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731.
732.
Notch1 functions as a tumor suppressor in mouse skin 总被引:24,自引:0,他引:24
Nicolas M Wolfer A Raj K Kummer JA Mill P van Noort M Hui CC Clevers H Dotto GP Radtke F 《Nature genetics》2003,33(3):416-421
Notch proteins are important in binary cell-fate decisions and inhibiting differentiation in many developmental systems, and aberrant Notch signaling is associated with tumorigenesis. The role of Notch signaling in mammalian skin is less well characterized and is mainly based on in vitro studies, which suggest that Notch signaling induces differentiation in mammalian skin. Conventional gene targeting is not applicable to establishing the role of Notch receptors or ligands in the skin because Notch1-/- embryos die during gestation. Therefore, we used a tissue-specific inducible gene-targeting approach to study the physiological role of the Notch1 receptor in the mouse epidermis and the corneal epithelium of adult mice. Unexpectedly, ablation of Notch1 results in epidermal and corneal hyperplasia followed by the development of skin tumors and facilitated chemical-induced skin carcinogenesis. Notch1 deficiency in skin and in primary keratinocytes results in increased and sustained expression of Gli2, causing the development of basal-cell carcinoma-like tumors. Furthermore, Notch1 inactivation in the epidermis results in derepressed beta-catenin signaling in cells that should normally undergo differentiation. Enhanced beta-catenin signaling can be reversed by re-introduction of a dominant active form of the Notch1 receptor. This leads to a reduction in the signaling-competent pool of beta-catenin, indicating that Notch1 can inhibit beta-catenin-mediated signaling. Our results indicate that Notch1 functions as a tumor-suppressor gene in mammalian skin. 相似文献
733.
CUL-4 ubiquitin ligase maintains genome stability by restraining DNA-replication licensing 总被引:20,自引:0,他引:20
To maintain genome stability, DNA replication is strictly regulated to occur only once per cell cycle. In eukaryotes, the presence of 'licensing proteins' at replication origins during the G1 cell-cycle phase allows the formation of the pre-replicative complex. The removal of licensing proteins from chromatin during the S phase ensures that origins fire only once per cell cycle. Here we show that the CUL-4 ubiquitin ligase temporally restricts DNA-replication licensing in Caenorhabditis elegans. Inactivation of CUL-4 causes massive DNA re-replication, producing cells with up to 100C DNA content. The C. elegans orthologue of the replication-licensing factor Cdt1 (refs 2, 3) is required for DNA replication. C. elegans CDT-1 is present in G1-phase nuclei but disappears as cells enter S phase. In cells lacking CUL-4, CDT-1 levels fail to decrease during S phase and instead remain constant in the re-replicating cells. Removal of one genomic copy of cdt-1 suppresses the cul-4 re-replication phenotype. We propose that CUL-4 prevents aberrant re-initiation of DNA replication, at least in part, by facilitating the degradation of CDT-1. 相似文献
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杨树不同杂交组合苗期性状遗传变异 总被引:4,自引:0,他引:4
对T120×S3107等8个杂交组合及各组合内无性系间的苗高、胸径、分枝情况等性状变异进行了研究。结果表明,组合间和无性系间在各性状上存在着显著的变异,苗高、胸径、侧枝的广义遗传力分别为77.75%,52.64%,56.96%。各杂交组合苗高和胸径平均值均超过对照T120和I 69。I 69×S3244,I 69×I 63组合的苗高和胸径性状表现都较好。因此,从这批材料中选出优良无性系是有可能的。 相似文献
735.
Iron in surface seawater has been demonstrated to be the limiting nutrient factor for primary productivity in certain oceanic regions where other major nutrients are abundant[1—5]. The available Fe to the phytoplankton in seawater is related to the uptake of carbon dioxide through the ocean and, in turn, to the global greenhouse effect[6—11]. Recent reports showed that the available Fe in the seawater is closely correlative to nitrogen fixation in the ocean[12—17]. Understanding which Fe s… 相似文献
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