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131.
Martin Lappann Heike Claus Tessa Van Alen Morten Harmsen Johannes Elias Søren Molin Ulrich Vogel 《Molecular microbiology》2010,75(6):1355-1371
Major pathogenic clonal complexes (cc) of Neisseria meningitidis differ substantially in their point prevalence among healthy carriers. We show that frequently carried pathogenic cc (e.g. sequence type ST‐41/44 cc and ST‐32 cc) depend on extracellular DNA (eDNA) to initiate in vitro biofilm formation, whereas biofilm formation of cc with low point prevalence (ST‐8 cc and ST‐11 cc) was eDNA‐independent. For initial biofilm formation, a ST‐32 cc type strain, but not a ST‐11 type strain, utilized eDNA. The release of eDNA was mediated by lytic transglycosylase and cytoplasmic N‐acetylmuramyl‐l ‐alanine amidase genes. In late biofilms, outer membrane phospholipase A‐dependent autolysis, which was observed in most cc, but not in ST‐8 and ST‐11 strains, was required for shear force resistance of microcolonies. Taken together, N. meningitidis evolved two different biofilm formation strategies, an eDNA‐dependent one yielding shear force resistant microcolonies, and an eDNA‐independent one. Based on the experimental findings and previous epidemiological observations, we hypothesize that most meningococcal cc display a settler phenotype, which is eDNA‐dependent and results in a stable interaction with the host. On the contrary, spreaders (ST‐11 and ST‐8 cc) are unable to use eDNA for biofilm formation and might compensate for poor colonization properties by high transmission rates. 相似文献
132.
133.
Sergey I. Zhadanov Matthew C. Dulik Michael Markley George W. Jennings Jill B. Gaieski George Elias Theodore G. Schurr 《American journal of physical anthropology》2010,142(4):579-589
The name “Wampanoag” means “Eastern People” or “People of the First Light” in the local dialect of the Algonquian language. Once extensively populating the coastal lands and neighboring islands of the eastern United States, the Wampanoag people now consist of two federally recognized tribes, the Aquinnah and Mashpee, the state‐recognized Seaconke Wampanoag tribe, and a number of bands and clans in present‐day southern Massachusetts. Because of repeated epidemics and conflicts with English colonists, including King Philip's War of 1675–76, and subsequent colonial laws forbidding tribal identification, the Wampanoag population was largely decimated, decreasing in size from as many as 12,000 individuals in the 16th century to less than 400, as recorded in 1677. To investigate the influence of the historical past on its biological ancestry and native cultural identity, we analyzed genetic variation in the Seaconke Wampanoag tribe. Our results indicate that the majority of their mtDNA haplotypes belongs to West Eurasian and African lineages, thus reflecting the extent of their contacts and interactions with people of European and African descent. On the paternal side, Y‐chromosome analysis identified a range of Native American, West Eurasian, and African haplogroups in the population, and also surprisingly revealed the presence of a paternal lineage that appears at its highest frequencies in New Guinea and Melanesia. Comparison of the genetic data with genealogical and historical information allows us to reconstruct the tribal history of the Seaconke Wampanoag back to at least the early 18th century. Am J Phys Anthropol 142:579–589, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
134.
Steven S. Xu C. G. Chu S. Chao D. L. Klindworth J. D. Faris E. M. Elias 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2010,120(8):1575-1585
The durum wheat cultivar ‘Golden Ball’ (GB) is a source of resistance to wheat sawfly due to its superior solid stem. In the
late 1980s, Dr. Leonard Joppa developed a complete set of 14 ‘Langdon’ (LDN)–GB disomic substitution (DS) lines by using GB
as the chromosome donor and LDN as the recipient. However, these substitution lines have not been previously characterized
and reported in the literature. The objectives of this study were to confirm the authenticity of the substituted chromosomes
and to analyze the genetic background of the 14 LDN–GB DS lines with the aid of molecular markers, and to further use the
substitution lines for chromosomal localization of DNA markers and genes conferring the superior stem solidness in GB. Results
from simple sequence repeat marker analysis validated the authenticity of the substituted chromosomes in 14 LDN–GB DS lines.
