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UCSF in Current Biology showed how the mitotic spindle repairs itself under stress and protects DNA division

Learn why the mitotic spindle, the key cellular "machine" for separating chromosomes, can withstand large forces. A team from UC San Francisco in Current Biology describes how fibers under load quickly renew and further strengthen. In an experiment with a microneedle in living cells, self-repair was recorded that helps DNA divide precisely into two cells.

UCSF in Current Biology showed how the mitotic spindle repairs itself under stress and protects DNA division
Photo by: Domagoj Skledar - illustration/ arhiva (vlastita)

UCSF Discovery: Microscopic Fibers That Repair Themselves as the Cell Divides

At every moment in the human body, millions of cell divisions are taking place. In this seemingly routine biology, there is no room for error: each cell must divide duplicated DNA into two equal "copies" so that the daughter cells receive the same genetic content. The key machine of this process is the mitotic spindle – a network of protein fibers that organizes around chromosomes on the eve of division, captures them, and pulls them to opposite sides of the cell with powerful mechanical forces. Even the slightest out-of-control deviation in this pulling can lead to the wrong distribution of chromosomes, a risk that biology tries to minimize.
For a long time, however, it was not known how the spindle withstands heavy loads without breaking or falling apart, while simultaneously remaining dynamic enough to finish the job within the exact time window of division. A team from the University of California, San Francisco (UCSF) has now shown that the spindle can locally "repair" itself during operation: when individual fibers find themselves under great mechanical stress, their internal "skeleton" rearranges and strengthens, replacing weakened bonds with new ones. In the UCSF announcement, the authors emphasize that such constant reinforcement helps the cell separate chromosomes precisely, reducing the probability that one daughter cell receives an excess or deficit of chromosomes – an error that, according to general medical and scientific consensus, can be linked to developmental disorders or biological processes that accompany the onset and progression of cancer.
The UCSF research report was published on January 27, 2026, and the study, according to the same announcement, appeared in the journal Current Biology dated January 23, 2026. Metadata accompanying the article also lists an online publication date of January 22, 2026, which is in practice a common difference between an early online edition and the official journal date.

Why the Mitotic Spindle Is More Than a "Rope" Pulling Chromosomes

The mitotic spindle is not a passive construction. It is a dynamic architecture composed of microtubules – hollow protein "tubes" built from tubulin – and a series of auxiliary proteins that link microtubules into bundles, stabilize them, and direct their behavior. During metaphase, when chromosomes line up in the center of the cell, the spindle must simultaneously keep the chromosomes aligned and prepare for separation in anaphase. This requires a combination of flexibility and strength: the structure must be "soft" enough to absorb local deformations and shifts, but also strong enough that, under load, it does not fall apart and lose the geometry needed for uniform pulling.
Precisely this mechanical reliability has intrigued biological physicists for decades. The strength and stability of such nanometer-sized constructions are difficult to measure directly in living cells, and approaches that "freeze" cells or roughly damage them often erase key details of the spindle's actual operation. Sophie Dumont, a professor at UCSF and the lead author of the paper, notes in the university's announcement that the spindle generates large forces, but that its durability is difficult to measure directly while it is in operation. That is exactly why the team sought a way to challenge and load the system while maintaining conditions as close as possible to natural division.

The Microneedle: A Glass Needle Thinner Than a Hair, but Precise Enough for a Single Thread

At the center of the experiment was a microneedle – a glass needle stretched to a thickness less than that of a human hair. Lead author Caleb Rux, then a doctoral student at UCSF, used it to physically load an individual spindle fiber within a living cell. The key was that the needle tip had to be smooth: piercing the membrane would kill the cell and turn the measurement into an artifact. According to the UCSF description, Rux positioned the microneedle above the selected fiber using precise commands and then engaged a finely calibrated motor that gradually increased the pull until the fiber reached its limit of endurance and snapped.
Such work required a combination of patience and microscopic precision. Under the microscope, Rux searched for elongated cells ready for division, with a clearly visible spindle stretching from one pole of the cell to the other and with chromosomes gathered in the middle. Only then would he select a bundle of microtubules that could be individually loaded. Bibliographic abstracts of the paper state that the authors used laser ablation and live microscopy alongside the microneedle to compare the consequences of mechanical loading and targeted "cuts" on similar structures. The goal was not only to see if the fiber breaks, but also how it behaves before and after the break, and if there is a way the system redistributes stability on its own.

