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The syntactic skills of Spanish-speaking children with Williams syndrome (WS) were assessed in different areas (phrase structure, recursion, and bound anaphora). Children were compared to typically-developing peers matched either in chronological age (CA-TD) or in verbal age (VA-TD). In all tasks children with WS performed significantly worse than CA-TD children, but similarly to VA-TD children. However, significant differences were observed in specific domains, particularly regarding sentences with cross-serial dependencies. At the same time, children with WS were less sensitive to syntactic constraints and exhibited a poorer knowledge of some functional words (specifically, of nonreflexive pronouns). A processing bottleneck or a computational constraint may account for this outcome. [ABSTRACT FROM AUTHOR]

Basic perceptual abilities are universal, and most people can distinguish between millions of distinct shades. However, languages differ in the set of basic color terms (BCTs) they have. Despite numerous prior studies, the exact number of BCTs in Mandarin (Sino‐Tibetan) and Spanish (Indo‐European) is still debated. In Mandarin, this number varies from 6 to 11, whereas in Spanish there are about 11 or 12 BCTs. Additionally, differences between these two languages can be expected with regard to the differing usage of BCTs in reference to color, as well as the naming strategies used for specifying references. To clarify this, we recruited a group of Mainland Mandarin speakers and a group of Castilian Spanish speakers and assessed them in two related tasks: the list task, in which participants were asked to write down as many color names as they could recall; and the color‐naming task, in which they were asked to name color chips from the Munsell color chart that were presented randomly. Our results suggest that Mandarin has nine BCTs, while Spanish has 12 BCTs. Furthermore, we found that Mandarin speakers use more modified terms and compounds to achieve precise color reference, whereas Spanish speakers rely more on monomorphemic non‐basic terms. Finally, we observed that Mandarin speakers use some colors (gray, blue, and purple) less consistently; although, the color space is partitioned similarly by these two languages. Our results reinforce the view that there are universal constraints on color naming that are compatible with subtle cross‐cultural differences in how colors are used. [ABSTRACT FROM AUTHOR]

The sequencing of the genomes from extinct hominins has revealed that changes in some brain-related genes have been selected after the split between anatomically-modern humans and Neanderthals/Denisovans. To date, no coherent view of these changes has been provided. Following a line of research we initiated in Boeckx and Benítez-Burraco (2014a), we hypothesize functional links among most of these genes and their products, based on the existing literature for each of the gene discussed. The genes we focus on are found mutated in different cognitive disorders affecting modern populations and their products are involved in skull and brain morphology, and neural connectivity. If our hypothesis turns out to be on the right track, it means that the changes affecting most of these proteins resulted in a more globular brain and ultimately brought about modern cognition, with its characteristic generativity and capacity to form and exploit cross-modular concepts, properties most clearly manifested in language. [ABSTRACT FROM AUTHOR]

The article discusses research being done on children with autism spectrum disorders (ASD). It references the study "Oral Motor Deficits in Speech-Impaired Children With Autism," by M. K. Belmonte et al. published in the 2013 issue of "Frontiers in Integrative Neuroscience." The role of expressive language deficits in autistic individuals, and the functions of RUNX2 gene, ROBO1 and FOXP2 interactomes and AUTS2 gene in language acquisition are also discussed.

This study builds on the hypothesis put forth in Boeckx and Benítez-Burraco (2014), according to which the developmental changes expressed at the levels of brain morphology and neural connectivity that resulted in a more globular braincase in our specieswere crucial to understand the origins of our language-ready brain. Specifically, this paper explores the links between twowell-known 'language-related' genes like FOXP2 and ROBO1 implicated in vocal learning and the initial set of genes of interest put forth in Boeckx and Benítez- Burraco (2014), with RUNX2 as focal point. Relying on the existing literature, we uncover potential molecular links that could be of interest to future experimental inquiries into the biological foundations of language and the testing of our initial hypothesis. Our discussion could also be relevant for clinical linguistics and for the interpretation of results from paleogenomics. [ABSTRACT FROM AUTHOR]

