Neural crest cell lineage restricts skeletal muscle progenitor cell differentiation through Neuregulin1-ErbB3 signaling

Coordinating the balance between progenitor self-renewal and myogenic differentiation is required for a regulated expansion of the developing muscles. Previous observation that neural crest cells (NCCs) migrate throughout the somite regions, where trunk skeletal muscles first emerge, suggests a potential role for these cells in influencing early muscle formation. However, specific signaling interactions between NCCs and skeletal muscle cells remain unknown. Here we show that mice with specific NCC and peripheral nervous system defects display impaired survival of skeletal muscle and show skeletal muscle progenitor cell (MPC) depletion due to precocious commitment to differentiation. We show that reduced NCC-derived Neuregulin1 (Nrg1) in the somite region perturbs ErbB3 signaling in uncommitted MPCs. Using a combination of explant culture experiments and genetic ablation in the mouse, we demonstrate that Nrg1 signals provided by the NCC lineage play a critical role in sustainable myogenesis, by restraining MPCs from precocious differentiation

Self-ordering of nanoparticles in magneto-organic composite films

Theis-Broehl K, Wolff M, Ennen I, Dewhurst CD, Hütten A, Toperverg BP. Self-ordering of nanoparticles in magneto-organic composite films. PHYSICAL REVIEW B. 2008;78(13): 134426.A combination of polarized neutron reflectometry and grazing incidence small-angle neutron scattering has been employed to deduce the structural and magnetic parameters of cobalt-oleyl amine nanocomplexes in thin films. It is demonstrated that inside the film the nanoparticles are self-organized into a three-dimensional paracrystallinelike lattice with the positional order well defined over a few interparticle spacings. Joint evaluation of the data elucidates the size of the saturated Co core and the CoO shell of the nanoparticles

dILA neurons in the dorsal spinal cord are the product of terminal and non-terminal asymmetric progenitor cell divisions, and require Mash1 for their development

dILA and dILB neurons comprise the major neuronal subtypes generated in the dorsal spinal cord, and arise in a salt-and-pepper pattern from a broad progenitor domain that expresses the bHLH factor Mash1. In this domain, Mash1-positive and Mash1-negative cells intermingle. Using a Mash1(GFP) allele in mice, we show here that Mash1+ progenitors give rise to dILA and dILB neurons. Using retroviral tracing in the chick, we demonstrate that a single progenitor can give rise to a dILA and a dILB neuron, and that dILA neurons are the product of asymmetric progenitor cell divisions. In Mash1-null mutant mice, the development of dILA, but not of dILB neurons is impaired. We provide evidence that a dual function of Mash1 in neuronal differentiation and specification accounts for the observed changes in the mutant mice. Our data allow us to assign to Mash1 a function in asymmetric cell divisions, and indicate that the factor coordinates cell cycle exit and specification in the one daughter that gives rise to a dILA neuron

A mutation of keratin 18 within the coil 1A consensus motif causes widespread keratin aggregation but cell type-restricted lethality in mice

Mutations in genes encoding epidermal keratins cause skin disorders, while those in internal epithelial keratins, such as K8 and K18, are risk factors for liver diseases. The effect of dominant mutations in K8 or K18 during embryonic development and tissue homeostasis has not been examined so far. Here we demonstrate that the dominant mutation hK18 R89C, that is highly similar to hK14 R125C, causing EBS in humans, leads to cell type-specific lethality in mice, depending on the ratio of mutant to endogenous keratins. Mice expressing hK18 R89C in the absence of endogenous K19 and K18 died at mid-gestation from defects in trophoblast giant cells, accompanied by haematomas. A single, endogenous K18 allele rescued embryonic lethality but caused aggregation of keratins in all adult internal epithelia, surprisingly without spontaneous cell fragility. Closer analysis revealed that both filaments and aggregates coexisted in the same cell, depending on the ratio of mutant to endogenous keratins. Our results demonstrate that balanced overexpression of a wild-type keratin rescued the lethal consequences of a dominant-negative mutation. This has important implications for therapy approaches of keratinopathies, suggesting that suppressing the mutant allele is not necessary in vivo

Colonization of the satellite cell niche by skeletal muscle progenitor cells depends on notch signals

Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite cells deregulate the expression of basal lamina components and adhesion molecules like integrin {alpha}7, collagen XVIII{alpha}1, Megf10, and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers

Polarized neutron reflectometry study on a magnetic film with an ion beam imprinted stripe pattern

Theis-Broehl K, Toperverg BP, Westphalen A, et al. Polarized neutron reflectometry study on a magnetic film with an ion beam imprinted stripe pattern. In: Superlattices and Microstructures. SUPERLATTICES AND MICROSTRUCTURES. Vol 41. ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD; 2007: 104-108.We used polarized neutron reflectometry for a quantitative study of the field dependent arrangement of the magnetization vector in the different regions of an ion beam imprinted stripe pattern in a magnetic film. For the magnetic patterning of the Co70Fe30 film we took advantage of the exchange bias to an antiferromagnetic Mn83Ir17 layer which was changed locally by He-ion bombardment. The exchange bias was set to be antiparallel in the two different striped regions. We found that after magnetization reversal of half of the stripes the magnetization in neighbouring regions is periodically canted with respect to the stripe axis so that the net magnetization of the ferromagnetic film tums almost perpendicular to the stripes. At the same time the projection of the magnetization vector onto the stripe axis has a periodically alternating sign. (c) 2007 Published by Elsevier Lt

Self-assembled iron oxide nanoparticle multilayer: x-ray and polarized neutron reflectivity

We have investigated the structure and magnetism of self-assembled, 20 nm diameter iron oxide nanoparticles covered by an oleic acid shell for scrutinizing their structural and magnetic correlations. The nanoparticles were spin-coated on an Si substrate as a single monolayer and as a stack of 5 ML forming a multilayer. X-ray scattering (reflectivity and grazing incidence small-angle scattering) confirms high in-plane hexagonal correlation and a good layering property of the nanoparticles. Using polarized neutron reflectivity we have also determined the long range magnetic correlations parallel and perpendicular to the layers in addition to the structural ones. In a field of 5 kOe we determine a magnetization value of about 80% of the saturation value. At remanence the global magnetization is close to zero. However, polarized neutron reflectivity reveals the existence of regions in which magnetic moments of nanoparticles are well aligned, while losing order over longer distances. These findings confirm that in the nanoparticle assembly the magnetic dipole-dipole interaction is rather strong, dominating the collective magnetic properties at room temperature. Accession Number: WOS:00029931600002