Neurobiology of speech and language has previously been studied in the KE family, in which half of the members have severe impairment in both speech and language. The gene responsible for the phenotype was mapped to chromosome 7q31 and identified as the FOXP2 gene, coding for a transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain. Because of linkage studies implicating 7q31 in autism, where language impairment is a component of the disorder, and in specific language impairment, FOXP2 has also been considered as a potential susceptibility locus for the language deficits in autism and͞or specific language impairment. In this study, we characterized mice with a disruption in the murine
This article is an up-to-date review of the literature available on the subject of ethanol to ethylene. The process of ethanol to ethylene has broad development prospects. Compared with the process of petroleum to ethylene, ethanol dehydration to ethylene is economically feasible. Researchers have been redirecting their interest to the ethylene production process, catalysts, and reaction mechanisms. A fluidized bed reactor, together with a wear-resistant, efficient, and stable catalyst will be the focus of future research that includes a deep understanding of the large-scale activated alumina catalyst and the molecular sieve catalyst used, and will promote the development of the ethanol dehydration to ethylene process and provide strong support for the market competiveness of the process.
In plants, auxin functions as a master controller of development, pattern formation, morphogenesis, and tropic responses. A sophisticated transport system has evolved to allow the establishment of precise spatiotemporal auxin gradients that regulate specific developmental programs. A critical unresolved question relates to how these gradients can be maintained in the presence of open plasmodesmata that allow for symplasmic exchange of essential nutrients and signaling macromolecules. Here we addressed this conundrum using genetic, physiological, and cell biological approaches and identified the operation of an auxin-GSL8 feedback circuit that regulates the level of plasmodesmal-localized callose in order to locally downregulate symplasmic permeability during hypocotyl tropic response. This system likely involves a plasmodesmal switch that would prevent the dissipation of a forming gradient by auxin diffusion through the symplasm. This regulatory system may represent a mechanism by which auxin could also regulate symplasmic delivery of a wide range of signaling agents.
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