Sunday, April 19, 2026

Anabaena learns a new trick

Cyanobacteria surprise scientists with evolutionary shift

Institute of Science and Technology Austria

Fluorescent Anabaena — image:
Fluorescent *Anabaena*. Fluorescently labelled CorM filaments inside Anabaena. These represent a newly discovered cytoskeleton in multicellular cyanobacteria.
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Credit: © Loose group | ISTA

Photosynthetic bacteria helped shape Planet Earth. Among them are cyanobacteria that produced the oxygen in our atmosphere and made complex life possible, captivating scientists for decades. Now, researchers at the Institute of Science and Technology Austria (ISTA) report a surprising new discovery—a system thought to separate DNA has developed to sculpt the shape of the cell in cyanobacteria instead. The results, published in Science, shed light on how protein systems evolve and how multicellularity emerged in this type of ecologically essential bacteria.

“Cyanobacteria are essentially pioneers of oxygenic photosynthesis,” says Benjamin Springstein, a postdoc in the Loose group at the Institute of Science and Technology Austria (ISTA).

“They are responsible for the Great Oxygenation Event about 2.5 billion years ago, when oxygen accumulated in the atmosphere and made aerobic life possible. Without them, it’s safe to say that none of us would be here today.”

Still today, these organisms remain vital by contributing significantly to global biomass production and playing key roles in carbon and nitrogen cycles. They thrive in some of Earth’s most extreme environments—from hot springs to the Arctic—and even on roofs and walls on urban buildings. Among them is Anabaena sp. PCC 7120 (or simply Anabaena), a multicellular cyanobacterium that has been the subject of research for more than 30 years.

Working in the group of Professor Martin Loose in collaboration with the Schur group at ISTA, as well as the Institut Pasteur de Montevideo (Uruguay), Kiel University (Germany), and the University of Zürich (Switzerland), Springstein and his colleagues now show that Anabaena, and likely many other multicellular cyanobacteria, have undergone a major evolutionary shift, transforming an ancient DNA segregation system into a new cytoskeleton that controls cell shape.

DNA in bacteria: A brief primer

Like all bacteria, Anabaena reproduce by cell division, which requires precise replication and distribution of its genetic material. This genetic material—the DNA—is tightly packed into chromosomes, much like a wire around a spool. Often present in multiple copies, chromosomes must be reliably inherited during cell division for daughter cells to remain viable.

Bacterial DNA exists in two main forms: chromosomes, which carry genes crucial for survival, and plasmids that contain additional, often non-essential genes. Plasmids are especially mobile, as they can easily be transferred from one bacterium to another, allowing bacteria to rapidly acquire new traits and evolve swiftly.

A DNA segregation system—until it was not

Since 2014, Springstein has been captivated by Anabaena, exploring their evolutionary and molecular mysteries. When the COVID-19 pandemic brought research to a halt and laboratories closed, he turned to reviewing literature on the topic while writing a review and found something surprising that proved worth following up.

“I made a serendipitous observation,” he recalls.

He noted that Anabaena and some other select multicellular cyanobacteria possess a so-called ParMR system that is encoded on their chromosomes. This system is traditionally associated with plasmid segregation and was previously only found on plasmids—the bacteria’s mobile gene storage site. This observation made him hypothesize that this system might actively segregate chromosomes—and not plasmids—during cell division to ensure the proper maintenance of its DNA.

Springstein then later joined ISTA and the Loose group as an IST-Bridge Fellow to test this idea. However, his experiments told a different story. One component, ParR, for instance, could not bind to the DNA anymore; instead, it associated with lipid membranes, particularly the inner cell membrane. Rather than forming filament bundles in the cytoplasm to segregate chromosomes, Anabaena’s ParM forms filament networks just underneath the inner cell membrane to assemble into an array of protein polymers like a cell cortex.

In other words, instead of generating spindle-like cytoplasmic structures as expected for a chromosome segregation system, it appeared to function through membrane-associated organization.

