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

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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

First video of immune cells eating live skin cancer in real time

Macrophages (green) engulfing melanoma cells (purple). Keith et al. / Garvan Institute, CC BY-SA Yuki Keith, Garvan Institute and Tri Phan, Garvan Institute

For the past 15 years or so, a class of drugs called immune checkpoint inhibitors have been used to treat melanoma – the most dangerous kind of skin cancer.

For many patients, they produce remarkable results. For others, they do nothing.

We still don’t really know why. But in new research published in the Journal of Experimental Medicine, we observed immune cells called macrophages attacking melanoma cells in real time – which may offer clues about how we can make those therapies work for all patients, not just some.

Tumours, hot and cold

One of us (Yuki) treated patients with melanoma in Japan as a dermatologist. The other (Tri Phan) runs a lab at the Garvan Institute in Sydney, where his team specialises in observing the cells of the immune system in real time.

When Yuki wanted to understand why immune checkpoint inhibitors were failing for many patients, she joined Tri Phan’s lab to continue her research.

The treatment fails in what oncologists call “cold” tumours, where the cancer’s environment actively prevents a kind of immune cell called a T cell attacking it. One of our lab’s aims is trying to work out how to make the tumours “hot”, allowing T cells to penetrate and destroy the cancer cells.

Our new findings suggest a different kind of immune cell, called macrophages, may hold the key.

Macrophages (green) engulfing melanoma cells (purple). Yuki Keith, CC BY

The housekeepers we’ve been ignoring

In 1908, Russian zoologist Ilya Mechnikov was awarded a Nobel Prize for the discovery of phagocytosis (“cell eating”) in the immune system, which is carried out by cells he called macrophages (from the Greek for “big eaters”).

These cells engulf and clear away the debris caused by tissue damage and cell death. They are often regarded as the body’s silent, no-fuss housekeepers.

However, their role in cancer has often been overlooked. Unlike other immune cells that move through the blood and patrol the whole body, macrophages are “tissue-resident” and stay in one place.

A microscopic view of a melanoma tumour growing in the skin shows CD169 macrophages in green and yellow forming a biological boundary wall around the tumour. Keith et al. / Garvan Institute, CC BY

Earlier studies of the role of macrophages in cancer assumed these housekeepers were all the same. But when we looked closely in the skin, it became clear that there were many different kinds of macrophages living in different layers.

One particular kind of macrophages (recognised by a protein called CD169) lives in a deeper part of the skin, called the hypodermis.

We found that these macrophages arranged themselves around the edges of a melanoma tumour, as if they were trying to wall it off. When we depleted the macrophages, the melanomas grew bigger, suggesting they were constraining the growth of the tumours.

Watching cancer cells being eaten alive

To understand what these CD169-positive macrophages were actually doing, we used an advanced imaging technique called intravital two-photon microscopy. This allows us to watch biological processes unfold in living tissue in real time.

What we saw was surprising: the macrophages were “nibbling” and actively engulfing live melanoma cells. While we had seen macrophages eat dead cells in our lab before, we had never seen them eat a live melanoma cell in a model organism.

What was even more surprising was that this immune attack was happening without the need for T cells, or antibodies made by another kind of immune cell called B cells – the immune players most commonly credited with fighting cancer.

We also confirmed this is not something that just happens in the lab. Our colleagues at the Melanoma Institute Australia analysed samples from human melanoma patients and found similar populations of CD169-expressing macrophages on the edges of the tumour, suggesting they may play a similar protective role there.

Calling in the cavalry – implications for therapies

Macrophages don’t just clear away debris. They can also alert the immune system to danger. After they have digested the debris, they can display it like a biological “red flag” to direct T cells to find and kill the cancer cells.

What makes a macrophage decide whether to silently dispose of debris without alerting the immune system, or wave the red flags to activate the immune system, is still unclear. Because the CD169-expressing macrophages are strategically positioned around the tumours, we suspect they may hold the key.

Macrophages are widespread in most solid tumours – including glioblastoma, breast cancer and many others. This is an army already in place waiting to be mobilised.

Our next step is to understand precisely how these macrophages eat live cancer cells and how they can communicate the danger to T cells, so we can harness this population with new treatments.

Yuki Keith, Postdoctoral Researcher, Immunology, Garvan Institute and Tri Phan, Program Director – Precision Immunology / Laboratory Head, Garvan Institute

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Read More........→May 27, 2026