SCIENCE · CELL BIOLOGY · REGENERATION

Cells that activate a death signal, survive and help rebuild damaged tissue

Approximate reading time: 8–10 minutes · Updated: September 2026

 

🧬 A story that seems like science fiction, but is born from experimental biology.

Research published in Nature Communications in December 2025 described two populations of epithelial cells that, in a model of Drosophila melanogaster —the fruit fly—, resist processes that normally lead to cell death and actively participate in regeneration after damage caused by ionizing radiation. The researchers named them DARE and NARE.

The news is usually summarized with the expression "zombie cells", but the term requires important precision: these cells are not the same "zombie cells" in the literature on cellular senescence. In this study, these are apoptosis-resistant cells that retain proliferative capacity and, in the case of DAREs, activate an initial signal of the apoptotic pathway without completing the death program.

🖼️ Recommended Scientific Images

The following images come from the Weizmann Institute of Science and show the epithelial tissue of the fly and the cells associated with the regeneration process. To respect provenance and rights of use, the document includes the absolute links to the original files.

🔗 Figure 1 — epithelial tissue before/after the damage (Weizmann Institute)

🔗 Image 2 — microscopic image associated with the study (Weizmann Institute)

🔗 Institutional page with context, authors and captions

🔬 The finding: cells that refuse to follow the script of death

Under normal conditions, apoptosis is one of the fundamental mechanisms by which an organism eliminates damaged, unnecessary, or potentially dangerous cells. The process is carefully regulated and depends on a family of enzymes called caspases. An initiating caspase activates a cascade that, if it progresses to the executing caspases, disassembles the cell in an orderly fashion.

The team led by Tslil Braun and Eli Arama of the Weizmann Institute of Science looked for precisely cells that had triggered an early signal of apoptosis but were still alive. To do this, they used genetic tools and a delayed sensor that identified cells in which the initiator caspase Dronc had been activated.

The result was the identification of DARE (Dronc-Activating Regeneration Enhancing) cells, capable of surviving an attack that causes apoptosis in many neighboring cells. After irradiation, these cells proliferated and contributed to tissue repair. The study indicates that their descendants managed to replace about half of the affected tissue in approximately 48 hours.

🧩 DARE and NARE: Two Populations, Different Functions

 

⚙️ How do they manage to survive?

The study provides a key piece of the mechanism. In DAREs, activation of Dronc does not automatically trigger the entire destructive cascade. The researchers implicated Myo1D, a molecular motor-associated protein, in the survival of these cells. Experimental evidence indicates that Myo1D helps keep the initiating caspase in a situation that prevents lethal activation of the executing caspases.

When the researchers silenced this protein, the DARE cells lost their ability to survive and tissue regeneration deteriorated. The finding is important because it shows that the same molecular machinery can participate in two apparently opposite outcomes: promoting cell death in a context and, under certain conditions, contributing to survival and repair.

🌱 When one cell dies activates the repair of others

Regeneration also does not occur in isolation. Cells that die after damage appear to emit signals capable of activating DAREs. From there, DAREs proliferate and promote the proliferation of nearby NARE cells.

The researchers also observed a negative feedback mechanism: DAREs stimulate the growth of NAREs, while NAREs produce signals that slow down the growth of DAREs. This circuit helps prevent a repair response from turning into uncontrolled growth.

In simple terms, tissue appears to use a combination of alarm, survival, expansion, and brake. Cell death is not just a loss: it can also become a signal that organizes reconstruction.

🛡️ The data that attracted the most attention: resistance in the descendants

The most striking aspect appears when the tissue is irradiated again. The researchers observed that, during the first hours of a second exposure, about half of the cells that had died during the first exposure died. In addition, the descendants of the DAREs were about seven times more resistant to cell death than the cells of the original tissue.

This does not mean that the cells have become "immortal". It means that, in the experimental model and under the conditions analyzed, the descendants of the DAREs showed much greater resistance to damage than the initial cells. That difference may be relevant to understanding how some tissues survive repeated aggressions.

The authors suggest that the mechanism could help to understand a known problem in oncology: some tumors that recur after treatment may have resistant populations. However, the study does not prove that this mechanism is, by itself, the explanation for the resistance of human tumors.

⚠️ "Zombie cells" doesn't mean the same thing in every study

Here is one of the main keys to correctly interpreting the news. In biology, "zombie cells" is often used as a popular expression for senescent cells: cells that stop dividing, remain metabolically active and can release molecules that modify the behavior of the tissue.

