Friday, 2 January 2015

Repairing fish

Fang Y, Lei X, Li X, Chen Y, Xu F, Feng X, Wei S, Li Y. A novel model of demyelination and remyelination in a GFP-transgenic zebrafish. Biol Open. 2014 Dec  pii: BIO201410736. doi: 10.1242/bio.201410736. [Epub ahead of print]

Demyelinating diseases consist of a variety of autoimmune conditions in which the myelin sheath is damaged due to genetic and/or environmental factors. During clinical treatment, some patients undergo partial remyelination, especially during the early disease stages. However, the mechanisms that regulate demyelination remain unclear. The myelin structure, myelin formation and myelin-related gene expression are highly conserved between mammals and zebrafish. Therefore, the zebrafish is an ideal model organism to study myelination. In this study, we generated a transgenic zebrafish Tg(mbp:nfsB-egfp) expressing a fusion protein composed of enhanced green fluorescent protein (EGFP) and NTR from the myelin basic protein (mbp) promoter. Tg(mbp:nfsB-egfp) expressed NTR-EGFP reproducibly and hereditarily in oligodendrocytes along the spinal cord. Treatment of zebrafish larvae Tg(mbp:nfsB-egfp) with metronidazole (Mtz) resulted in the selective ablation of oligodendrocytes and led to demyelination, accompanied by behavioral changes, including decreased total movement distance, velocity, total movement time and fast movement time. After withdrawal of Mtz for a seven day recovery period, the expression of EGFP and MBP protein was observed again which indicates remyelination. Additionally, locomotor capacity was restored. Collectively, Tg(mbp:nfsB-egfp), a heritable and stable transgenic line, provides a novel, powerful tool to study the mechanisms of demyelination and remyelination.

Zebrafish have transparent bodies so you can see through them and the larva have a yolk sac so you don't need to feed them.  You can add genes to them so their myelin glows under ultraviolet or laser light. You can use them to watch how myelination occurs. In this study they demyelinated them and showed loss of movement behaviours and then allowed them to remyelinate and the behaviours returned, As you can see the default pathway is repair and this occurred quickly. Can this system be used to find triggers that promote remyelination.

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