Genome-wide scans using the target region amplification polymorphism (TRAP) marker system produced a total of 359 polymorphic
fragments that were used to compare the genetic background of substitution lines with that of LDN. Among the polymorphic TRAP
markers, 134 (37.3%) and 185 (51.5%) were present in LDN and GB, respectively, with only 10 (2.8%) derived from Chinese Spring.
Therefore, marker analysis demonstrated that each LDN–GB DS line had a pair of chromosomes from GB with a genetic background
similar to that of LDN. Of the TRAP markers generated in this study, 200 were successfully assigned to specific chromosomes
based on their presence or absence in the corresponding LDN–GB DS lines. Also, evaluation of stem solidness in the substitution
lines verified the presence of a major gene for stem solidness in chromosome 3B. Results from this research provides useful
information for the utilization of GB and LDN–GB DS lines for genetic and genomic studies in tetraploid wheat and for the
improvement of stem solidness in both durum and bread wheat. 相似文献
135.
Background
In species with single locus complementary sex determination (sl-CSD), the sex of individuals depends on their genotype at one single locus with multiple alleles. Haploid individuals are always males. Diploid individuals are females when heterozygous, but males when homozygous at the sex-determining locus. Diploid males are typically unviable or effectively sterile, hence imposing a genetic load on populations. Diploid males are produced from matings of partners that share an allele at the sex-determining locus. The lower the allelic diversity at the sex-determining locus, the more diploid males are produced, ultimately impairing the growth of populations and jeopardizing their persistence. The gregarious endoparasitoid wasp Cotesia glomerata is one of only two known species with sl-CSD and fertile diploid males. 相似文献136.
Elias A Rahal Leigh A Henricksen Yuling Li R Scott Williams John A Tainer Kathleen Dixon 《Cell cycle (Georgetown, Tex.)》2010,9(14):2866-2877
The human disorder ataxia telangiectasia (AT), which is characterized by genetic instability and neurodegeneration, results from mutation of the ataxia telangiectasia mutated (ATM) kinase. The loss of ATM leads to cell cycle checkpoint deficiencies and other DNA damage signaling defects that do not fully explain all pathologies associated with A-T including neuronal loss. In addressing this enigma, we find here that ATM suppresses DNA double-strand break (DSB) repair by microhomology-mediated end joining (MMEJ). We show that ATM repression of DNA end-degradation is dependent on its kinase activities and that Mre11 is the major nuclease behind increased DNA end-degradation and MMEJ repair in A-T. Assessment of MMEJ by an in vivo reporter assay system reveals decreased levels of MMEJ repair in Mre11-knockdown cells and in cells treated with Mre11-nuclease inhibitor mirin. Structure-based modeling of Mre11 dimer engaging DNA ends suggests the 5′ ends of a bridged DSB are juxtaposed such that DNA unwinding and 3′–5′ exonuclease activities may collaborate to facilitate simultaneous pairing of extended 5′ termini and exonucleolytic degradation of the 3′ ends in MMEJ. Together our results provide an integrated understanding of ATM and Mre11 in MMEJ: ATM has a critical regulatory function in controlling DNA end-stability and error-prone DSB repair and Mre11 nuclease plays a major role in initiating MMEJ in mammalian cells. These functions of ATM and Mre11 could be particularly important in neuronal cells, which are post-mitotic and therefore depend on mechanisms other than homologous recombination between sister chromatids to repair DSBs.Key words: ATM, Mre11, MRN complex, DNA degradation, double-strand break repair, microhomology-mediated end joining, PI-3-kinase-like kinases 相似文献
137.
Jennifer W. Hill Carol F. Elias Makoto Fukuda Kevin W. Williams Eric D. Berglund William L. Holland You-Ree Cho Jen-Chieh Chuang Yong Xu Michelle Choi Danielle Lauzon Charlotte E. Lee Roberto Coppari James A. Richardson Jeffrey M. Zigman Streamson Chua Philipp E. Scherer Bradford B. Lowell Jens C. Brüning Joel K. Elmquist 《Cell metabolism》2010,11(4):286-297
138.
