Directing Coupled Motion with Light:A Key Step Toward Machine-Like Function

Molecular photoactuators can control shape and chemical or physical properties of the responsive system they are embedded in. These effects are usually mediated by supramolecular interactions and can be amplified to perform work at the micro- and macroscopic scale, for instance, in materials and biomimetic systems. While many studies focus on the observable outcome of these events, photoresponsive structures can also translate their conformational change to molecular components and perform work against random Brownian motion. Stereochemical cascades can amplify light-generated motion to a distant moiety of the same molecule or molecular assembly, via conformationally restricted stereogenic elements. Being able to control the conformation or motion of molecular systems remotely provides prospects for the design of the smallest machines imaginable. This Focus Review emphasizes the emergence of directed, coupled motion of remote functionalities triggered by light-powered switches and motors as a tool to control molecular topology and function

β-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis

Mutations in the gene encoding β-III spectrin give rise to spinocerebellar ataxia type 5 (SCA5), a neurodegenerative disease characterized by progressive thinning of the molecular layer, loss of Purkinje cells and increasing motor deficits. A mouse lacking full-length β-III spectrin (β-III(−/−)) displays a similar phenotype. In vitro and in vivo analyses of Purkinje cells lacking β-III spectrin, reveal a critical role for β-III spectrin in Purkinje cell morphological development. Disruption of the normally well-ordered dendritic arborization occurs in Purkinje cells from β-III(−/−) mice, specifically showing a loss of monoplanar organization, smaller average dendritic diameter and reduced densities of Purkinje cell spines and synapses. Early morphological defects appear to affect distribution of dendritic, but not axonal, proteins. This study confirms that thinning of the molecular layer associated with disease pathogenesis is a consequence of Purkinje cell dendritic degeneration, as Purkinje cells from 8-month old β-III(−/−) mice have drastically reduced dendritic volumes, surface areas and total dendritic lengths compared to 5–6 week old β-III(−/−) mice. These findings highlight a critical role of β-III spectrin in dendritic biology and are consistent with an early developmental defect in β-III(−/−) mice, with abnormal Purkinje cell dendritic morphology potentially underlying disease pathogenesis