An important challenge for neuroscientists is to find cures for diseases that affect the central nervous system, such as autism, Alzheimer’s, or Parkinson’s disease. For this purpose, researchers use several vertebrate species as model organisms. The zebrafish has recently received much attention because it has many advantages over other vertebrate models. For example, development of its nervous system can be followed from its earliest stages in naturally behaving individuals.
Thomas Pietri and colleagues from six institutes in France, Spain, and the USA developed a strain of zebrafish with a nonfunctional mecp2 gene (“methyl CpG binding protein 2″, which controls many other genes). In humans, defects in mecp2 cause Rett syndrome, a disease within the family of autism spectrum disorders. Patients with Rett syndrome (mostly girls and women, since mecp2 lies on the X chromosome) often show mental retardation, stereotyped hand movements, seizures, and an increased response to sensory stimuli.
Surprisingly, zebrafish without mecp2 survive and reproduce normally, unlike mice with defective mecp2. But Pietri and colleagues found that the mutation modifies the behavior of zebrafish: mutant embryos respond more to tactile stimulation, while mutant larvae swim less and appear to have a reduced preference for the walls of their tank. Understanding why zebrafish without mecp2 develop only mild symptoms could lead to new directions in the search for treatments of Rett sydrome in humans.
The first mecp2-null zebrafish model shows altered motor behaviors, Thomas Pietri, Angel-Carlos Roman, Nicolas Guyon, Sebastián A. Romano, Philip Washbourne, Cecilia B. Moens, Gonzalo G. de Polavieja and Germán Sumbre
News From ‘Frontiers’: July 16, 2013