The DAREs and NAREs in the Weizmann Institute study should not be automatically confused with those senescent cells. In fact, independent work has shown that certain senescent cells can play beneficial roles during tissue repair, while other senescent populations can contribute to inflammation and disease. Cell biology is therefore much more nuanced than the picture of a simply "good" or "bad" cell.

In 2026, for example, a study published in Nature Cell Biology described a rapid senescence response in skin cells after an injury and found that this response is involved in repair. That work is relevant to the overall context of "cells that appear damaged but help repair," but it's not the same mechanism as the one described for DARE/NARE.

🧪 Was the discovery made in humans?

No. The central study was conducted using Drosophila melanogaster and, in particular, epithelial tissue related to wing development. This point is critical. Just because a molecular pathway exists in a model organism and can have equivalents in other animals does not mean that the same behavior has been demonstrated in humans.

The fruit fly is a widely used model in genetics and developmental biology because numerous cellular pathways are conserved between species. So the results can guide further research. But it still needs to be shown which equivalent cells exist in human tissues, how they are regulated, and whether they produce comparable benefits or risks.

🧠 Why may this finding be important for medicine?

The first possibility lies in regeneration. If it is possible to understand how cells survive intense damage and coordinate repair, new strategies could appear to improve healing or the recovery of certain tissues. The authors themselves suggest that these mechanisms could help to develop ways to accelerate regeneration after an injury.

The second possibility is in oncology. If a cell manages to avoid apoptosis after suffering genetic damage, that ability can be useful for healthy tissue that needs to be repaired, but it could also be problematic if a tumor cell uses similar mechanisms to escape treatment.

The third issue is therapeutic: the challenge is not simply to increase cell resistance. The goal would be to learn how to control when that resistance is beneficial and when it can promote abnormal growth. The research is still at a basic stage and is not a treatment available to patients.

🔭 A Shift in Perspective on Apoptosis

For a long time, apoptosis was primarily presented as the mechanism by which a cell "commits suicide" to protect the organism. Modern research has shown that caspases may have additional functions and that signaling associated with death may influence processes such as proliferation, repair, and response to damage.

The work of Braun and his colleagues adds a particularly interesting piece: some cells can activate a part of the apoptotic machinery and, without completing the death process, convert that signal into a regenerative advantage. The boundary between "death," "survival," and "repair" thus becomes much less rigid than simplified definitions suggest.

📌 What we know and what we don't know yet

🧾 Conclusion

The term "zombie cells" is attractive to describe this discovery, but the scientific reality is even more interesting. The researchers identified DARE cells that, in a fruit fly model, activate a signal associated with apoptosis, survive an attack that kills other cells, proliferate, and help rebuild tissue. They also identified NARE cells that are involved in regeneration and a signal circuit that limits growth.

The fact that the descendants of DAREs were much more resistant to a second injury opens up a question of great interest to biology and medicine: how can a cell convert an experience of damage into a subsequent ability to survive? The answer could contribute both to improving tissue regeneration and to understanding why some cells, including certain cancer cells, manage to resist therapeutic aggressions.

For now, however, it is convenient to separate the evidence from the expectations. The finding is solid within the experimental model used, but it does not yet demonstrate a therapy for humans or allow us to affirm that there are "zombie cells" with identical behavior in our body.

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Recommended H1: "Zombie" cells? The cells that survive apoptosis and help regenerate tissues

Excerpt/pompadour: A study in Nature Communications identified DARE and NARE cells capable of resisting cell death and coordinating regeneration after severe damage. The finding also raises questions about tumor resistance.

FAQ: What are DARE cells? · What are NARE cells? · Do zombie cells really exist? · Were DARE cells found in humans? · How do they relate to apoptosis? · Why may they be important for cancer?

Entities / topics: Apoptosis · caspases · Dronc · tissue regeneration · Drosophila melanogaster · cellular senescence · cancer · ionizing radiation

📚 Scientific sources and absolute links

🔗 Nature Communications — original article, published December 4, 2025

🔗 Weizmann Institute of Science — Resurrected Tissue, 24 de diciembre de 2025

🔗 eLife / PMC — regeneration after necrosis and non-apoptotic caspase activity

🔗 Nature Cell Biology — rapid senescence during healing, 2026

🔗 PubMed — abstract of the study on rapid senescence and repair

🔗 UCSF — context on senescent cells and tissue repair