imprint:
Proceedings of the National Academy of Sciences, 2016
Published in:Proceedings of the National Academy of Sciences
Language:
English
DOI:
10.1073/pnas.1516697113
ISSN:
0027-8424;
1091-6490
Origination:
Footnote:
Description:
<jats:title>Significance</jats:title>
<jats:p>
Neuronal morphology is tightly linked to the actin cytoskeleton, which provides stability for synapses while retaining the potential for changes during learning and memory processes (synaptic plasticity). Despite biochemical similarity, isoforms of the small actin-binding protein profilin perform astonishingly diverse tasks in neurons, influencing actin dynamics in an opposing manner. Although the ubiquitous isoform profilin1 supports synaptogenesis, the evolutionary more recent and brain-specific isoform profilin2a mediates synapse function and plasticity. Moreover, we show that in
<jats:italic>mammalia</jats:italic>
, only profilin1 is bound by Fragile X mental retardation protein, and therefore is most likely crucial in the cause of and in the devastating outcome of Fragile X syndrome, one of the most common forms of inherited cognitive impairment.
</jats:p>