天然1型欧泊的分类

详细介绍了欧泊咨询机构对闪电岭地区贵欧泊的品质 (价值 )进行评估和描述的一种非常实用的方法。这套体系基于量化决定欧泊价值的正面因素 (体色调、亮度、样式、色彩条厚度及颜色 ) ,扣除瑕疵因素的影响 (裂痕和细裂纹、台面上的砂或石膏、颜色不在台面上、拙劣的切磨、形状和抛光 ) ,然后描述欧泊的切磨形状。相应的编码系统可以准确描述一颗欧泊。

The promoter analysis of the human C17orf25 gene, a novel chromosome 17pl3.3 gene

The human C17orf25 gene (Accession No. AF177342) is one of thirteen genes cloned from a region displaying a high score of loss of heterozygosity within chromosome 17pl3.3 in human hepatocellular carcinoma in China[l]. To unveil the underlying mechanisms for the transcription regulation of this gene and understand its implication to the hepatocellular carcinogenesis, we looked into the relevant aspects by both bioinformatic and experimental executions. We found: 1, The abundant expression of the C17orf25 gene was evident in all the cell lines and tissue samples tested, showing little hepatoma-selectivity; 2, Its transcription starts at a single site, locating at -60 from the translation initiation codon; 3, A 58 bp fragment containing the transcription start, extending from -112 to -55, represents the minimal promoter; 4, The consensus sequence within this fragment recognized by SP1 contributes predominantly to the activity of the minimal promoter; 5, The bioinformatic analysis suggests that the C17orf25 gene may encode a protein in the family of the glyoxalase. Our data has provided some deep insight into both function and regulation of the C1 7orf25 gene in the context of the normal liver and hepatocellular carcinoma.

The ATF/CREB site is the key element for transcription of the human RNA methyltransferase like1(RNMTL1) gene, a newly discovered 17p13.3 gene

The human RNA methyltransferase like 1 gene (RNMTL1) is one of thirteen newly discovered genes within a 116 Kb segment of the chromosome 17pl3.3 that suffers from a high frequent loss of heterozygosity in human hepatocellular carcinoma in China[1-5]. To understand the molecular mechanisms underlying transcription control of the RNMTL1 gene in human cancers, we decline using of the conventional approach where the cis-elements bound by the known transcription factors are primary targets, and carried out the systematic analyses to dissect the promoter structure and identify/characterize the key cis-elements that are responsible for its strong expression in cell. The molecular approaches applied included 1, the primer extension for mapping of the transcription starts; 2, the transient transfection/reporter assays on a large number of deletion and site-specific mutants of the promoter segment for defining the minimal promoter and the crucial elements within; and 3, the electrophoresis mobility shift assay with specific antibodies for reconfirming the nature of the transcription factors and their cognate cis-elements. We have shown that the interaction of an ATF/CREB element (-38 to -31) and its cognate transcription factors play a predominant role in the promoter activity of the RNMTL1 gene. The secondary DNA structures of the ATF/CREB element play a more vital role in the protein-DNA interaction. Finally, we reported a novel mechanism underlying the YY1 mediated transcription repression, namely, the ATF/CREB dependent transcription-repression by YY1 is executed in absence of its own sequence-specific binding.

Chromatin remodeling regulated by steroid and nuclearreceptors

Coactivators and corepressors regulate transcriptionby controlling interactions between sequence-specific transcription factors, the basal transcriptional machinery andthe chromatin environment. This review consider the access of nuclear and steroid receptors to chromatin, theiruse of corepressors and coactivators to modify chromatinstructure and the implications for transcriptional control.The assembly of specific nucleoprotein architectures andtargeted histone modification emerge as central controlling elements for gene expression.

Conditional Mutations in Drosophila

The aim of this study was to obtain unusual mutations called conditional. The mutations manifest in some, not all representatives of a species. Collections of these mutations in chromosomes X, 2, and 3 of Drosophila melanogaster were established. Sex of fly or chromosomal rearrangement was the conditions providing ＂manifestation-non manifestation＂ of these mutations. The mutations differ from the usual by a set of properties. The salient differences in addition to conditional manifestation include： manifestation dependence on the spatial arrangement of chromosomal material in the genome, parental effects （maternal or paternal） of the mutant, capacity for transferring the genome from stable to unstable state. It is suggested that conditional mutations are mutant variants of Drosophila regulatory genes contained by the large Genomic Regulatory Network of Drosophila. Thus, the genes of this category can be detected by using special breeding procedures, mutations of these genes have unusual manifestation.

Mitosis-specific acetylation tunes Ran effector binding for chromosome segregation

Stable transmission of genetic information during cell division requires faithful mitotic spindle assembly and chromosome segregation. The Ran GTPase plays a key role in mitotic spindle assembly. However, how the generation of a chemical gradient of Ran-GTP at the spindle is coupled to mitotic post-translational modifications has never been characterized. Here, we solved the complex structure of Ran with the nucleotide release factor Mogl and delineated a novel mitosis-specific acetylation-regulated Ran-Mogl interaction dur- ing chromosome segregation. Our structure-guided functional analyses revealed that Mogl compotes with RCCl for Ran binding in a GTP/GDP-dependent manner. Biochemical characterization demonstrated that Mogl-bound Ran prevents RCCl binding and subse- quent GTP loading. Surprisingly, Ran is a bono fide substrate of TIP60, and the acetylation of Lys134 by TIP60 liberates Mogl from Ran binding during mitosis. Importantly, this acetylation-elicited switch of Ran binding to RCC1 promotes high level of Ran-GTP, which is essential for chromosome alignment. These results establish a previously uncharacterized regulatory mechanism in which TIP60 pro- vides a homeostatic control of Ran-GTP level by tuning Ran effector binding for chromosome segregation in mitosis.

Regulation of sister chromatid cohesion during the mitotic cell cycle

Orderly execution of two critical events during the cell cycle––DNA replication and chromosome segregation––ensures the stable transmission of genetic materials. The cohesin complex physically connects sister chromatids during DNA replication in a process termed sister chromatid cohesion. Timely establishment and dissolution of sister chromatid cohesion is a prerequisite for accurate chromosome segregation, and is tight regulated by the cell cycle machinery and cohesin-associated proteins. In this review, we discuss recent progress in the molecular understanding of sister chromatid cohesion during the mitotic cell cycle.

Epigenetic control of meiotic recombination in plants

Meiotic recombination is a deeply conserved process within eukaryotes that has a profound effect on patterns of natural genetic variation. During meiosis homologous chromosomes pair and undergo DNA double strand breaks generated by the Spo11 endonuclease. These breaks can be repaired as crossovers that result in reciprocal exchange between chromosomes. The frequency of recombination along chromosomes is highly variable, for example, crossovers are rarely observed in heterochromatin and the centromeric regions. Recent work in plants has shown that crossover hotspots occur in gene promoters and are associated with specific chromatin modifications, including H2 A.Z. Meiotic chromosomes are also organized in loop-base arrays connected to an underlying chromosome axis, which likely interacts with chromatin to organize patterns of recombination.Therefore, epigenetic information exerts a major influence on patterns of meiotic recombination along chromosomes, genetic variation within populations and evolution of plant genomes.