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When the researchers added plastin 3 back to motor neurons in zebrafish that were genetically altered so they couldn’t produce SMN, the zebrafish regained most of their swimming abilities movement that had been severely limited by their reduced SMN. These findings tied the presence of plastin 3 – alone, without SMN – to the recovery of lost movement

without SMN in their cells still eventually died, so the addition of plastin 3 alone is not a therapeutic option

using animal studies to pinpoint the role of plastin 3 in this disease

In zebrafish genetically altered so they don’t produce SMN, plastin 3 levels remained low, as well.

lowering plastin 3 first in the fish – SMN was unaffected. This showed that the plastin 3 decrease occurred only when SMN was lowered first

SMN production was stimulated in zebrafish initially lacking the protein, plastin 3 levels were restored as well

researchers determined that decreased SMN influences plastin 3 production at a late point in the process called translation, when amino acids are strung together to form the protein’s initial shape

lack of SMN creates conditions in which too little plastin 3 is made to complete the protein’s normal functions – in these animals, the reduction was about four-fold

maybe SMN is affecting translation of other proteins that could be contributing to spinal muscular atrophy

That hasn’t been shown before

examination of zebrafish motor neurons suggested that decreased plastin 3 affects these cells in at least two ways

damaging axons, branch-like extensions that allow for communication among nerve cells

destabilizing synapses, structures through which those signals pass

result of the added plastin 3, the fish recovered their ability to turn and swim, movements they were previously unable to make.

rescued axons, synaptic proteins and behavior all by putting plastin 3 back in motor neurons,” she said. “That’s very encouraging.”