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81.
Repression of the tyrosine, lysine, and methionine biosynthetic pathways in a hisT mutant of Salmonella typhimurium.
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B A Brown S R Lax L Liang B J Dabney L L Spremulli J M Ravel 《Journal of bacteriology》1977,129(2):1168-1170
A comparison was made of the repressibility of certain enzymes in the tyrosine, methionine, and lysine biosynthetic pathways in wild-type Salmonella typhimurium and a hisT mutant. The results show that (i) tyrosine represses the synthesis of the tyrosine-sensitive 3-deoxy-D-arabino-heptulsonic acid 7-phosphate synthetase and the tyrosine aminotransferase to the same extent in a hisT mutant as in wild type and (ii) there is no detectable alteration in the extent to which methionine represses O-succinylhomoserine synthetase or in the extent to which lysine represses the lysine-sensitive beta-aspartokinase as a result of the hisT mutation. 相似文献
82.
Localization of thyroglobulin antigenicity in rat thyroid sections using antibodies labled with peroxidase or (125)I-radioiodine
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In the hope of localizing thyroglobulin within focullar cells of the thyroid gland, antibodies raised against rat thyroglobulin were labeled with the enzyme horseradish peroxidase or with (125)I-radioiodine. Sections of rat thyroids fixed in glutaraldehyde and embedded in glycol methacrylate or Araldite were placed in contact with the labeled antibodies. The sites of antibody binding were detected by diaminobenzidine staining in the case of peroxidase labeling, and radioautography in the case of 125(I) labeling. Peroxidase labeling revealed that the antibodies were bound by the luminal colloid of the thyroid follicles and, within focullar cells, by colloid droplets, condensing vacuoles, and apical vesicles. (125)I labeling confirmed these findings, and revealed some binding of antibodies within Golgi saccules and rough endoplasmic reticulum. This method provides a visually less distinct distribution than peroxidase labeling, but it allowed ready quantitation of the reactions by counts of silver grains in the radioautographs. The counts revealed that the concentration of label was similar in the luminal colloid of different follicles, but that it varied within the compartments of follicular cells. A moderate concentration was detected in rough endoplasmic reticulum and Golgi saccules, whereas a high concentration was found in condensing vacuoles, apical vesicles, and in the luminal colloid. Varying amounts of label were observed over the different types of colloid droplets, and this was attributed to various degrees of lysosomal degradation of thyroglobulin. It is concluded that the concentration of thyroglobulin antigenicity increases during transport from the ribosomal site of synthesis to the follicular colloid, and then decreases during the digestion of colloid droplets which leads to the release of the thyoid hormone. 相似文献
83.
The clock gene period (per) controls a number of biological rhythms in
Drosophila. In D. melanogaster, per has a repetitive region that encodes a
number of alternating threonine-glycine residues. We sequenced and compared
this region from several different Drosophila species belonging to various
groups within the Drosophila and Sophophora subgenera. This part of per
shows a great variability in both DNA sequence and length. Furthermore,
analysis of the data suggests that changes in the length of this variable
region might be associated with amino acid replacements in the more
conserved flanking sequences.
相似文献
84.
Feng Ding Yelena Prints Madhu S. Dhar Dabney K. Johnson Carmen Garnacho–Montero Robert D. Nicholls Uta Francke 《Mammalian genome》2005,16(6):424-431
Prader–Willi syndrome (PWS) is a neurobehavioral disorder caused by the lack of paternal expression of imprinted genes in the human chromosome region 15q11–13. Recent studies of rare human translocation patients narrowed the PWS critical genes to a 121-kb region containing PWCR1/HBII-85 and HBII-438 snoRNA genes. The existing mouse models of PWS that lack the expression of multiple genes, including Snrpn, Ube3a, and many intronic snoRNA genes, are characterized by 80%–100% neonatal lethality. To define the candidate region for PWS-like phenotypes in mice, we analyzed the expression of several genetic elements in mice carrying the large radiation-induced p30PUb deletion that includes the p locus. Mice having inherited this deletion from either parent develop normally into adulthood. By Northern blot and RT-PCR assays of brain tissue, we found that Pwcr1/MBII-85 snoRNAs are expressed normally, while MBII-52 snoRNAs are not expressed when the deletion is paternally inherited. Mapping of the distal deletion breakpoint indicated that the p30PUb deletion includes the entire MBII-52 snoRNA gene cluster and three previously unmapped EST sequences. The lack of expression of these elements in mice with a paternal p30PUb deletion indicates that they are not critical for the neonatal lethality observed in PWS mouse models. In addition, we identified MBII-436, the mouse homolog of the HBII-436 snoRNA, confirmed its imprinting status, and mapped it outside of the p30PUb deletion. Taking together all available data, we conclude that the lack of Pwcr1/MBII-85 snoRNA expression is the most likely cause for the neonatal lethality in PWS model mice. 相似文献
85.
