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111.
112.
The patterns of seedling recruitment in animal-dispersed plants result from the interactions among environmental and behavioral variables. However, we know little on the contribution and combined effect of both kinds of variables. We designed a field study to assess the interplay between environment (vegetation structure, seed abundance, rodent abundance) and behavior (seed dispersal and predation by rodents, and rooting by wild boars), and their contribution to the spatial patterns of seedling recruitment in a Mediterranean mixed-oak forest. In a spatially explicit design, we monitored intensively all environmental and behavioral variables in fixed points at a small spatial scale from autumn to spring, as well as seedling emergence and survival. Our results revealed that the spatial patterns of seedling emergence were strongly related to acorn availability on the ground, but not by a facilitationeffect of vegetation cover. Rodents changed seed shadows generated by mother trees by dispersing most seeds from shrubby to open areas, but the spatial patterns of acorn dispersal/predation had no direct effect on recruitment. By contrast, rodents had a strong impact on recruitment as pilferers of cached seeds. Rooting by wild boars also reduced recruitment by reducing seed abundance, but also by changing rodent’s behavior towards higher consumption of acorns in situ. Hence, seed abundance and the foraging behavior of scatter-hoarding rodents and wild boars are driving the spatial patterns of seedling recruitment in this mature oak forest, rather than vegetation features. The contribution of vegetation to seedling recruitment (e.g. facilitation by shrubs) may be context dependent, having a little role in closed forests, or being overridden by directed seed dispersal from shrubby to open areas. We warn about the need of using broad approaches that consider the combined action of environment and behavior to improve our knowledge on the dynamics of natural regeneration in forests. 相似文献
113.
Background
Genomic imprinting is an epigenetic mechanism that can lead to differential gene expression depending on the parent-of-origin of a received allele. While most studies on imprinting address its underlying molecular mechanisms or attempt at discovering genomic regions that might be subject to imprinting, few have focused on the amount of phenotypic variation contributed by such epigenetic process. In this report, we give a brief review of a one-locus imprinting model in a quantitative genetics framework, and provide a decomposition of the genetic variance according to this model. Analytical deductions from the proposed imprinting model indicated a non-negligible contribution of imprinting to genetic variation of complex traits. Also, we performed a whole-genome scan analysis on mouse body mass index (BMI) aiming at revealing potential consequences when existing imprinting effects are ignored in genetic analysis.Results
10,021 SNP markers were used to perform a whole-genome single marker regression on mouse BMI using an additive and an imprinting model. Markers significant for imprinting indicated that BMI is subject to imprinting. Marked variance changed from 1.218 ×10−4 to 1.842 ×10−4 when imprinting was considered in the analysis, implying that one third of marked variance would be lost if existing imprinting effects were not accounted for. When both marker and pedigree information were used, estimated heritability increased from 0.176 to 0.195 when imprinting was considered.Conclusions
When a complex trait is subject to imprinting, using an additive model that ignores this phenomenon may result in an underestimate of additive variability, potentially leading to wrong inferences about the underlying genetic architecture of that trait. This could be a possible factor explaining part of the missing heritability commonly observed in genome-wide association studies (GWAS). 相似文献114.
Timothy M Beissinger Guilherme JM Rosa Shawn M Kaeppler Daniel Gianola Natalia de Leon 《遗传、选种与进化》2015,47(1)
Background
High-density genomic data is often analyzed by combining information over windows of adjacent markers. Interpretation of data grouped in windows versus at individual locations may increase statistical power, simplify computation, reduce sampling noise, and reduce the total number of tests performed. However, use of adjacent marker information can result in over- or under-smoothing, undesirable window boundary specifications, or highly correlated test statistics. We introduce a method for defining windows based on statistically guided breakpoints in the data, as a foundation for the analysis of multiple adjacent data points. This method involves first fitting a cubic smoothing spline to the data and then identifying the inflection points of the fitted spline, which serve as the boundaries of adjacent windows. This technique does not require prior knowledge of linkage disequilibrium, and therefore can be applied to data collected from individual or pooled sequencing experiments. Moreover, in contrast to existing methods, an arbitrary choice of window size is not necessary, since these are determined empirically and allowed to vary along the genome.Results
Simulations applying this method were performed to identify selection signatures from pooled sequencing FST data, for which allele frequencies were estimated from a pool of individuals. The relative ratio of true to false positives was twice that generated by existing techniques. A comparison of the approach to a previous study that involved pooled sequencing FST data from maize suggested that outlying windows were more clearly separated from their neighbors than when using a standard sliding window approach.Conclusions
We have developed a novel technique to identify window boundaries for subsequent analysis protocols. When applied to selection studies based on FST data, this method provides a high discovery rate and minimizes false positives. The method is implemented in the R package GenWin, which is publicly available from CRAN. 相似文献115.