Abdel-Massih RM Rizkallah HD Al-Din RS Baydoun EA Brett CT 《Journal of plant physiology》2007,164(1):1-10
Microsomal membranes were prepared from etiolated pea (Pisum sativum L.) epicotyls and used to form nascent [Uronic acid-14C]pectin. The enzyme products were characterized by selective enzymic degradation, gel permeation chromatography and analysis of cellulose binding properties. The product obtained had a molecular weight of around 40 kDa, which was significantly lower than that of nascent [Gal-14C]pectin prepared from the same tissues. It is composed mainly of polygalacturonan and perhaps also rhamnogalacturonan (RG-I). Evidence was obtained for the presence of a protein attached to the nascent [Uronic acid-14C]pectin, but it was unaffected by endoglucanase and did not bind to cellulose. Hence, no xyloglucan appeared to be attached to the nascent [Uronic acid-14C]pectin. A model is proposed in which xyloglucan is attached to nascent pectin after formation of homogalacturonan, but before the pectin leaves the Golgi apparatus. 相似文献
139.
Bhandari V Choo-Wing R Homer RJ Elias JA 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(8):4993-5000
IL-13 is a critical effector at sites of Th2 inflammation and remodeling. As a result, anti-IL-13-based therapies are being actively developed to treat a variety of diseases and disorders. However, the beneficial effects of endogenous IL-13 in the normal and diseased lung have not been adequately defined. We hypothesized that endogenous IL-13 is an important regulator of oxidant-induced lung injury and inflammation. To test this hypothesis, we compared the effects of 100% O(2) in mice with wild-type and null IL-13 loci. In this study, we demonstrate that hyperoxia significantly augments the expression of the components of the IL-13R, IL-13Ralpha1, and IL-4Ralpha. We also demonstrate that, in the absence of IL-13, hyperoxia-induced tissue inflammation is decreased. In contrast, in the IL-13 null mice, DNA injury, cell death, caspase expression, and activation and mortality are augmented. Interestingly, the levels of the cytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in the bronchoalveolar lavage fluid. These studies demonstrate that the expression of the IL-13R is augmented and that the endogenous IL-13-IL-13R pathway contributes to the induction of inflammation and the inhibition of injury in hyperoxic acute lung injury. 相似文献
140.
Chapoval SP Al-Garawi A Lora JM Strickland I Ma B Lee PJ Homer RJ Ghosh S Coyle AJ Elias JA 《Journal of immunology (Baltimore, Md. : 1950)》2007,179(10):7030-7041
IL-13 is a major Th2 cytokine that is capable of inducing inflammation, excessive mucus production, airway hyperresponsiveness, alveolar remodeling, and fibrosis in the murine lung. Although IL-13 through its binding to IL-4Ralpha/IL-13Ralpha1 uses the canonical STAT6-signaling pathway to mediate these tissue responses, recent studies have demonstrated that other signaling pathways may also be involved. Previous studies from our laboratory demonstrated that IL-13 mediates its tissue effects by inducing a wide variety of downstream genes many of which are known to be regulated by NF-kappaB. As a result, we hypothesized that NF-kappaB activation plays a critical role in the pathogenesis of IL-13-induced tissue alterations. To test this hypothesis, we compared the effects of transgenic IL-13 in mice with normal and diminished levels of NF-kappaB activity. Three pharmacologic approaches were used to inhibit NF-kappaB including 1) PS1145, a small molecule inhibitor of IkappaBalpha kinase (IKK2), 2) antennapedia-linked NF-kappaB essential modulator-binding domain (NBD) peptide (wild-type NBD), and 3) an adenoviral construct expressing a dominant-negative version of IKK2. We also crossed IL-13-transgenic mice with mice with null mutations of p50 to generate mice that overproduced IL-13 in the presence and absence of this NF-kappaB component. These studies demonstrate that all these interventions reduced IL-13-induced tissue inflammation, fibrosis and alveolar remodeling. In addition, we show that both PS1145 and wild-type NBD inhibit lung inflammatory and structural cell apoptosis. PS1145 inhibits caspase activation and up-regulates inhibitor of apoptosis protein cellular-inhibitor of apoptosis protein 1 (c-IAP-1). Therefore, NF-kappaB is an attractive target for immunotherapy of IL-13-mediated diseases. 相似文献