNA levels remained higher, which could be critical for maintaining energy production in vulnerable tissues such as the heart and brain.

Mitochondrial DNA loss is increasingly linked to a range of diseases, from multi-organ mitochondrial depletion syndromes to chronic inflammatory conditions such as diabetes, Alzheimer’s, arthritis, and inflammatory bowel disease. When mtDNA fragments escape from mitochondria into the rest of the cell, they can act as distress signals that activate immune responses.

“If we can retain the DNA inside the mitochondria, we might be able to prevent those downstream signals that cause inflammation,” Zhao said.

Importantly, the researchers found that the protected DNA remained functional, despite being chemically tagged.

“We thought adding a bulky chemical might prevent the DNA from working properly,” Zhao said. “But to our surprise, it was still able to support transcription, the process cells use to turn DNA into RNA, and then into proteins. That opens the door for therapeutic applications.”

The Hallmarks of Aging – credit Rebelo-Marques et al, Frontiers, CC 4.0. BY-SA

The project builds on more than two years of research into the cellular mechanisms that govern mtDNA processing. While additional studies are needed to explore clinical potential, the new molecule represents a paradigm shift.

Indeed, DNA damage makes up two of the 8 hallmarks of aging first outlined in a landmark paper in 2013, which also includes mitochondrial dysfunction as an antagonistic hallmark, i.e. a result of DNA damage.“This is a chemical approach to prevention, not just repair,” Zhao said. “It’s a new way of thinking about how to defend the genome under stress.” Chemical Shield Stops DNA Damage from Triggering Disease–’A Paradigm Shift’

Read More........→August 01, 2025