One of the major attributes of autosegmental phonology is the possibility of reducing procedural techniques of morphological exponence to a generalised concept of concatenation. This research programme, which equates the triggers of non-concatenative processes with affixes consisting of incomplete autosegmental or prosodic representations, is called Generalised Non-linear Affixation in Bermú dez-Otero (2012). In this paper, we argue that the Generalised Non-linear Affixation analysis of segmental lengthening by mora affixation extends naturally to subtractive morphology. Defective (phonetically uninterpretable) integration of an affix mora into the prosodic structure of its base triggers deletion and shortening. We show that this approach derives all major types of quantitymanipulating morphology (vowel shortening, segmental subtraction and vowellength polarity), and thus demonstrate that Generalised Non-linear Affixation extends fully to subtractive morphology, which has been seen as the ultimate problem for a concatenative reanalysis (Anderson 1992).
Hydrated Arabidopsis thaliana seeds are coated by a gelatinous layer called mucilage, which is mainly composed of cell wall polysaccharides. Since mucilage is rich in pectin, its architecture can be visualized with the ruthenium red (RR) dye. We screened the seeds of around 280 Arabidopsis natural accessions for variation in mucilage structure, and identified a large number of novel variants that differed from the Col-0 wild-type. Most of the accessions released smaller RR-stained capsules compared to the Col-0 reference. By biochemically characterizing the phenotypes of 25 of these accessions in greater detail, we discovered that distinct changes in polysaccharide structure resulted in gelatinous coatings with a deceptively similar appearance. Monosaccharide composition analysis of total mucilage extracts revealed a remarkable variation (from 50 to 200% of Col-0 levels) in the content of galactose and mannose, which are important subunits of heteromannan. In addition, most of the natural variants had altered Pontamine Fast Scarlet 4B staining of cellulose and significantly reduced birefringence of crystalline structures. This indicates that the production or organization of cellulose may be affected by the presence of different amounts of hemicellulose. Although, the accessions described in this study were primarily collected from Western Europe, they form five different phenotypic classes based on the combined results of our experiments. This suggests that polymorphisms at multiple loci are likely responsible for the observed mucilage structure. The transcription of MUCILAGE-RELATED10 (MUCI10), which encodes a key enzyme for galactoglucomannan synthesis, was severely reduced in multiple variants that phenocopied the muci10-1 insertion mutant. Although, we could not pinpoint any causal polymorphisms in this gene, constitutive expression of fluorescently-tagged MUCI10 proteins complemented the mucilage defects of a muci10-like accession. This leads us to hypothesize that some accessions might disrupt a transcriptional regulator of MUCI10. Therefore, this collection of publicly-available variants should provide insight into plant cell wall organization and facilitate the discovery of genes that regulate polysaccharide biosynthesis.
This book investigates the phenomenon of Morphological Length-Manipulation: processes of segment lengthening, shortening, deletion, and insertion that cannot be explained by phonological means but crucially rely on morpho-syntactic information. A unified theoretical account of these phenomena is presented and it is argued that Morphological Length-Manipulation is best analysed inside the framework termed ‘Prosodically Defective Morphemes’: if all possible Prosodically Defective Morpheme representations and their potential effects for the resulting surface structure are taken into account, instances of length-manipulating non-concatenative morphology and length-manipulating morpheme-specific phonology are predicted. The argumentation in this book is hence in line with the general claim that all morphology results from combination and that non-concatenative exponents are epiphenomenal and arise from affixation of autosegmental elements. Although this position has been defended various times for specific phenomena, it has rarely been discussed against the background of a broad typological survey. In contrast to most existing claims, the argumentation in this book is based on a representative data set for attested morphological length-manipulating patterns in the languages of the world that serves as basis for the theoretical arguments. It is argued that alternative accounts suffer from severe under- and overgeneration problems if they are tested against the full range of attested phenomena.
ObjectivesDMBT is an antibacterial pattern recognition and scavenger receptor. In this study, we analyzed the role of DMBT1 single nucleotide polymorphisms (SNPs) regarding inflammatory bowel disease (IBD) susceptibility and examined their functional impact on transcription factor binding and downstream gene expression.MethodsSeven SNPs in the DMBT1 gene region were analyzed in 2073 individuals including 818 Crohn’s disease (CD) patients and 972 healthy controls in two independent case-control panels. Comprehensive epistasis analyses for the known CD susceptibility genes NOD2, IL23R and IL27 were performed. The influence of IL23R variants on DMBT1 expression was analyzed. Functional analysis included siRNA transfection, quantitative PCR, western blot, electrophoretic mobility shift and luciferase assays.ResultsIL-22 induces DMBT1 protein expression in intestinal epithelial cells dependent on STAT3, ATF-2 and CREB1. IL-22 expression-modulating, CD risk-associated IL23R variants influence DMBT1 expression in CD patients and DMBT1 levels are increased in the inflamed intestinal mucosa of CD patients. Several DMBT1 SNPs were associated with CD susceptibility. SNP rs2981804 was most strongly associated with CD in the combined panel (p = 3.0×10−7, OR 1.42; 95% CI 1.24–1.63). All haplotype groups tested showed highly significant associations with CD (including omnibus P-values as low as 6.1×10−18). The most strongly CD risk-associated, non-coding DMBT1 SNP rs2981804 modifies the DNA binding sites for the transcription factors CREB1 and ATF-2 and the respective genomic region comprising rs2981804 is able to act as a transcriptional regulator in vitro. Intestinal DMBT1 expression is decreased in CD patients carrying the rs2981804 CD risk allele.ConclusionWe identified novel associations of DMBT1 variants with CD susceptibility and discovered a novel functional role of rs2981804 in regulating DMBT1 expression. Our data suggest an important role of DMBT1 in CD pathogenesis.
Ghost segments are best analysed as weakly active elements under the assumption of Gradient Symbolic Representations (Smolensky & Goldrick, 2016; Rosen, 2016). This assumption allows to predict the attested interactions between phonological markedness constraints and the (non)appearance of ghost segments we find in the languages of the world: first, the co-existence of different types of ghost segments that differ in whether they appear to resolve a markedness problem or whether they disappear to avoid a markedness problem, and, second, the weak contribution to markedness of ghosts. The assumption that all underlying phonological elements have a certain activation that can gradiently differ and might persist into the output structure predicts these two phenomena straightforwardly that are challenging under alternative accounts to ghost segments
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