It has been suggested that language disorders can serve as real windows onto language evolution. We examine this claim in this paper. We see ourselves forced to qualify three central assumptions of the the 'disorders-as-windows' hypothesis. After discussing the main outcome of decades of research on the linguistic ontogeny of pathological populations, we argue that language disorders should be construed as conditions for which canalization has failed to cope fully with developmental perturbations. We conclude that a robust link exists between developmental disturbances and evolutionary history that allows language disorders to be used as real windows onto the evolution of the neuronal substrate of language, and emphasize that our conclusion is more compatible with views of language evolution as the result of reorganizational changes as opposed to radically novel emergences. [ABSTRACT FROM AUTHOR]

Recent advances in genetics and neurobiology have greatly increased the degree of variation that one finds in what is taken to provide the biological foundations of our species-specific linguistic capacities. In particular, this variation seems to cast doubt on the purportedly homogeneous nature of the language faculty traditionally captured by the concept of 'Universal Grammar.' In this article we discuss what this new source of diversity reveals about the biological reality underlying Universal Grammar. Our discussion leads us to support (1) certain hypotheses advanced in evolutionary developmental biology that argue for the existence of robust biological mechanisms capable of canalizing variation at different levels, and (2) a bottom-up perspective on comparative cognition. We conclude by sketching future directions for what we call 'comparative biolinguistics,' specifying which experimental directions may help us succeed in this new research avenue. [ABSTRACT FROM AUTHOR]

Copyright of Moenia: Revista Lucense de Lingüística & Literatura is the property of Universidad de Santiago de Compostela, Servicio de Publicaciones and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Any comprehensive neurobiological depiction of the language faculty (but also the elucidation of the etiology of different inherited language impairments) demands, among other things, the identification (and the structural and functional characterization) of genes which can be properly regarded as involved in the regulation of the development of the neuronal substrate of the "language organ". Such genes can also be plausibly considered as casual (or risk) factors for the appearance of such impairments. Different molecular techniques have been developed for cloning and molecular characterising the so-called "language genes". In spite of their noteworthy analytic yield, the real significance of their output can only be truly apprehended when methodological caveats and shortcomings are also considered. One of the most significant concerns the way in which the phenotype (which is a starting point for these cloning techniques) is defined, categorised, and delimited. [ABSTRACT FROM AUTHOR]

Copyright of Verba: Anuario Galego de Filoloxia is the property of Universidad de Santiago de Compostela, Servicio de Publicaciones and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

An increasing corpus of clinical, neuroanatomical, neurophysiological, and genetic evidences seems to put into question the idiosyncratic nature of the so-called specific language impairments. Methodological caveats could be in part responsible for some of the problems that arise when trying to precisely characterize and distinctively define this kind of cognitive disorders. However, those evidences also seem to demand a thorough re-examination of the conventional description pf how the "language organ" is structured, and how it develops and works. A main conclusion here will be that the "language organ" emerges during ontogeny as a result of an innate programme (genetically encoded to some extent), which, nevertheless, is always conditioned by the molecular and the ontogenetic background of the organism, and also by the environment in which the subject lives. Inside this "organ" different neuronal structures jointly work in order to properly process linguistic stimuli, though each of these components are simultaneously able to compute different types of inputs. [ABSTRACT FROM AUTHOR]

Two Neanderthals from El Sidrón (Asturias, Spain) have been recently analyzed for possible mutations in FOXP2, a gene involved in the faculty of language. Although this gene was believed to be specific to modern humans, the analysis in question revealed otherwise. The present article reflects on the meaning of this finding, and raises some concerns about the interpretation suggested in Krause et al. (2007). [ABSTRACT FROM AUTHOR]

Two genomic clones corresponding to putative pectate lyase genes (plA and plB) were isolated and characterized in strawberry (Fragaria×ananassa cv. Chandler). The corresponding ORFs for the plA and plB genes revealed deduced proteins of 451 and 439 amino acids, respectively, that differ from that of the previously isolated strawberry plC gene. Southern blot analysis has shown that while the plB gene is a single copy gene, the plA gene is probably encoded by a small multigene family. By using specific probes corresponding to the untranslated 3′ terminal region of the pl genes, and QRT‐PCR methodology, the spatio‐temporal expression pattern of both strawberry pl genes have been compared with that of the plC gene. The three transcripts were specifically expressed only in fruit and mainly during the ripening stages. Moreover, the expression of the plA and plB genes was induced in green de‐achened fruit, but this increase was reduced by the external application of auxins as was the expression of plC. The expression of both pl genes was also strongly reduced in harvested fruit kept in controlled atmosphere (CA) containing high CO2 levels. Immunolocalization studies using antibodies raised against the strawberry PL proteins placed the proteins in the cell wall of parenchymatic cells of the fruit receptacle. The role of pl genes in cell‐wall disassembly and fruit ripening softening is discussed. [ABSTRACT FROM PUBLISHER]