Cells lose their shape

To unravel this mystery further, the researchers rebuilt the system outside living cells using purified components. In these in vitro reconstitution experiments, they observed that the filaments showed dynamic instability—they grew before suddenly collapsing during disassembly, a behavior well known from microtubules in eukaryotic cells.

To understand the structural basis of this behavior, the Loose group teamed up with the group of ISTA Professor Florian Schur and his PhD student Manjunath Javoor. Using cryo-electron microscopy—a technique that captures molecular structures at near-atomic resolution—the researchers examined the architecture of these filaments. Their discovery: Unlike the plasmid-encoded ParMR system in other bacteria, which forms polar filaments, Anabaena filaments are bipolar, meaning they can grow and shrink from both ends.

The functional consequences became quite clear when the system was removed from living cells.

“Cells lacking the system lost their normal rectangular-like cell shape and instead became round and swollen,” Springstein explains.

Similar defects are often seen in mutations of cell-shape maintenance genes in other bacteria, strongly indicating that this system plays a role in controlling cell morphology rather DNA segregation.

Reflecting on its newly uncovered function and their distinct location in the cell, the researchers renamed the system “CorMR.”

Four steps to a new function

Multicellular cyanobacteria evolved from single-celled ancestors through a gradual increase in cellular complexity. Bioinformatic analyses by collaborator Daniela Megrian from the Institut Pasteur in Montevideo, Uruguay, shed light on how the CorMR system evolved—an adaptation that did not arise all at once but rather through a series of changes.

The transformation likely unfolded in four key steps: the system moved from a plasmid to the chromosome; its components changed in size and structure; new membrane-binding capabilities emerged, and the system came under the control of an additional protein system. Together, these changes turned an ancient DNA-segregation machinery into one that controls cell shape.

Journal

Science

DOI

10.1126/science.aea6343

Method of Research

Experimental study

Subject of Research

Cells

Article Title

Repurposing of a DNA segregation machinery into a cytoskeletal system controlling cell shape

Article Publication Date

16-Apr-2026

High-resolution image of CorM filaments in Anabaena. Green corresponds to CorM filaments while purple shows cyanobacterial photosynthetic pigments.

Credit

Down to the core. From left to right: When rebuilt outside of living cells, CorM forms dynamic filaments. Cryo-electron microscopy (cryo-EM) image of purified CorM filaments. Successive zoom-ins show the reconstructed 3D electron density map of the CorM filament, followed by the corresponding atomic model, illustrating the filaments’ assembly into a bipolar double-stranded filament.

Credit

MIT study shows youth may increase vulnerability to a carcinogen found in contaminated water and some drugs

The new study suggests that the chemical NDMA is much more likely to cause cancerous mutations after exposure early in life.

Massachusetts Institute of Technology

CAMBRIDGE, MA -- A new study from MIT suggests that a carcinogen that has been found in medications and in drinking water contaminated by chemical plants may have a much more severe impact on children than adults.

In a study of mice, the researchers found that juveniles exposed to drinking water containing this compound, known as NDMA, showed dramatically higher rates of DNA damage and cancer than adults.

The findings may help to explain an epidemiological association between childhood cancer and prenatal exposure to NDMA in people living near a contaminated site in Wilmington, Massachusetts, the researchers say. The study also suggests that it is critical to evaluate the impact of potential carcinogens across all ages.

“We really hope that groups that do safety testing will change their paradigm and start looking at young animals, so that we can catch potential carcinogens before people are exposed,” says Bevin Engelward, an MIT professor of biological engineering. “As a solution to cancer, cancer prevention is clearly much better than cancer treatment, so we hope we can spot dangerous chemicals before people are exposed, and therefore prevent extensive cancer risk.”

MIT postdoc Lindsay Volk is the lead author of the paper. Engelward is the senior author of the study, which appears in Nature Communications.

From DNA damage to cancer

NDMA (N-Nitrosodimethylamine) can be generated as a byproduct of many industrial chemical processes, and it is also found in cigarette smoke and processed meats. In recent years, NDMA has been detected in some formulations of the drugs valsartan, ranitidine, and metformin. It was also found in drinking water in Wilmington, Massachusetts, in the 1990s, as a result of contamination from the Olin Chemical site.

