Chromosomal mapping, differential origin and evolution of the S100 gene family

S100 proteins are calcium-binding proteins, which exist only in vertebrates and which constitute a large protein family. The origin and evolution of the S100 family in vertebrate lineages remain a challenge. Here, we examined the synteny conservation of mammalian S100A genes by analysing the sequence of available vertebrate S100 genes in databases. Five S100A gene members, unknown previously, were identified by chromosome mapping analysis. Mammalian S100A genes are duplicated and clustered on a single chromosome while two S100A gene clusters are found on separate chromosomes in teleost fish, suggesting that S100A genes existed in fish before the fish-specific genome duplication took place. During speciation, tandem gene duplication events within the cluster of S100A genes of a given chromosome have probably led to the multiple members of the S100A gene family. These duplicated genes have been retained in the genome either by neofunctionalisation and/or subfunctionalisation or have evolved into non-coding sequences. However in vertebrate genomes, other S100 genes are also present i.e. S100P, S100B, S100G and S100Z, which exist as single copy genes distributed on different chromosomes, suggesting that they could have evolved from an ancestor different to that of the S100A genes

Characterization of Bovidae sex-determining gene SRY

In mammals, testis determination is under the control of the sex-determining gene SRY. This Y-linked gene encodes a protein with a DNA binding domain similar to those found in high-mobility-group proteins. Here we report the cloning and sequences of the SRY genes of yak and Chinese native cattle. Our data show that SRY genes in Bovidae are less divergent, especially in the coding and 3' regions

Squaring the cube:a family of octametallic lanthanide complexes including a Dy8 single-molecule magnet

International audienceA series of isostructural octanuclear lanthanide complexes of general formula [Ln(8)(sao)(4)(mu(3)-OH)(4)( NO3)(12)(DMF)(12)] (Ln = Nd (1), Sm (2), Eu (3), Gd (4), Tb (5), Dy (6), Ho (7), Er (8); DMF = dimethylformamide) have been prepared via reactions of salicylaldoxime (saoH(2)), tetramethylammonium hydroxide (Me4NOH) with the appropriate lanthanide nitrate salt (Ln(NO3)(3)center dot 6H(2)O). The metallic skeletons of the complexes describe [Ln(4)] tetrahedra encapsulated inside a [Ln(4)] square with the inner core stabilised through mu(3)-OH-ions and the periphery by mu(4)-sao(2)-ligands. The magnetic properties of compounds 2-8 were investigated by dc and ac magnetometry. Temperature dependent ac magnetic susceptibility data reveal that the dysprosium analogue (6) displays an out-of-phase signal in the absence of an applied magnetic field indicative of slow relaxation of the magnetization typical of a Single-Molecule Magnet (SMM). Micro-SQUID measurements reveal temperature and sweep rate dependent hysteresis below 1.0 K

Tumor Suppressor RASSF1A Promoter: p53 Binding and Methylation

Oncogenes and tumor suppressors work in concert to regulate cell growth or death, which is a pair of antagonist factors for regulation of tumorigenesis. Here we show promoter characteristic of tumor suppressor RASSF1A, which revealed a p53 binding site in the distal and a GC-rich region in the proximal promoter region of RASSF1A, in despite of TATA box-less. The GC-rich region, which is ∼300 bp upstream from the RASSF1A ATG, showed the strongest promoter activity in an assay of RASSF1A-driving GFP expression. Methylation analysis of the CpG island showed that 78.57% of the GC sties were methylated in testis tumor samples compared with methylation-less in normal testis. Hypermethylation of the GC-rich region is associated with RASSF1A silencing in human testis tumors. In addition, electrophoretic mobility shift assay indicated that p53 protein bound to the RASSF1A promoter. Further chromatin immunoprecipitation confirmed p53 binding to the RASSF1A. Moreover, p53 binding to the promoter down-regulated RASSF1A expression. These results suggest that p53 protein specifically binds to the RASSF1A promoter and inhibits its expression. Our results provide new insight into the mechanism of action of tumor suppressors and may be a starting point for development of new approaches to cancer treatment

A Global View of Cancer-Specific Transcript Variants by Subtractive Transcriptome-Wide Analysis

