A rapid and dynamic role for FMRP in the plasticity of adult neurons.

Fragile X syndrome (FXS) is a neuro-developmental disorder caused by silencing , which encodes the RNA-binding protein FMRP. Although is expressed in adult neurons, it has been challenging to separate acute from chronic effects of loss of in models of FXS. We have used the precision of genetics to test if acutely affects adult neuronal plasticity , focusing on the s-LNv circadian pacemaker neurons that show 24 hour rhythms in structural plasticity.

Overexpression of Lin28a delays Xenopus metamorphosis and down-regulates albumin independently of its translational regulation domain.

Background: Lin28 regulates stem cell biology and developmental timing. At the molecular level Lin28 inhibits the biogenesis of the micro RNA let-7 and directly controls the transcription and translation of several genes. In Xenopus, Lin28 overexpression delays metamorphosis and affects the expression of genes of the thyroid hormone (TH) axis.

The heterochronic gene Lin28 regulates amphibian metamorphosis through disturbance of thyroid hormone function.

Metamorphosis is a classic example of developmental transition, which involves important morphological and physiological changes that prepare the organism for the adult life. It has been very well established that amphibian metamorphosis is mainly controlled by Thyroid Hormone (TH). Here, we show that the heterochronic gene Lin28 is downregulated during Xenopus laevis metamorphosis.