Unexpected Break: The Fiber Snaps Where It Is Pulled, Not at the Ends

One expectation was almost intuitive: if a bundle of microtubules is pulled outward, the "anchoring points" – the ends of the bundle where connections are transferred to the rest of the spindle – should be the most sensitive. However, as the load increased, the fiber did not fall apart at the poles. It broke exactly in the zone where the microneedle was pulling – at the point of maximum force. "We expected the fiber to break at the ends, but instead it broke where the needle was pulling," UCSF quoted Caleb Rux.
Even more important was what happened after the break. In many conditions, microtubules are prone to dynamic instability: they can suddenly transition from growth to rapid shortening and collapse. In this case, however, the severed end maintained its shape and did not scatter. This surprised the team, especially because earlier experiments from the same laboratory, according to UCSF, showed that laser "cutting" of the fiber could lead to its rapid disintegration. The difference between mechanical breaking and laser ablation became an important clue that in the mechanical case, a process is activated that stabilizes the damaged site and prevents immediate collapse.

Real-Time Self-Repair: Damage as a Trigger for Strengthening

Post-experiment analyses suggest a two-phase scenario. In the first, as the bundle bends and begins to "give way" under the force, part of the protein bonds holding the microtubules linked in the bundle is temporarily lost. This is the moment when the system could become vulnerable and prone to snapping. However, according to the UCSF description, a rapid replacement immediately follows: the lost bonds are replaced with new, stronger ones, using proteins that already exist in the cell and can be integrated into the site of damage. The bundle, therefore, does not stay in a weakened state for long, but quickly transitions into a reinforced version of itself.
Bibliographic abstracts of the paper emphasize that local force can damage the microtubule lattice, but that this damage encourages remodeling and stabilization. One sign of such stabilization is the behavior of the new microtubule ends in the break zone: they often show arrested dynamics and resist degradation, which is consistent with the observation that the broken part does not retract and disintegrate immediately. In the popular UCSF announcement, this effect is summarized simply: by the time the fiber finally breaks, it is stronger than it was before the initial loading.
Such a conclusion changes the classic image of the spindle as a structure that "must endure" while working. Here it is suggested that the spindle distributes its durability, strengthening itself where the forces are greatest. If this mechanism is general, it is an elegant solution: instead of the entire system being built with a large safety margin, it reinforces itself locally when and where necessary, while the rest remains dynamic enough for adjustments.

Why One Error in Chromosome Number Can Have Great Consequences

The biological stakes of such mechanisms are high. If chromosomes are not distributed equally, aneuploidy occurs – a condition in which a cell has an excess or deficit of whole chromosomes. In a medical context, aneuploidy is linked to pregnancy outcomes and developmental disorders; medical reviews state that changes in chromosome number can increase the risk of miscarriages and lead to chromosomal disorders that affect development. On the other hand, modern reviews in oncology emphasize that aneuploidy is a common and clinically important feature of many tumors and can play a role in development, progression, and response to therapy.
That is precisely why researchers are interested in how cells achieve extreme accuracy at the moment when mechanics could throw the system "out of balance." The spindle must withstand forces while simultaneously maintaining proper chromosome alignment and preparing for the separation that will pull them toward the poles. If the most loaded parts of the spindle can strengthen themselves in real time, it potentially reduces the probability that a break will occur during crucial seconds that changes the direction of pulling and increases the risk of missegregation.

