Stratigraphic architecture of the Neoproterozoic glacial rocks in the “Xiang-Qian-Gui” region of the central Yangtze Block, South China

Recently ,theinterestinglowlatitudeandlowaltitudeSnowballEarthhypothesis[1,2 ] iswidelyreco gnized ,and greatlystimulatingthestudyoftheNeoproterozoicglaciations ,whichmaybecloselyre latedtothewell knownEarlyCambrianbio radiationevent.By 1980 ,theNeoproterozoicglaciationinSouthChinaisbelievedtobedividedintotwoglaciationsandoneinterglaciation[3～ 5] ,namely ,theearlyChang’anGlaciation ,lateNantuoGlaciationandFu luInterglaciation .However ,thereweredifferentwaysofcorrelation ,themostobvious…     

DNA sequence of human chromosome 17 and analysis of rearrangement in the human lineage

Chromosome 17 is unusual among the human chromosomes in many respects. It is the largest human autosome with orthology to only a single mouse chromosome, mapping entirely to the distal half of mouse chromosome 11. Chromosome 17 is rich in protein-coding genes, having the second highest gene density in the genome. It is also enriched in segmental duplications, ranking third in density among the autosomes. Here we report a finished sequence for human chromosome 17, as well as a structural comparison with the finished sequence for mouse chromosome 11, the first finished mouse chromosome. Comparison of the orthologous regions reveals striking differences. In contrast to the typical pattern seen in mammalian evolution, the human sequence has undergone extensive intrachromosomal rearrangement, whereas the mouse sequence has been remarkably stable. Moreover, although the human sequence has a high density of segmental duplication, the mouse sequence has a very low density. Notably, these segmental duplications correspond closely to the sites of structural rearrangement, demonstrating a link between duplication and rearrangement. Examination of the main classes of duplicated segments provides insight into the dynamics underlying expansion of chromosome-specific, low-copy repeats in the human genome.     

Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cells

Double-strand breaks occur during DNA replication and are also induced by ionizing radiation. There are at least two pathways which can repair such breaks: non-homologous end joining and homologous recombination (HR). Although these pathways are essentially independent of one another, it is possible that the proteins Mre11, Rad50 and Xrs2 are involved in both pathways in Saccharomyces cerevisiae. In vertebrate cells, little is known about the exact function of the Mre11-Rad50-Nbs1 complex in the repair of double-strand breaks because Mre11- and Rad50-null mutations are lethal. Here we show that Nbs1 is essential for HR-mediated repair in higher vertebrate cells. The disruption of Nbs1 reduces gene conversion and sister chromatid exchanges, similar to other HR-deficient mutants. In fact, a site-specific double-strand break repair assay showed a notable reduction of HR events following generation of such breaks in Nbs1-disrupted cells. The rare recombinants observed in the Nbs1-disrupted cells were frequently found to have aberrant structures, which possibly arise from unusual crossover events, suggesting that the Nbs1 complex might be required to process recombination intermediates.     

Apolipoprotein L-I is the trypanosome lytic factor of human serum

Human sleeping sickness in east Africa is caused by the parasite Trypanosoma brucei rhodesiense. The basis of this pathology is the resistance of these parasites to lysis by normal human serum (NHS). Resistance to NHS is conferred by a gene that encodes a truncated form of the variant surface glycoprotein termed serum resistance associated protein (SRA). We show that SRA is a lysosomal protein, and that the amino-terminal alpha-helix of SRA is responsible for resistance to NHS. This domain interacts strongly with a carboxy-terminal alpha-helix of the human-specific serum protein apolipoprotein L-I (apoL-I). Depleting NHS of apoL-I, by incubation with SRA or anti-apoL-I, led to the complete loss of trypanolytic activity. Addition of native or recombinant apoL-I either to apoL-I-depleted NHS or to fetal calf serum induced lysis of NHS-sensitive, but not NHS-resistant, trypanosomes. Confocal microscopy demonstrated that apoL-I is taken up through the endocytic pathway into the lysosome. We propose that apoL-I is the trypanosome lytic factor of NHS, and that SRA confers resistance to lysis by interaction with apoL-I in the lysosome.     

Chlorpyrifos (Dursban®) resistance inCulex pipiens pipiens L. from Southern France: Inheritance and linkage

Summary InCulex pipiens mosquitos from Southern France, resistance to the organophosphorus insecticide chlorpyrifos is due to the dominant allele (Chl ^R) of an autosomal gene. TheChl gene is localized between thea-Gpd andEst-2 loci at 26.8 and 5.8 units of crossing-over respectively.     

Perlecan, the major proteoglycan of basement membranes, is altered in patients with Schwartz-Jampel syndrome (chondrodystrophic myotonia)

Schwartz-Jampel syndrome (SJS1) is a rare autosomal recessive disorder characterized by permanent myotonia (prolonged failure of muscle relaxation) and skeletal dysplasia, resulting in reduced stature, kyphoscoliosis, bowing of the diaphyses and irregular epiphyses. Electromyographic investigations reveal repetitive muscle discharges, which may originate from both neurogenic and myogenic alterations. We previously localized the SJS1 locus to chromosome 1p34-p36.1 and found no evidence of genetic heterogeneity. Here we describe mutations, including missense and splicing mutations, of the gene encoding perlecan (HSPG2) in three SJS1 families. In so doing, we have identified the first human mutations in HSPG2, which underscore the importance of perlecan not only in maintaining cartilage integrity but also in regulating muscle excitability.     

A belt of moonlets in Saturn's A ring

The origin and evolution of planetary rings is one of the prominent unsolved problems of planetary sciences, with direct implications for planet-forming processes in pre-planetary disks. The recent detection of four propeller-shaped features in Saturn's A ring proved the presence of large boulder-sized moonlets in the rings. Their existence favours ring creation in a catastrophic disruption of an icy satellite rather than a co-genetic origin with Saturn, because bodies of this size are unlikely to have accreted inside the rings. Here we report the detection of eight new propeller features in an image sequence that covers the complete A ring, indicating embedded moonlets with radii between 30 m and 70 m. We show that the moonlets found are concentrated in a narrow 3,000-km-wide annulus 130,000 km from Saturn. Compared to the main population of ring particles (radius s < 10 m), such embedded moonlets have a short lifetime with respect to meteoroid impacts. Therefore, they are probably the remnants of a shattered ring-moon of Pan size or larger, locally contributing new material to the older ring. This supports the theory of catastrophic ring creation in a collisional cascade.