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31.
Cook RK Christensen SJ Deal JA Coburn RA Deal ME Gresens JM Kaufman TC Cook KR 《Genome biology》2012,13(3):R21-14
Background
Chromosomal deletions are used extensively in Drosophila melanogaster genetics research. Deletion mapping is the primary method used for fine-scale gene localization. Effective and efficient deletion mapping requires both extensive genomic coverage and a high density of molecularly defined breakpoints across the genome.Results
A large-scale resource development project at the Bloomington Drosophila Stock Center has improved the choice of deletions beyond that provided by previous projects. FLP-mediated recombination between FRT-bearing transposon insertions was used to generate deletions, because it is efficient and provides single-nucleotide resolution in planning deletion screens. The 793 deletions generated pushed coverage of the euchromatic genome to 98.4%. Gaps in coverage contain haplolethal and haplosterile genes, but the sizes of these gaps were minimized by flanking these genes as closely as possible with deletions. In improving coverage, a complete inventory of haplolethal and haplosterile genes was generated and extensive information on other haploinsufficient genes was compiled. To aid mapping experiments, a subset of deletions was organized into a Deficiency Kit to provide maximal coverage efficiently. To improve the resolution of deletion mapping, screens were planned to distribute deletion breakpoints evenly across the genome. The median chromosomal interval between breakpoints now contains only nine genes and 377 intervals contain only single genes.Conclusions
Drosophila melanogaster now has the most extensive genomic deletion coverage and breakpoint subdivision as well as the most comprehensive inventory of haploinsufficient genes of any multicellular organism. The improved selection of chromosomal deletion strains will be useful to nearly all Drosophila researchers. 相似文献32.
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Polybrominated diphenyl ethers (PBDEs) are widely used as additive flame-retardants and have been detected in human blood,
adipose tissue, and breast milk. Developmental and long-term exposures to these chemicals may pose a human health risk, especially
to children. We have previously demonstrated that polychlorinated biphenyls (PCBs), which are structurally similar to PBDEs
and cause neurotoxicity, perturb intracellular signaling events including calcium homeostasis and protein kinase C translocation,
which are critical for neuronal function and development of the nervous system. The objective of the present study was to
test whether environmentally relevant PBDE congeners 47 and 99 are also capable of disrupting Ca2 + homeostasis. Calcium buffering was determined by measuring 45Ca2 + -uptake by microsomes and mitochondria, isolated from adult male rat brain (frontal cortex, cerebellum, hippocampus, and hypothalamus).
Results show that PBDEs 47 and 99 inhibit both microsomal and mitochondrial 45Ca2 + -uptake in a concentration-dependent manner. The effect of these congeners on 45Ca2 + -uptake is similar in all four brain regions though the hypothalamus seems to be slightly more sensitive. Among the two preparations,
the congeners inhibited 45Ca2 + -uptake in mitochondria to a greater extent than in microsomes. These results indicate that PBDE 47 and PBDE 99 congeners
perturb calcium signaling in rat brain in a manner similar to PCB congeners, suggesting a common mode of action of these persistent
organic pollutants.
The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory
of the US Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily
reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement
or recommendation for use.
These results will be presented at the 21th Biennial Meeting of International Society for Neurochemistry and American Society
for Neurochemistry in Cancun, Mexico (August 19–24, 2007).
Special issue article in honor of Dr. Frode Fonnum. 相似文献
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Jessica L. Teo Vanesa M. Tomatis Luke Coburn Anne K. Lagendijk Irin-Maya Schouwenaar Srikanth Budnar Thomas E. Hall Suzie Verma Robert W. McLachlan Benjamin M. Hogan Robert G. Parton Alpha S. Yap Guillermo A. Gomez 《Molecular biology of the cell》2020,31(23):2557
Epithelia can eliminate apoptotic cells by apical extrusion. This is a complex morphogenetic event where expulsion of the apoptotic cell is accompanied by rearrangement of its immediate neighbors to form a rosette. A key mechanism for extrusion is constriction of an actomyosin network that neighbor cells form at their interface with the apoptotic cell. Here we report a complementary process of cytoskeletal relaxation that occurs when cortical contractility is down-regulated at the junctions between those neighbor cells themselves. This reflects a mechanosensitive Src family kinase (SFK) signaling pathway that is activated in neighbor cells when the apoptotic cell relaxes shortly after injury. Inhibiting SFK signaling blocks both the expulsion of apoptotic cells and the rosette formation among their neighbor cells. This reveals the complex pattern of spatially distinct contraction and relaxation that must be established in the neighboring epithelium for apoptotic cells to be extruded. 相似文献
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The use of inflatable breast implants 总被引:1,自引:0,他引:1