Wallace S.H. Chick Sarah E. Mentzer Donald A. Carpenter Eugene M. Rinchik Dabney Johnson Yun You 《Mammalian genome》2005,16(9):661-671
Chromosomal deletions have long been used as genetic tools in dissecting the functions of complex genomes, and new methodologies
are still being developed to achieve the maximum coverage. In the mouse, where the chromosomal deletion coverage is far less
extensive than that in Drosophila, substantial coverage of the genome with deletions is strongly desirable. This article reports the generation of three deletion
complexes in the distal part of mouse Chromosome (Chr) 15. Chromosomal deletions were efficiently induced by X rays in embryonic
stem (ES) cells around the Otoconin 90 (Oc90), SRY-box-containing gene 10 (Sox10), and carnitine palmitoyltransferase 1b (Cpt1b) loci. Deletions encompassing the Oc90 and Sox10 loci were transmitted to the offspring of the chimeric mice that were generated from deletion-bearing ES cells. Whereas deletion
complexes encompassing the Sox10 and the Cpt1b loci overlap each other, no overlap of the Oc90 complex with the Sox10 complex was found, possibly indicating the existence of a haploinsufficient gene located between Oc90 and Sox10. Deletion frequency and size induced by X rays depend on the selective locus, possibly reflecting the existence of haplolethal
genes in the vicinity of these loci that yield fewer and smaller deletions. Deletions induced in ES cells by X rays vary in
size and location of breakpoints, which makes them desirable for mapping and for functional genomics studies. 相似文献
86.
The Collaborative Cross at Oak Ridge National Laboratory: developing a powerful resource for systems genetics 总被引:3,自引:0,他引:3
87.
88.
Kelvin KL Wong Pongpat Thavornpattanapong Sherman CP Cheung Zhonghua Sun Jiyuan Tu 《BMC cardiovascular disorders》2012,12(1):1-18
Background
This study characterizes the distribution and components of plaque structure by presenting a three-dimensional blood-vessel modelling with the aim of determining mechanical properties due to the effect of lipid core and calcification within a plaque. Numerical simulation has been used to answer how cap thickness and calcium distribution in lipids influence the biomechanical stress on the plaque.Method
Modelling atherosclerotic plaque based on structural analysis confirms the rationale for plaque mechanical examination and the feasibility of our simulation model. Meaningful validation of predictions from modelled atherosclerotic plaque model typically requires examination of bona fide atherosclerotic lesions. To analyze a more accurate plaque rupture, fluid-structure interaction is applied to three-dimensional blood-vessel carotid bifurcation modelling. A patient-specific pressure variation is applied onto the plaque to influence its vulnerability.Results
Modelling of the human atherosclerotic artery with varying degrees of lipid core elasticity, fibrous cap thickness and calcification gap, which is defined as the distance between the fibrous cap and calcification agglomerate, form the basis of our rupture analysis. Finite element analysis shows that the calcification gap should be conservatively smaller than its threshold to maintain plaque stability. The results add new mechanistic insights and methodologically sound data to investigate plaque rupture mechanics.Conclusion
Structural analysis using a three-dimensional calcified model represents a more realistic simulation of late-stage atherosclerotic plaque. We also demonstrate that increases of calcium content that is coupled with a decrease in lipid core volume can stabilize plaque structurally. 相似文献89.
High-throughput sequencing technologies frequently necessitate the use of PCR for sequencing library amplification. PCR is a sometimes enigmatic process and is known to introduce biases. Here we perform a simple amplification-sequencing assay using 10 commercially available polymerase-buffer systems to amplify libraries prepared from both modern and ancient DNA. We compare the performance of the polymerases with respect to a previously uncharacterized template length bias, as well as GC-content bias, and find that simply avoiding certain polymerase can dramatically decrease the occurrence of both. For amplification of ancient DNA, we found that some commonly used polymerases strongly bias against amplification of endogenous DNA in favor of GC-rich microbial contamination, in our case reducing the fraction of endogenous sequences to almost half. 相似文献
90.
Bas E Dutilh Cristiane C Thompson Ana CP Vicente Michel A Marin Clarence Lee Genivaldo GZ Silva Robert Schmieder Bruno GN Andrade Luciane Chimetto Daniel Cuevas Daniel R Garza Iruka N Okeke Aaron Oladipo Aboderin Jessica Spangler Tristen Ross Elizabeth A Dinsdale Fabiano L Thompson Timothy T Harkins Robert A Edwards 《BMC genomics》2014,15(1)