Given the clinical challenges associated with repairing damaged nerves, using model organisms to define the molecular mechanisms controlling spontaneous modes of functional regeneration can be advantageous. In the last five years, using the nematode Caenorhabditis elegans as a model system, we have gained major insights into the molecular control of a highly efficient repair paradigm known as axonal fusion. In this key biological process, individually transected axons regrow, reconnect, and fuse, with their own separated distal axon fragments, restoring the original axonal tract and the full neuronal function. Excitingly, similar paradigms that have been optimised in rodent and canine models have now been successfully used in the clinic.
However, based on the current literature and from conversations with colleagues, it has become apparent that there are conceptual differences in the way axonal fusion is analysed and quantified, potentially leading to the publication of misleading or incorrect findings. Thus, it is essential that a unifying view is developed to clarify how to precisely examine and score this biological event in order to prevent the publication and dissemination of erroneous interpretations. In our manuscript, we address this by providing clear examples of how fusion should be assessed and the errors that can result from incorrect analysis. We hope that our article will be a helpful guide as more groups focus on regenerative axonal fusion.