The Genetics of Language: From complex genes to complex communication

This chapter discusses the genetic foundations of the human capacity for language. It reviews the molecular structure of the genome and the complex molecular mechanisms that allow genetic information to influence multiple levels of biology. It goes on to describe the active regulation of genes and their formation of complex genetic pathways that in turn control the cellular environment and function. At each of these levels, examples of genes and genetic variants that may influence the human capacity for language are given. Finally, it discusses the value of using animal models to understand the genetic underpinnings of speech and language. From this chapter will emerge the complexity of the genome in action and the multidisciplinary efforts that are currently made to bridge the gap between genetics and language

A chromosomal rearrangement in a child with severe speech and language disorder separates FOXP2 from a functional enhancer

Mutations of FOXP2 in 7q31 cause a rare disorder involving speech apraxia, accompanied by expressive and receptive language impairments. A recent report described a child with speech and language deficits, and a genomic rearrangement affecting chromosomes 7 and 11. One breakpoint mapped to 7q31 and, although outside its coding region, was hypothesised to disrupt FOXP2 expression. We identified an element 2 kb downstream of this breakpoint with epigenetic characteristics of an enhancer. We show that this element drives reporter gene expression in human cell-lines. Thus, displacement of this element by translocation may disturb gene expression, contributing to the observed language phenotype

Ab-initio calculation of Kerr spectra for semi-infinite systems including multiple reflections and optical interferences

Based on Luttinger's formulation the complex optical conductivity tensor is calculated within the framework of the spin-polarized relativistic screened Korringa-Kohn-Rostoker method for layered systems by means of a contour integration technique. For polar geometry and normal incidence ab-initio Kerr spectra of multilayer systems are then obtained by including via a 2x2 matrix technique all multiple reflections between layers and optical interferences in the layers. Applications to Co|Pt5 and Pt3|Co|Pt5 on the top of a semi-infinite fcc-Pt(111) bulk substrate show good qualitative agreement with the experimental spectra, but differ from those obtained by applying the commonly used two-media approach.Comment: 32 pages (LaTeX), 5 figures (Encapsulated PostScript), submitted to Phys. Rev.

Non-collinear magnetic structures: a possible cause for current induced switching

Current induced switching in Co/Cu/Co trilayers is described in terms of ab-initio determined magnetic twisting energies and corresponding sheet resistances. In viewing the twisting energy as an energy flux the characteristic time thereof is evaluated by means of the Landau-Lifshitz-Gilbert equation using ab-initio parameters. The obtained switching times are in very good agreement with available experimental data. In terms of the calculated currents, scalar quantities since a classical Ohm's law is applied, critical currents needed to switch magnetic configurations from parallel to antiparallel and vice versa can unambiguously be defined. It is found that the magnetoresistance viewed as a function of the current is essentially determined by the twisting energy as a function of the relative angle between the orientations of the magnetization in the magnetic slabs, which in turn can also explain in particular cases the fact that after having switched off the current the system remains in the switched magnetic configuration. For all ab-initio type calculations the fully relativistic Screened Korringa-Kohn-Rostoker method and the corresponding Kubo-Greenwood equation in the context of density functional theory are applied.Comment: 20 pages, 4 tables and 15 figures, submitted to PR

Modeling mycorrhizal fungi dispersal by the mycophagous swamp wallaby (Wallabia bicolor)

Despite the importance of mammal-fungal interactions, tools to estimate the mammal-assisted dispersal distances of fungi are lacking. Many mammals actively consume fungal fruiting bodies, the spores of which remain viable after passage through their digestive tract. Many of these fungi form symbiotic relationships with trees and provide an array of other key ecosystem functions. We present a flexible, general model to predict the distance a mycophagous mammal would disperse fungal spores. We modelled the probability of spore dispersal by combining animal movement data from GPS-telemetry with data on spore gut-retention time. We test this model using an exemplar generalist mycophagist, the swamp wallaby (Wallabia bicolor). We show that swamp wallabies disperse fungal spores hundreds of metres—and occasionally up to 1265 m—from the point of consumption, distances that are ecologically significant for many mycorrhizal fungi. In addition to highlighting the ecological importance of swamp wallabies as dispersers of mycorrhizal fungi in eastern Australia, our simple modelling approach provides a novel and effective way of empirically describing spore dispersal by a mycophagous animal. This approach is applicable to the study of other animal-fungi interactions in other ecosystems.Funding provided by: Hermon Slade FoundationCrossref Funder Registry ID: http://dx.doi.org/10.13039/501100001109Award Number: HSF08-6Funding provided by: Australian Research CouncilCrossref Funder Registry ID: http://dx.doi.org/10.13039/501100000923Award Number: DP0557022Methods are described in the published article

The efficacy of epidermal growth factor receptor-specific antibodies against glioma xenografts is influenced by receptor levels, activation status, and heterodimerization

Purpose: Factors affecting the efficacy of therapeutic monoclonal antibodies (mAb) directed to the epidermal growth factor receptor (EGFR) remain relatively unknown, especially in glioma. Experimental Design: We examined the efficacy of two EGFR-specific mAbs (mAbs 806 and 528) against U87MG-derived glioma xenografts expressing EGFR variants. Using this approach allowed us to change the form of the EGFR while keeping the genetic background constant. These variants included the de2-7 EGFR (or EGFRvIII), a constitutively active mutation of the EGFR expressed in glioma. Results: The efficacy of the mAbs correlated with EGFR number; however, the most important factor was receptor activation. Whereas U87MG xenografts expressing the de2-7 EGFR responded to therapy, those exhibiting a dead kinase de2-7 EGFR were refractory. A modified de2-7 EGFR that was kinase active but autophosphorylation deficient also responded, suggesting that these mAbs function in de2-7 EGFR–expressing xenografts by blocking transphosphorylation. Because de2-7 EGFR–expressing U87MG xenografts coexpress the wild-type EGFR, efficacy of the mAbs was also tested against NR6 xenografts that expressed the de2-7 EGFR in isolation. Whereas mAb 806 displayed antitumor activity against NR6 xenografts, mAb 528 therapy was ineffective, suggesting that mAb 528 mediates its antitumor activity by disrupting interactions between the de2-7 and wild-type EGFR. Finally, genetic disruption of Src in U87MG xenografts expressing the de2-7 EGFR dramatically enhanced mAb 806 efficacy. Conclusions: The effective use of EGFR-specific antibodies in glioma will depend on identifying tumors with activated EGFR. The combination of EGFR and Src inhibitors may be an effective strategy for the treatment of glioma