Background and AimsUnderstanding the genetic basis underlying domestication-related traits (DRTs) is important in order to use wild germplasm efficiently for improving yield, stress tolerance and quality of crops. This study was conducted to characterize the genetic basis of DRTs in soybean (Glycine max) using quantitative trait locus (QTL) mapping.MethodsA population of 96 recombinant inbred lines derived from a cultivated (ssp. max) × wild (ssp. soja) cross was used for mapping and QTL analysis. Nine DRTs were examined in 2004 and 2005. A linkage map was constructed with 282 markers by the Kosambi function, and the QTL was detected by composite interval mapping.Key ResultsThe early flowering and determinate habit derived from the max parent were each controlled by one major QTL, corresponding to the major genes for maturity (e1) and determinate habit (dt1), respectively. There were only one or two significant QTLs for twinning habit, pod dehiscence, seed weight and hard seededness, which each accounted for approx. 20–50 % of the total variance. A comparison with the QTLs detected previously indicated that in pod dehiscence and hard seededness, at least one major QTL was common across different crosses, whereas no such consistent QTL existed for seed weight.ConclusionsMost of the DRTs in soybeans were conditioned by one or two major QTLs and a number of genotype-dependent minor QTLs. The common major QTLs identified in pod dehiscence and hard seededness may have been key loci in the domestication of soybean. The evolutionary changes toward larger seed may have occurred through the accumulation of minor changes at many QTLs. Since the major QTLs for DRTs were scattered across only six of the 20 linkage groups, and since the QTLs were not clustered, introgression of useful genes from wild to cultivated soybeans can be carried out without large obstacles.
BackgroundEpidemiological studies have revealed a link between dental infection and preterm birth or low birth weight (PTB/LBW), however, the underlying mechanisms remain unclear. Progress in understanding the associated mechanisms has been limited in part by lack of an animal model for chronic infection-induced PTB/LBW, mimicking pregnancy under conditions of periodontitis. We aimed to establish a mouse model of chronic periodontitis in order to investigate the link between periodontitis and PTB/LBW.MethodsTo establish chronic inflammation beginning with dental infection, we surgically opened mouse (female, 8 weeks old) 1st molar pulp chambers and directly infected with w83 strain Porphyromonas gingivalis (P.g.), a keystone periodontal pathogen. Mating was initiated at 6 wks post-infection, by which time dental granuloma tissue had developed and live P.g. was cultured from extracted tooth root, which serves as a persistent source of P.g. The gestational day (gd) and birth weight were recorded during for P.g.-infected and control mice, and serum and placental tissues were collected at gd 15 to evaluate the systemic and local conditions during pregnancy.ResultsDental infection with P.g. significantly increased circulating TNF-α (2.5-fold), IL-17 (2-fold), IL-6 (2-fold) and IL-1β (2-fold). The P.g.-infected group delivered at gd 18.25 vs. gd 20.45 in the non-infected control (NC) group (p < 0.01), and pups exhibited LBW compared to controls (p < 0.01). P.g. was localized to placental tissues by immunohistochemistry and PCR, and defects in placental tissues of P.g. infected mice included premature rupture of membrane, placental detachment, degenerative changes in trophoblasts and endothelial cells, including necrotic areas. P.g. infection caused significantly increased numbers of polymorphonuclear leukocytes (PMNLs) and macrophages in placental tissues, associated with increased local expression of pro-inflammatory mediators including TNF-α and COX-2. Further placental tissue damage was indicated in P.g. infected mice by decreased CD-31 in endothelial cells, increased expression of 8OHdG, an indicator of oxidative DNA damage, and cleaved caspase-3, a marker of apoptosis. In vitro, P.g. lipopolysaccharide significantly increased expression of COX-2, IL-8 and TNF-α, in HTR-8 trophoblasts in an NF-κB-dependent fashion.ConclusionsOur novel mouse model supports previous epidemiological studies signifying dental infection as predisposing factor for PTB/LBW. We demonstrate PTB and LBW in infected mice, translocation of P.g to placental tissues, increased circulating and local pro-inflammatory markers, and the capability of P.g. LPS to directly induce cytokine production in trophoblasts, in vitro. These findings further underscore the importance of local and systemic infections and inflammation during pregnancy and suggest that prevention and/or elimination of dental infections such as marginal or periapical periodontitis before pregnancy may have a beneficial effect on PTB/LBW.
Two experiments compared young and older adults in order to examine whether aging leads to a larger dependence on visual articulatory movements in auditory-visual speech perception. These experiments examined accuracy and response time in syllable identification for auditory-visual (AV) congruent and incongruent stimuli. There were also auditory-only (AO) and visual-only (VO) presentation modes. Data were analyzed only for participants with normal hearing. It was found that the older adults were more strongly influenced by visual speech than the younger ones for acoustically identical signal-to-noise ratios (SNRs) of auditory speech (Experiment 1). This was also confirmed when the SNRs of auditory speech were calibrated for the equivalent AO accuracy between the two age groups (Experiment 2). There were no aging-related differences in VO lipreading accuracy. Combined with response time data, this enhanced visual influence for the older adults was likely to be associated with an aging-related delay in auditory processing.
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