Shane Deegan Svetlana Saveljeva Susan E Logue Karolina Pakos-Zebrucka Sanjeev Gupta Peter Vandenabeele Mathieu JM Bertrand Afshin Samali 《Autophagy》2014,10(11):1921-1936
Endoplasmic reticulum (ER) stress-induced cell death is normally associated with activation of the mitochondrial apoptotic pathway, which is characterized by CYCS (cytochrome c, somatic) release, apoptosome formation, and caspase activation, resulting in cell death. In this study, we demonstrate that under conditions of ER stress cells devoid of CASP9/caspase-9 or BAX and BAK1, and therefore defective in the mitochondrial apoptotic pathway, still undergo a delayed form of cell death associated with the activation of caspases, therefore revealing the existence of an alternative stress-induced caspase activation pathway. We identified CASP8/caspase-8 as the apical protease in this caspase cascade, and found that knockdown of either of the key autophagic genes, ATG5 or ATG7, impacted on CASP8 activation and cell death induction, highlighting the crucial role of autophagy in the activation of this novel ER stress-induced death pathway. In line with this, we identified a protein complex composed of ATG5, FADD, and pro-CASP8 whose assembly coincides with caspase activation and cell death induction. Together, our results reveal the toxic potential of autophagy in cells undergoing ER stress that are defective in the mitochondrial apoptotic pathway, and suggest a model in which the autophagosome functions as a platform facilitating pro-CASP8 activation. Chemoresistance, a common problem in the treatment of cancer, is frequently caused by the downregulation of key mitochondrial death effector proteins. Alternate stress-induced apoptotic pathways, such as the one described here, may become of particular relevance for tackling the problem of chemoresistance in cancer cells. 相似文献
116.
JM Mcnulty 《Biotechnic & histochemistry》2013,88(5-6):191-196
Zirconyl hematoxylin stains acidic mucins darkly and specifically using a solution of 100 mg hematoxylin, 5 ml ethanol, 5 ml 0.5% sodium iodate, 400 mg zirconyl chloride octahydrate, and 30 ml 25% aqueous glycerol. The stain is especially advantageous for studying goblet cells and Paget cells. 相似文献
117.
118.
Firdaus AA Mohamed Hoesein Pieter Zanen Pim A de Jong Bram van Ginneken H Marike Boezen Harry JM Groen Mathijs Oudkerk Harry J de Koning Dirkje S Postma Jan-Willem J Lammers 《Respiratory research》2013,14(1):55
Background
Little is known about the factors associated with CT-quantified emphysema progression in heavy smokers. The objective of this study was to investigate the effect of length of smoking cessation and clinical / demographical factors on the rate of emphysema progression and FEV1-decline in male heavy smokers.Methods
3,670 male smokers with mean (SD) 40.8 (17.9) packyears underwent chest CT scans and pulmonary function tests at baseline and after 1 and 3 years follow-up. Smoking status (quitted ≥5, ≥1-<5, <1 years or current smoker) was noted. Rate of progression of emphysema and FEV1-decline after follow-up were assessed by analysis of variance adjusting for age, height, baseline pulmonary function and emphysema severity, packyears, years in study and respiratory symptoms. The quitted ≥5 group was used as reference.Results
Median (Q1-Q3) emphysema severity,<-950 HU, was 8.8 (5.1 – 14.1) and mean (SD) FEV1 was 3.4 (0.73) L or 98.5 (18.5) % of predicted. The group quitted ‘>5 years’ showed significantly lower rates of progression of emphysema compared to current smokers, 1.07% and 1.12% per year, respectively (p<0.001). Current smokers had a yearly FEV1-decline of 69 ml, while subjects quit smoking >5 years had a yearly decline of 57.5 ml (p<0.001).Conclusion
Quit smoking >5 years significantly slows the rate of emphysema progression and lung function decline.Trial registration
Registered at http://www.trialregister.nl with trial number ISRCTN63545820. 相似文献119.
Akkelies E Dijkstra Dirkje S Postma Nick ten Hacken Judith M Vonk Matthijs Oudkerk Peter MA van Ooijen Pieter Zanen Firdaus A Mohamed Hoesein Bram van Ginneken Michael Schmidt Harry JM Groen 《Respiratory research》2013,14(1):11
Background
Increased airway wall thickness (AWT) and parenchymal lung destruction both contribute to airflow limitation. Advances in computed tomography (CT) post-processing imaging allow to quantify these features. The aim of this Dutch population study is to assess the relationships between AWT, lung function, emphysema and respiratory symptoms.Methods
AWT and emphysema were assessed by low-dose CT in 500 male heavy smokers, randomly selected from a lung cancer screening population. AWT was measured in each lung lobe in cross-sectionally reformatted images with an automated imaging program at locations with an internal diameter of 3.5 mm, and validated in smaller cohorts of patients. The 15th percentile method (Perc15) was used to assess the severity of emphysema. Information about respiratory symptoms and smoking behavior was collected by questionnaires and lung function by spirometry.Results
Median AWT in airways with an internal diameter of 3.5 mm (AWT3.5) was 0.57 (0.44 - 0.74) mm. Median AWT in subjects without symptoms was 0.52 (0.41-0.66) and in those with dyspnea and/or wheezing 0.65 (0.52-0.81) mm (p<0.001). In the multivariate analysis only AWT3.5 and emphysema independently explained 31.1%and 9.5%of the variance in FEV1%predicted, respectively, after adjustment for smoking behavior.Conclusions
Post processing standardization of airway wall measurements provides a reliable and useful method to assess airway wall thickness. Increased airway wall thickness contributes more to airflow limitation than emphysema in a smoking male population even after adjustment for smoking behavior. 相似文献120.
Roland F Hoffmann Sina Zarrintan Simone M Brandenburg Arjan Kol Harold G de Bruin Shabnam Jafari Freark Dijk Dharamdajal Kalicharan Marco Kelders Harry R Gosker Nick HT ten Hacken Johannes J van der Want Antoon JM van Oosterhout Irene H Heijink 《Respiratory research》2013,14(1):97