Becker SF et al. (2016) Curr Opin Genet Dev "Natural and induced direct reprogramming: mechanisms, concepts and general principles-from the worm to vertebrates."

Becker SF, Jarriault S

[Curr Opin Genet Dev, 2016]

Elucidating the mechanisms underlying cell fate determination, cell identity maintenance and cell reprogramming in vivo is one of the main challenges in today's science. Such knowledge of fundamental importance will further provide new leads for early diagnostics and targeted therapy approaches both in regenerative medicine and cancer research. This review focuses on recent mechanistic findings and factors that influence the differentiated state of cells in direct reprogramming events, aka transdifferentiation. In particular, we will look at the mechanistic and conceptual advances brought by the use of the nematode Caenorhabditis elegans and highlight common themes across phyla.

Sleigh JN et al. (2010) Translational Neuroscience "C. elegans models of neuromuscular diseases expedite translational research"

Sleigh JN, Sattelle DB

[Translational Neuroscience, 2010]

The nematode Caenorhabditis elegans is a genetic model organism and the only animal with a complete nervous system wiring diagram. With only 302 neurons and 95 striated muscle cells, a rich array of mutants with defective locomotion and the facility for individual targeted gene knockdown by RNA interference, it lends itself to the exploration of gene function at nerve muscle junctions. With approximately 60% of human disease genes having a C. elegans homologue, there is growing interest in the deployment of lowcost, high-throughput, drug screens of nematode transgenic and mutant strains mimicking aspects of the pathology of devastating human neuromuscular disorders. Here we explore the contributions already made by C. elegans to our understanding of muscular dystrophies (Duchenne and Becker), spinal muscular atrophy, amyotrophic lateral sclerosis, Friedreichs ataxia, inclusion body myositis and the prospects for contributions to other neuromuscular disorders. A bottleneck to low-cost, in vivo, large-scale chemical library screening for new candidate therapies has been rapid, automated, behavioural phenotyping. Recent progress in quantifying simple swimming (thrashing) movements is making such screening possible and is expediting the translation of drug candidates towards the clinic.