Was the universal common ancestry proved?

The question of whether or not all life on Earth shares a single common ancestor has been a central problem of evolutionary biology since Darwin. Although the theory of universal common ancestry (UCA) has gathered a compelling list of circumstantial evidence, as given in ref. 2, there has been no attempt to test statistically the UCA hypothesis among the three domains of life (eubacteria, archaebacteria and eukaryotes) by using molecular sequences. Theobald recently challenged this problem with a formal statistical test, and concluded that the UCA hypothesis holds. Although his attempt is the first step towards establishing the UCA theory with a solid statistical basis, we think that the test of Theobald is not sufficient enough to reject the alternative hypothesis of the separate origins of life, despite the Akaike information criterion (AIC) of model selection giving a clear distinction between the competing hypotheses.     

Plasmodium cynomolgi genome sequences provide insight into Plasmodium vivax and the monkey malaria clade

P. cynomolgi, a malaria-causing parasite of Asian Old World monkeys, is the sister taxon of P. vivax, the most prevalent malaria-causing species in humans outside of Africa. Because P. cynomolgi shares many phenotypic, biological and genetic characteristics with P. vivax, we generated draft genome sequences for three P. cynomolgi strains and performed genomic analysis comparing them with the P. vivax genome, as well as with the genome of a third previously sequenced simian parasite, Plasmodium knowlesi. Here, we show that genomes of the monkey malaria clade can be characterized by copy-number variants (CNVs) in multigene families involved in evasion of the human immune system and invasion of host erythrocytes. We identify genome-wide SNPs, microsatellites and CNVs in the P. cynomolgi genome, providing a map of genetic variation that can be used to map parasite traits and study parasite populations. The sequencing of the P. cynomolgi genome is a critical step in developing a model system for P. vivax research and in counteracting the neglect of P. vivax.     

过渡流态下槽道流动间歇性结构PIV实验研究

为了研究槽道湍流与层流过渡流态下流场中的大尺度流动结构,采用粒子图像测速仪对过渡雷诺数下平板槽道内的流场进行了定量测量,捕捉到了高速区域与低速区域相间的瞬时流场,并基于Taylor假设对所测流场进行了重构,从多个瞬时流场中提取出大尺度条纹状结构。结果表明:这种条纹结构与流动方向之间存在一定的夹角,大约为25°～30°;倾斜因子和平坦因子的绝对值随雷诺数的减小而减小,即湍流猝发事件减少,间歇性减弱,流动趋于有序,逐渐向层流转化。从流场及统计量的变化还可以看出:当1 300≤Rem≤1 600时,流场的变化最显著。     

Mechanical twisting of a guest by a photoresponsive host

Molecular analogues of a variety of mechanical devices such as shuttles, brakes, unidirectional rotors and tweezers have been created. But these 'molecular machines' have not yet been used to mechanically manipulate a second molecule in a controlled and reversible manner. Here we show that light-induced scissor-like conformational changes of one molecule can give rise to mechanical twisting of a non-covalently bound guest molecule. To realize this coupling of molecular motions, we use a previously designed system: a ferrocene moiety with an azobenzene strap, each end of which is attached to one of the two cyclopentadienyl rings of the ferrocene unit, acts as a pivot so that photoisomerization of the strap rotates the ferrocene rings relative to each other and thereby also changes the relative position of two 'pedal' moieties attached to the ferrocene rings. We translate this effect into intermolecular coupling of motion by endowing the pedals with binding sites, which allow the host system to form a stable complex with a bidentate rotor molecule. Using circular dichroism spectroscopy, we show that the photoinduced conformational changes of the host are indeed transmitted and induce mechanical twisting of the rotor molecule. This design concept, which significantly extends the successful coupling of motion beyond the intramolecular level seen in synthetic allosteric receptors, might allow for the remote control of molecular events in larger interlocked molecular systems.     

Topical drug rescue strategy and skin protection based on the role of Mc1r in UV-induced tanning

Ultraviolet-light (UV)-induced tanning is defective in numerous 'fair-skinned' individuals, many of whom contain functional disruption of the melanocortin 1 receptor (MC1R). Although this suggested a critical role for the MC1R ligand melanocyte stimulating hormone (MSH) in this response, a genetically controlled system has been lacking in which to determine the precise role of MSH-MC1R. Here we show that ultraviolet light potently induces expression of MSH in keratinocytes, but fails to stimulate pigmentation in the absence of functional MC1R in red/blonde-haired Mc1r(e/e) mice. However, pigmentation could be rescued by topical application of the cyclic AMP agonist forskolin, without the need for ultraviolet light, demonstrating that the pigmentation machinery is available despite the absence of functional MC1R. This chemically induced pigmentation was protective against ultraviolet-light-induced cutaneous DNA damage and tumorigenesis when tested in the cancer-prone, xeroderma-pigmentosum-complementation-group-C-deficient genetic background. These data emphasize the essential role of intercellular MSH signalling in the tanning response, and suggest a clinical strategy for topical small-molecule manipulation of pigmentation.