Yes / The morphology transition from micelles to vesicles of a solution-state self-assembled block copolymer, containing a fluorescent dye at the core–shell interface, has been induced by an addition–elimination reaction using a thiol, and has been shown to be coupled to a simultaneous ON-to-OFF switch in particle fluorescence. / EPSRC and the IAS at the University of Warwick

Chiral nematic liquid crystals or cholesteric liquid crystals (CLC) can be obtained by adding a chiral dopant into a nematic liquid crystal. Liquid crystal molecules spontaneously rotate along a long axis to form helical structures in CLC system. Both pitch size and orientation of the helical structure is determined by the boundary conditions and can be further tuned by external stimuli. Particularly, the uniform lying helical structure of CLC has attracted intensive attention due to its beam steering and diffraction abilities. Up to now, studies have worked on controlling the in-plane orientation of lying helix through surface rubbing and external stimuli. However, it remains challenging to achieve steady and uniform lying helical structure due to its higher energy, comparing with other helical configurations. Here, by varying the surface anchoring, uniform lying helical structure with long-range order is achieved as thermodynamically stable state without external support. Poly (6-(4-methoxy-azobenzene-4'-oxy) hexyl methacrylate) (PMMAZO), a liquid crystalline polymer, is deposited onto the silicon substrate to fine-tune the surface anchoring. By changing the grafting density of PMMAZO, both pitch size and orientation of lying helical structure are precisely controlled. As the grafting density increases, the enhanced titled deformation of helical structure suppresses the pitch size of CLC at the same cell thickness; as the cell thickness increases, the morphology transition from long-range order stripe to small fingerprint domain is facilitated.

Mitochondria are usually considered simply as the “powerhouses of the cell”, however in recent years it has become apparent that mitochondria are also of fundamental importance in programmed cell death (PCD), which refers to cell death resulting from a controlled, genetically defined pathway. In Arabidopsis, PCD induced by either heat shock or treatment with strong oxidants is found to be correlated with an early and irreversible change in mitochondrial morphology which manifests as an increase in the size of individual mitochondria. In addition, PCD causes a clustering of mitochondria and loss of motility. In this study, I have used two arginase negative mutant Arabidopsis lines (argah1-1 and argah2-1) which have elevated cellular NO concentrations to examine the effect of nitrosative stress on mitochondria undergoing PCD. Another three different Arabidopsis lines (mito-GFP/mTalin-mCherry, mito-GFP/MAP4-mCherry, mito- mCherry/EB1b-GFP) were used to visualize cytoskeletal elements alongside mitochondria to examine the mechanisms responsible for the mitochondrial morphology transition, clustering and motility inhibition. Results indicate that the elevated concentration of NO found in arginase negative mutants is not sufficient to induce PCD. There was no significant mitochondrial morphology or dynamic change detected between arginase negative mutants and wild type plants, with or without a heat shock. Disruption of either actin or microtubule (MT) cytoskeletal elements leads to the formation of mitochondrial clusters, although they showed different cluster morphology and sizes. Mitochondrial clusters were observed to be moving along the remaining actin cables after a mild heat treatment or cytoskeletal depolymerizing drug treatment. Intact microtubules or MT plus ends visualized with EB1b did not show any interaction with mitochondria under normal conditions. However, after a mild heat stress, EB1b appeared to be associated with clusters of enlarged, possibly swollen mitochondria.