LEM-3 loss leaves some worm neurons connected to their sisters
A peer-reviewed study in a model worm found lasting cellular bridges after the final stage of division failed. Shared proteins sometimes accompanied changes in neuronal identity, while other connected nuclei retained different gene-expression programmes. The experiments distinguish physical separation from specialization and concern development in worms, without establishing an equivalent disease mechanism in humans.
Science··Morning
Daughter cells retain a physical bridge
Some developing neurons in Caenorhabditis elegans, a small worm widely used in biological research, remained attached to their sister cells when LEM-3 function was disrupted. This enzyme helps clear DNA links left between separating chromosomes. The single peer-reviewed study found that incomplete final separation could leave two nuclei sharing connected cytoplasm. Such connections survived development and were still visible in adult animals, even as the linked cell bodies moved apart.[1]
Protein sharing differs from gene activity
Fluorescent markers appeared in both connected cell bodies, but measurements of messenger RNA showed that their genes were not necessarily active in both. Proteins could travel through the bridge from their cell of origin. In some pairs, the nuclei therefore preserved distinct transcriptional programmes despite sharing cellular contents. In other pairs, the programme associated with touch-sensing neurons suppressed parts of the sister cell’s alternative identity; the outcome varied by neuronal type.[1]
Connected neurons accompany changed behaviour
The bridges contained components of the cellular skeleton alongside DNA and protruding nuclear membranes in some cases. Worms with particular linked neurons responded differently in behavioural tests while retaining basic touch sensitivity. The experiments connect successful separation with the preservation of specialized neuronal identities in this organism. LEM-3 has a human counterpart called ANKLE1, but these worm results do not establish a human neurological disease mechanism or a therapy.[1]