Broader Scientific Context: The Search for Rules of "Robustness" in Cell Division

Mechanical approaches in cell biology have been gaining more space in recent years. It is becoming clear that cellular structures cannot be explained solely by chemical reactions, but also by the laws of force, stress, and elasticity. Review papers on the assembly and robustness of the mitotic spindle highlight that microtubules and associated proteins self-organize into a structure that must be stable and simultaneously adaptable, and that constant regulation of growth and degradation takes place during division. In such a framework, it is logical to ask not only how the spindle is built, but also how it remains functional when local damage or unexpected loads occur.
Sophie Dumont's laboratory had previously developed physical methods to challenge the spindle with a microneedle to see how the system distributes forces without ending the cell's life. The new research goes a step further because it shows that loading is not just a threat, but also a trigger for rearrangement. Interestingly, the idea of microtubule repair exists outside the context of division: part of the literature describes the exchange of building units along the microtubule wall as a way to remediate damage. Here, however, the emphasis is on the repair being linked to sites of maximum mechanical stress within the spindle, exactly in the phase when the accuracy of chromosome distribution is crucial.

From the Cell to Engineering: Can Biology Inspire Self-Repairing Materials?

In the UCSF announcement, Sophie Dumont draws a parallel with engineering: buildings are designed to survive earthquakes, roads to withstand winters, and materials to endure repeated loads. If it is understood how biological structures locally strengthen under stress, some of those principles could inspire the development of materials that respond to damage not by snapping, but by reorganization. In material sciences, "self-repairing" concepts are already being developed, but cellular systems offer an example of an extremely fast response, in which stabilization can happen in a time measurable in seconds or minutes, while the process is still ongoing.
It is important, however, to remain cautious regarding direct applications. This research primarily explains a fundamental mechanism in living cells and does not offer a ready-made technology. But in scientific practice, exactly these kinds of discoveries often become a starting point: they define rules of reliability at the molecular level and help understand how a system that must work under load can remain stable, yet simultaneously lively enough to finish the task.

Who Is Behind the Study, When Was It Published, and Who Funded It

Alongside Caleb J. Rux and Sophie Dumont, the authors of the paper include Megan K. Chong, Valerie Myers, and Nathan H. Cho. According to the UCSF announcement, the research was financially supported by the US National Institutes of Health (NIH) through grant R35GM136420, the National Science Foundation (NSF) through the Graduate Research Fellowship Program, and several university and philanthropic programs, including UCSF fellowships, joint UC Berkeley and UCSF programs, and the Chan Zuckerberg Biohub.
UCSF states that the paper appeared in the journal Current Biology dated January 23, 2026, while metadata accompanying the article also lists an online publication date of January 22, 2026. Abstracts of the paper emphasize that mechanical force locally damages the spindle's microtubule bundles, but that this damage encourages remodeling and stabilization of the lattice, making the bundle more resistant exactly at the site of maximum load. Such a conclusion provides a new explanation for why the spindle proves extremely reliable under normal conditions, even when exposed to forces that, at first glance, should be destructive.

What Is Currently Firmly Shown and What Remains Open

Based on available data, it is clear that mechanical loading can trigger local strengthening of spindle fibers and that such stabilization happens quickly, in a time relevant to the cell division itself. This explains how the spindle can endure large forces and remain functional until the moment the chromosomes are separated. Nevertheless, questions remain about universality: does the same type of strengthening occur in all cell types and tissues, and how does the mechanism behave in cells that are already under chronic stress or have altered regulatory pathways, as is often the case in a tumor environment?
The question of which proteins are crucial for replacing "weak links" with stronger ones and how the cell "knows" to reinforce the structure exactly at that spot also remains open. The authors suggest that reinforcement appears where the force is greatest, which suggests a kind of mechanical sensor in the architecture of the microtubules and associated proteins themselves. Clarifying these details could help in understanding why errors in chromosome segregation occur in some states, despite the basic division machine being extremely reliable in healthy cells.

Sources:
  • UC San Francisco (UCSF News Center) – report on mitotic spindle research, author quotes, and description of the microneedle experiment (link)
  • Phys.org – summary of the announcement and bibliographic data of the paper in Current Biology, including DOI (link)
  • Scilit – metadata about the article in the journal Current Biology (date and DOI) (link)
  • bioRxiv – preprint of the study (technical details of methodology and interpretation of stabilization under force) (link)
  • Nature Reviews (Molecular Cell Biology) – review on the mechanisms of assembly and robustness of the mitotic spindle (link)
  • Nature Genetics – review paper on aneuploidy as a factor in cancer development and progression (link)
  • Cleveland Clinic – medical overview of aneuploidy and consequences for pregnancy (link)

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