In 2021, a study from the Massachusetts Department of Health suggested a link between that water contamination and an elevated incidence of childhood cancer in Wilmington. Between 1990 and 2000, 22 Wilmington children were diagnosed with cancer. The contaminated wells were closed in 2003.

Also in 2021, Engelward and others at MIT published a study on the mechanism of how NDMA can lead to cancer. In the new Nature Communications paper, Engelward and her colleagues set out to see if they could determine why the compound appears to affect children more than adults.

Most studies that evaluate potential carcinogens are performed in mice that are at least 4 to 6 weeks old, and often older. For this study, the researchers studied two groups of mice — one 3 weeks old (juvenile), and one 6 months old (adult). Each group was given drinking water with low levels of NDMA, about five parts per million, for two weeks.

Inside the body, NDMA is metabolized by a liver enzyme called CYP2E1. This produces toxic metabolites that can damage DNA by adding a small chemical group known as a methyl group to DNA bases, creating lesions known as adducts.

When the researchers examined the livers of the mice, they found that juveniles and adults showed similar levels of DNA adducts. However, there were dramatic differences in what happened after that initial damage. In juvenile mice, DNA adducts led to significant accumulation of double-stranded DNA breaks, which occur when cells try to repair adducts. These breaks produce mutations that eventually lead to the development of liver cancer.

In the adult mice, the researchers saw essentially no double-stranded breaks and significantly fewer mutations compared to juveniles. Furthermore, the livers did not develop severe pathology, including tumors, even though they experienced the same initial level of DNA adducts.

“The initial structural changes to the DNA had very different consequences depending on age,” Engelward says. “The double-stranded breaks were exclusively observed in the young.”

Further experiments revealed that these differences stem from differences in the rates of cell proliferation. Cells in the juvenile liver divide rapidly, giving them more opportunity to turn DNA adducts into mutations, while cells of the adult liver rarely divide.

“This really emphasizes the overall problem that we’re trying to highlight in the paper,” Volk says. “With toxicological studies, oftentimes the standard is to use fully grown mice. At that point, they’re already slowing down cell division, so if we are testing the harmful effects of NDMA in adult mice, then we’re completely missing how vulnerable particular groups are, such as younger animals.”

While most of these effects were seen in the liver, because that is where NDMA is metabolized, a few of the mice developed other types of cancer, including lung cancer and lymphoma.

Adult risk is not zero

For most of these studies, the researchers used mice that had two of their DNA repair systems knocked out. This speeds up the mutation process, allowing the researchers to see the effects of NDMA exposure more easily, without needing to study a large population of mice.

However, a small study in mice with normal DNA repair showed that juveniles experienced NDMA-induced double-strand breaks, regenerative proliferation, and large-scale mutations that were completely absent in adults. This occurs because the fast-growing juveniles possess highly active DNA replication machinery that encounters the DNA adducts before the cell has time to repair them.

The researchers also found that if they treated adult mice with thyroid hormone, which stimulates proliferation of liver cells, those cells began accumulating mutations as quickly as the juvenile liver cells. Previous work done in the Engelward laboratory has shown that inflammation can also stimulate cell proliferation-driven vulnerability to DNA damage, so the findings of this study suggest that anything that causes liver inflammation could make the adult liver more vulnerable to damage caused by agents such as NDMA.

“We certainly don’t want to say that adults are completely resistant to NDMA,” Volk says. “Everything impacts your susceptibility to a carcinogen, whether that’s your genetics, your age, your diet, and so forth. In adults, if they have a viral infection, or a high fat diet, or chronic binge alcohol drinking, this can impact proliferation within the liver and potentially make them susceptible to NDMA.”

The researchers are now investigating how a high-fat diet might influence cancer development in mice that also have exposure to NDMA.

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This collaborative effort across several MIT labs was funded by the National Institutes of Environmental and Health Sciences (NIEHS) Superfund Research Program, a NIEHS Core Center Grant, a National Institutes of Health Training Grant, and the Anonymous Fund for Climate Action.