As a mouse embryo’s spinal neural tube closes, two edges of tissue meet and fuse in a process researchers call zippering. A study by Abigail R. Marshall and colleagues, published in PLOS Biology on November 2, 2026, reports that the protein CFL1 helps coordinate cell behaviours that move this seam along. When the researchers conditionally removed CFL1 from the embryo’s surface ectoderm, zippering slowed by about 30%, and roughly 30% of the altered embryos developed spina bifida.
The neural tube is the embryonic precursor of the brain and spinal cord. As it forms, the left and right neural folds come together at the dorsal midline. The surface ectoderm, which later contributes to the epidermis, fuses there as closure advances from the upper spinal region toward the lower spine. If closure is interrupted, a neural tube defect such as spina bifida can result.
Marshall and colleagues describe zippering as a sequence of cell actions. Actomyosin cables link cells along the edges; cells extend thin protrusions that can explore across the midline; cell borders constrict, bringing opposing protrusions closer; and new attachments form as the seam advances. The researchers propose that these steps work together, while noting that their imaging could not capture every step at once.
CFL1 is involved in the turnover of F-actin, the protein filaments that help shape cells and form their cables and protrusions. The team found CFL1 enriched near the leading edge of surface ectoderm cells beside the zippering point, particularly at earlier stages. They then used a conditional gene-deletion approach to reduce CFL1 in the surface ectoderm during early closure and examined the embryos’ cell structures and movements.
Without surface-ectoderm CFL1, cells accumulated denser actin fibres. Their filopodia—slender protrusions—were more numerous and persisted longer, but showed less exploratory movement in live imaging. In control embryos, some protrusions made brief contacts across the midline and withdrew, while others formed contacts that became stable. The authors suggest that this exploratory behaviour may help establish the contacts that let the seam progress.
The altered embryos also showed less constriction of cell borders at the zippering point. In control embryos, this tightening helps draw protrusions from opposite sides closer together. The study did not find reduced tension in the actomyosin cables or in the measured cell junctions after CFL1 deletion, narrowing the proposed explanation for slower zippering. The authors instead point to reduced filopodial movement and border constriction as changes that may limit the sequence of cell behaviours.
The results connect a specific actin-regulating protein to both cell movement and tissue-level closure in living mouse embryos. They also suggest why a disruption in one cell layer could affect whether spinal closure completes. But the proposed chain of events remains a model: the researchers could not observe the full sequence simultaneously, and they say further work may identify additional steps or relationships. The findings concern a targeted genetic change in mice; they do not establish the same mechanism or risk in humans.
The article page labels the paper an uncorrected proof.