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  • 1
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    Apoptotic force and tissue dynamics during Drosophila embryogenesis (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: Understanding cell morphogenesis during metazoan development requires knowledge of how cells and the extracellular matrix produce and respond to forces. We investigated how apoptosis, which remodels tissue by eliminating supernumerary cells, also contributes forces to a tissue (the amnioserosa) that promotes cell-sheet fusion (dorsal closure) in the Drosophila embryo. We showed that expression in the amnioserosa of proteins that suppress or enhance apoptosis slows or speeds dorsal closure, respectively. These changes correlate with the forces produced by the amnioserosa and the rate of seam formation between the cell sheets (zipping), key processes that contribute to closure. This apoptotic force is used by the embryo to drive cell-sheet movements during development, a role not classically attributed to apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757114/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757114/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toyama, Yusuke -- Peralta, Xomalin G -- Wells, Adrienne R -- Kiehart, Daniel P -- Edwards, Glenn S -- GM33830/GM/NIGMS NIH HHS/ -- R01 GM033830/GM/NIGMS NIH HHS/ -- R01 GM033830-24/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1683-6. doi: 10.1126/science.1157052.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physics Department and Free Electron Laser Laboratory, Duke University, Durham, NC 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Movement ; Cell Shape ; Drosophila melanogaster/cytology/*embryology ; Embryo, Nonmammalian/*cytology ; *Embryonic Development ; Epidermis/cytology/embryology ; Epithelial Cells/*cytology/physiology ; Epithelium/*embryology ; Female ; Microscopy, Confocal ; *Morphogenesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    An X chromosome gene, WTX, is commonly inactivated in Wilms tumor (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: Wilms tumor is a pediatric kidney cancer associated with inactivation of the WT1 tumor-suppressor gene in 5 to 10% of cases. Using a high-resolution screen for DNA copy-number alterations in Wilms tumor, we identified somatic deletions targeting a previously uncharacterized gene on the X chromosome. This gene, which we call WTX, is inactivated in approximately one-third of Wilms tumors (15 of 51 tumors). Tumors with mutations in WTX lack WT1 mutations, and both genes share a restricted temporal and spatial expression pattern in normal renal precursors. In contrast to biallelic inactivation of autosomal tumor-suppressor genes, WTX is inactivated by a monoallelic "single-hit" event targeting the single X chromosome in tumors from males and the active X chromosome in tumors from females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivera, Miguel N -- Kim, Woo Jae -- Wells, Julie -- Driscoll, David R -- Brannigan, Brian W -- Han, Moonjoo -- Kim, James C -- Feinberg, Andrew P -- Gerald, William L -- Vargas, Sara O -- Chin, Lynda -- Iafrate, A John -- Bell, Daphne W -- Haber, Daniel A -- P01-CA101942/CA/NCI NIH HHS/ -- R37 CA054358/CA/NCI NIH HHS/ -- R37 CA054358-17/CA/NCI NIH HHS/ -- R37-CA058596/CA/NCI NIH HHS/ -- T32-CA009216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):642-5. Epub 2007 Jan 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Harvard Medical Center, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204608" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Alleles ; Amino Acid Sequence ; Animals ; Cell Line ; Chromosome Deletion ; Chromosomes, Human, X/*genetics ; Female ; Gene Expression ; *Gene Silencing ; *Genes, Wilms Tumor ; Heterozygote ; Humans ; In Situ Hybridization, Fluorescence ; Kidney/embryology/metabolism ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Point Mutation ; Tumor Suppressor Proteins/chemistry/*genetics/physiology ; Wilms Tumor/*genetics ; beta Catenin/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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