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Stochastic mesoscale inhomogeneity of material properties and material symmetries are investigated in a 3D-printed material. The analysis involves a spatially-dependent characterization of the microstructure in 316 L stainless steel, obtained through electron backscatter diffraction imaging. These data are subsequently fed into a Voigt–Reuss–Hill homogenization approxima- tion to produce maps of elasticity tensor coefficients along the path of experimental probing. Information-theoretic stochastic models corresponding to this stiffness random field are then introduced. The case of orthotropic fields is first defined as a high-fidelity model, the realizations of which are consistent with the elasticity maps. To investigate the role of material symmetries, an isotropic approximation is next introduced through ad-hoc projections (using various metrics). Both stochastic representations are identified using the dataset. In particular, the correlation length along the characterization path is identified using a maximum likelihood estimator. Uncertainty propagation is finally performed on a complex geometry, using a Monte Carlo analysis. It is shown that mechanical predictions in the linear elastic regime are mostly sensitive to material symmetry but weakly depend on the spatial correlation length in the considered propagation scenario. 

To complete mitosis, the bridge that links the two daughter cells needs to be cleaved. This step is carried out by the endosomal sorting complex required for transport (ESCRT) machinery. AKTIP, a protein discovered to be associated with telomeres and the nuclear membrane in interphase cells, shares sequence similarities with the ESCRT I component TSG101. Here we present evidence that during mitosis AKTIP is part of the ESCRT machinery at the midbody. AKTIP interacts with the ESCRT I subunit VPS28 and forms a circular supra-structure at the midbody, in close proximity with TSG101 and VPS28 and adjacent to the members of the ESCRT III module CHMP2A, CHMP4B and IST1. Mechanistically, the recruitment of AKTIP is dependent on MKLP1 and independent of CEP55. AKTIP and TSG101 are needed together for the recruitment of the ESCRT III subunit CHMP4B and in parallel for the recruitment of IST1. Alone, the reduction of AKTIP impinges on IST1 and causes multinucleation. Our data altogether reveal that AKTIP is a component of the ESCRT I module and functions in the recruitment of ESCRT III components required for abscission.