The identification of QTL controlling ergot sclerotia size in hexaploid wheat implicates a role for the Rht dwarfing alleles

The fungal pathogen Claviceps purpurea infects ovaries of a broad range of temperate grasses and cereals, including hexaploid wheat, causing a disease commonly known as ergot. Sclerotia produced in place of seed carry a cocktail of harmful alkaloid compounds that result in a range of symptoms in humans and animals, causing ergotism. Following a field assessment of C. purpurea infection in winter wheat, two varieties ‘Robigus’ and ‘Solstice’ were selected which consistently produced the largest differential effect on ergot sclerotia weights. They were crossed to produce a doubled haploid mapping population, and a marker map, consisting of 714 genetic loci and a total length of 2895 cM was produced. Four ergot reducing QTL were identified using both sclerotia weight and size as phenotypic parameters; QCp.niab.2A and QCp.niab.4B being detected in the wheat variety ‘Robigus’, and QCp.niab.6A and QCp.niab.4D in the variety ‘Solstice’. The ergot resistance QTL QCp.niab.4B and QCp.niab.4D peaks mapped to the same markers as the known reduced height (Rht) loci on chromosomes 4B and 4D, Rht-B1 and Rht-D1, respectively. In both cases, the reduction in sclerotia weight and size was associated with the semi-dwarfing alleles, Rht-B1b from ‘Robigus’ and Rht-D1b from ‘Solstice’. Two-dimensional, two-QTL scans identified significant additive interactions between QTL QCp.niab.4B and QCp.niab.4D, and between QCp.niab.2A and QCp.niab.4B when looking at sclerotia size, but not between QCp.niab.2A and QCp.niab.4D. The two plant height QTL, QPh.niab.4B and QPh.niab.4D, which mapped to the same locations as QCp.niab.4B and QCp.niab.4D, also displayed significant genetic interactions

Stochastic loss and gain of symmetric divisions in the C. elegans epidermis perturbs robustness of stem cell number

Biological systems are subject to inherent stochasticity. Nevertheless, development is remarkably robust, ensuring the consistency of key phenotypic traits such as correct cell numbers in a certain tissue. It is currently unclear which genes modulate phenotypic variability, what their relationship is to core components of developmental gene networks, and what is the developmental basis of variable phenotypes. Here, we start addressing these questions using the robust number of Caenorhabditis elegans epidermal stem cells, known as seam cells, as a readout. We employ genetics, cell lineage tracing, and single molecule imaging to show that mutations in lin-22, a Hes-related basic helix-loop-helix (bHLH) transcription factor, increase seam cell number variability. We show that the increase in phenotypic variability is due to stochastic conversion of normally symmetric cell divisions to asymmetric and vice versa during development, which affect the terminal seam cell number in opposing directions. We demonstrate that LIN-22 acts within the epidermal gene network to antagonise the Wnt signalling pathway. However, lin-22 mutants exhibit cell-to-cell variability in Wnt pathway activation, which correlates with and may drive phenotypic variability. Our study demonstrates the feasibility to study phenotypic trait variance in tractable model organisms using unbiased mutagenesis screens

Fabrication of a nanoscale Ti-Ta-Nb alloy coating and its effect on osteoblast precursor initial response

The aim of this study was to prepare a novel titanium-10tantalum-10niobium (Ti-Ta-Nb) alloy nanoscale coatings using sputter deposition and to evaluate their effect on osteoblast response. The three groups of Ti alloy used in this study were: (1) as-sputtered Ti-Ta-Nb coatings; (2) Ti-Ta-Nb disks; and (3) Ti6Al4V alloy disks as controls. The three surfaces were characterized using a x-ray diffractometer, a scanning electron microscope, a surface profilometer, and a contact angle measuring instrument. ATCC CRL 1486 human embryonic palatal mesenchymal cells were used to evaluate the cell responses. Cell attachment was measured using a coulter counter. After 4 days incubation, dsDNA, total protein, and alkaline phosphatase of the attached cells were assayed. The assputtered Ti-Ta-Nb coatings consisted of dense nanoscale grains. The Ti-Ta-Nb coatings exhibited significantly greater cell attachments compared to the two polished microgroove groups at 30minutes and Ihour. No significant differences were observed in dsDNA amount, total protein production and alkaline phosphatase specific activity among the three groups. These results demonstrated an equivalent performance for the Ti-Ta-Nb alloy and its nanoscale Ti-Ta-Nb coatings, suggesting an alternative biocompatible metal for use in dentistry and orthopedics. Copyright © 2006 by ASME

Enhancing osseointegration using surface-modified titanium implants

Osseointegrated dental implants are used to replace missing teeth. The success of implants is due to osseointegration or the direct contact of the implant surface and bone without a fibrous connective tissue interface. This review discusses the enhancement of osseointegration by means of anodized microporous titanium surfaces, functionally macroporous graded titanium coatings, nanoscale titanium surfaces, and different bioactive factors