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Weninger, W. J.

Publications and source records attributed to Weninger, W. J..

2 recordsLinked to original sources

Imaging the microscopic viscoelastic anisotropy in living cells

Maintaining and modulating the mechanical anisotropy is essential for biological processes. How this is achieved on the microscopic scale in living soft matter is however not always clear. Here we introduce Brillouin Light Scattering Anisotropy Microscopy (BLAM) for mapping the high-frequency viscoelastic anisotropy inside living cells. Following proof-of-principle experiments on muscle myofibers, we apply this to study two fundamental biological processes. In plant cell walls we show how a phase-transition driven switch between anisotropic-isotropic wall properties may lead to asymmetric growth. In mammalian cell nuclei we uncover a spatio-temporally oscillating elastic anisotropy correlated to chromatin condensation, with long range orientational correlations that may provide a dynamic framework for coordinating intra-nuclear processes. Our results highlight the direct and indirect role the high-frequency mechanics can play in providing dynamic structure that lead to the regulation of diverse fundamental processes in biological systems, and offer a means for studying these. BLAM should find diverse biomedical and material characterization applications.

biophysics↗

The imprinted Mir483 is a growth suppressor and metabolic regulator functioning through IGF1

Mir483 is a conserved and highly expressed microRNA in placental mammals, embedded within the Igf2 gene. Here, we uncover the control mechanisms and physiological functions of Mir483 in vivo, by generating constitutive loss-of-function and over-expressing mice. Mir483 expression is imprinted and dependent on the Igf2 promoters and Igf2/H19 imprinting control region. Over-expression of Mir483 causes severe mid-gestation fetal, but not placental, growth restriction, and late lethality. Fetal death is prevented by restoring Mir483 to endogenous levels using an inducible transgenic system. Continuous postnatal Mir483 over-expression induces growth stunting, elevated hepatic lipid content, increased adiposity, reduced local and systemic IGF1 levels and increased GH. The growth phenotypes are rescued by IGF1 infusion. Our findings provide evidence for a novel functional antagonism between a growth-suppressor microRNA and its growth-promoter host gene, and suggest that Mir483 evolved to limit excessive tissue growth through repression of IGF ligand signalling.

developmental biology↗