BACKGROUND: Alternative pre-mRNA splicing (AS) plays a central role in generating complex proteomes and influences development and disease. However, the regulation and etiology of AS in human tumorigenesis is not well understood. METHODOLOGY/PRINCIPAL FINDINGS: A Basic Local Alignment Search Tool database was constructed for the expressed sequence tags (ESTs) from all available databases of human cancer and normal tissues. An insertion or deletion in the alignment of EST/EST was used to identify alternatively spliced transcripts. Alignment of the ESTs with the genomic sequence was further used to confirm AS. Alternatively spliced transcripts in each tissue were then subtractively cross-screened to obtain tissue-specific variants. We systematically identified and characterized cancer/tissue-specific and alternatively spliced variants in the human genome based on a global view. We identified 15,093 cancer-specific variants of 9,989 genes from 27 types of human cancers and 14,376 normal tissue-specific variants of 7,240 genes from 35 normal tissues, which cover the main types of human tumors and normal tissues. Approximately 70% of these transcripts are novel. These data were integrated into a database HCSAS (http://202.114.72.39/database/human.html, pass:68756253). Moreover, we observed that the cancer-specific AS of both oncogenes and tumor suppressor genes are associated with specific cancer types. Cancer shows a preference in the selection of alternative splice-sites and utilization of alternative splicing types. CONCLUSIONS/SIGNIFICANCE: These features of human cancer, together with the discovery of huge numbers of novel splice forms for cancer-associated genes, suggest an important and global role of cancer-specific AS during human tumorigenesis. We advise the use of cancer-specific alternative splicing as a potential source of new diagnostic, prognostic, predictive, and therapeutic tools for human cancer. The global view of cancer-specific AS is not only useful for exploring the complexity of the cancer transcriptome but also widens the eyeshot of clinical research

DNA Demethylation and USF Regulate the Meiosis-Specific Expression of the Mouse Miwi

Miwi, a member of the Argonaute family, is required for initiating spermiogenesis; however, the mechanisms that regulate the expression of the Miwi gene remain unknown. By mutation analysis and transgenic models, we identified a 303 bp proximal promoter region of the mouse Miwi gene, which controls specific expression from midpachytene spermatocytes to round spermatids during meiosis. We characterized the binding sites of transcription factors NF-Y (Nuclear Factor Y) and USF (Upstream Stimulatory Factor) within the core promoter and found that both factors specifically bind to and activate the Miwi promoter. Methylation profiling of three CpG islands within the proximal promoter reveals a markedly inverse correlation between the methylation status of the CpG islands and germ cell type–specific expression of Miwi. CpG methylation at the USF–binding site within the E2 box in the promoter inhibits the binding of USF. Transgenic Miwi-EGFP and endogenous Miwi reveal a subcellular co-localization pattern in the germ cells of the Miwi-EGFP transgenic mouse. Furthermore, the DNA methylation profile of the Miwi promoter–driven transgene is consistent with that of the endogenous Miwi promoter, indicating that Miwi transgene is epigenetically modified through methylation in vivo to ensure its spatio-temporal expression. Our findings suggest that USF controls Miwi expression from midpachytene spermatocytes to round spermatids through methylation-mediated regulation. This work identifies an epigenetic regulation mechanism for the spatio-temporal expression of mouse Miwi during spermatogenesis

Chromosomal mapping, differential origin and evolution of the S100 gene family

S100 proteins are calcium-binding proteins, which exist only in vertebrates and which constitute a large protein family. The origin and evolution of the S100 family in vertebrate lineages remain a challenge. Here, we examined the synteny conservation of mammalian S100A genes by analysing the sequence of available vertebrate S100 genes in databases. Five S100A gene members, unknown previously, were identified by chromosome mapping analysis. Mammalian S100A genes are duplicated and clustered on a single chromosome while two S100A gene clusters are found on separate chromosomes in teleost fish, suggesting that S100A genes existed in fish before the fish-specific genome duplication took place. During speciation, tandem gene duplication events within the cluster of S100A genes of a given chromosome have probably led to the multiple members of the S100A gene family. These duplicated genes have been retained in the genome either by neofunctionalisation and/or subfunctionalisation or have evolved into non-coding sequences. However in vertebrate genomes, other S100 genes are also present i.e. S100P, S100B, S100G and S100Z, which exist as single copy genes distributed on different chromosomes, suggesting that they could have evolved from an ancestor different to that of the S100A genes

Can Digital Finance Promote Comprehensive Carbon Emission Performance? Evidence from Chinese Cities

Improving urban comprehensive carbon emission performance (CCEP) is the inevitable choice for China’s low-carbon development. With the continuous integration of digital technology and financial elements, the development of urban digital finance has also been significantly improved. To further explore the impact of urban digital finance on urban low-carbon development, using the data of 281 cities in China from 2011 to 2019, this paper firstly evaluates the urban CCEP, and further empirically investigates how digital finance influences CCEP. The empirical results show that: (1) Digital finance significantly improves the urban CCEP, and after conducting robustness tests and addressing the endogeneity issue, the above conclusion is robust. (2) For the sub-indicators, there is a U-shaped relationship between the coverage breadth of digital finance and CCEP. Moreover, the improvement of usage depth and digital support services could promote CCEP. (3) The channel tests indicate that digital finance improves the CCEP mainly by promoting green technology innovation and the development of urban tertiary industry. Meantime, digital finance has a stronger impact on improving CCEP in cities with more developed traditional finance, and the positive effect is significant in non-old industrial base cities and a two-control zone. Finally, this paper puts forward relevant policy suggestions