Purpose: Chromosome 16p11.2 deletion syndrome (OMIM #611913) is a rare genetic condition resulting from the partial deletion of approximately 35 genes located at Chromosome 16. Affected people exhibit a variable clinical profile, featuring mild dysmorphisms, motor problems, developmental delay, mild intellectual disability (ID), socialization deficits and/or autism spectrum disorder (ASD) traits, and problems with language. Specifically, a precise characterization of the speech, language, and communication (dis)abilities of people with this condition is still pending. Method: We used standardized tests and samples of naturalistic speech to provide a longitudinal profile of the speech, language, and communication problems of a boy with Chromosome 16p11.2 deletion syndrome and without ID or ASD. Results: The proband shows impaired expressive abilities as well as problems with receptive language, dysprosody, and ASD-like communication deficits, such as impaired interactive skills, perseverative verbal behavior, overabundance of tangential responses, and lack of metapragmatic awareness and communicative use of gaze, meeting the criteria for social pragmatic communication disorder. Conclusions: Our results support the view that language and communication impairment should be regarded as one core symptom of Chromosome 16p11.2 deletion syndrome, even without a diagnosis of ASD or ID. Clinical implications of our results, with a focus on therapeutic interventions for children with 16p11.2 deletion syndrome and no ASD or ID, are also discussed. [ABSTRACT FROM AUTHOR]

The authors comment on the article "FOXP2 drives neuronal differentiation by interacting with retinoic acid signaling pathways" by P. Devanna and colleagues. The authors state that FOXP2 gene emulates and potentiates the retinoic acid (RA) in the induction of genes during the differentiation of neurons. Moreover, they stated the significance of RA signalling in brain differentiation and growth.

Williams syndrome is a complex condition resulting from the heterozygous deletion of nearly 30 genes in chromosome 7. However, precise genotype-to-phenotype mappings are not available for most of its distinctive features. Because WS entails changes in the expression patterns of multiple genes outside the WS region, it can be expected that many other genes besides the deleted genes contribute to this condition. In this paper, we hypothesise that genes that have changed recently in our history could account for some key aspects of the WS phenotype, because of the robust link that exists between human evolution and complex, human-specific diseases. Supporting this view, we have found that protein-coding genes that are dysregulated in the blood of subjects with WS are significantly enriched in protein-coding genes that have been positively selected in our species compared to extinct hominins. These genes play biological roles and are expressed in body regions of relevance for the WS phenotype. We conclude that the genes we highlight in the paper should be regarded as important etiological factors of the WS clinical profile. [ABSTRACT FROM AUTHOR]

Background: Mutations in the coding region of FOXP2 are known to cause speech and language impairment. However, it is not clear how dysregulation of the gene contributes to language deficit. Interestingly, microdeletions of the region downstream the gene have been associated with cognitive deficits. Methods: Here, we investigate changes in FOXP2 expression in the SK-N-MC neuroblastoma human cell line after deletion by CRISPR-Cas9 of two enhancers located downstream of the gene. Results: Deletion of any of these two functional enhancers downregulates FOXP2, but also upregulates the closest 3′ gene MDFIC. Because this effect is not statistically significant in a HEK 293 cell line, derived from the human kidney, both enhancers might confer a tissue specific regulation to both genes. We have also found that the deletion of any of these enhancers downregulates six well-known FOXP2 target genes in the SK-N-MC cell line. Conclusions: We expect these findings contribute to a deeper understanding of how FOXP2 and MDFIC are regulated to pace neuronal development supporting cognition, speech and language. [ABSTRACT FROM AUTHOR]

The unique divergence of the BRCA2 gene in Neanderthals compared to modern humans has been hypothesized to account for a differential susceptibility to cancer. However, the role of the gene in brain development and its connection with autism suggest that these differences might be (also) related to the more encapsulated nature of the Neanderthal cognition and their (inferred) autistic-like features. [ABSTRACT FROM AUTHOR]