Selection overrides gene flow to break down maladaptive mimicry

Predators typically avoid dangerous species, and batesian mimicry evolves when a palatable species (the 'mimic') co-opts a warning signal from a dangerous species (the 'model') and thereby deceives its potential predators. Because predators would not be under selection to avoid the model and any of its look-alikes in areas where the model is absent (that is, allopatry), batesian mimics should occur only in sympatry with their model. However, contrary to this expectation, batesian mimics often occur in allopatry. Here we focus on one such example--a coral snake mimic. Using indirect DNA-based methods, we provide evidence suggesting that mimics migrate from sympatry, where mimicry is favoured, to allopatry, where it is disfavoured. Such gene flow is much stronger in nuclear genes than in maternally inherited mitochondrial genes, indicating that dispersal by males may explain the presence of mimetic phenotypes in allopatry. Despite this gene flow, however, individuals from allopatry resemble the model less than do individuals from sympatry. We show that this breakdown of mimicry probably reflects predator-mediated selection acting against individuals expressing the more conspicuous mimetic phenotype in allopatry. Thus, although gene flow may explain why batesian mimics occur in allopatry, natural selection may often override such gene flow and promote the evolution of non-mimetic phenotypes in such areas.     

Amygdala intercalated neurons are required for expression of fear extinction

Congruent findings from studies of fear learning in animals and humans indicate that research on the circuits mediating fear constitutes our best hope of understanding human anxiety disorders. In mammals, repeated presentations of a conditioned stimulus that was previously paired to a noxious stimulus leads to the gradual disappearance of conditioned fear responses. Although much evidence suggests that this extinction process depends on plastic events in the amygdala, the underlying mechanisms remain unclear. Intercalated (ITC) amygdala neurons constitute probable mediators of extinction because they receive information about the conditioned stimulus from the basolateral amygdala (BLA), and contribute inhibitory projections to the central nucleus (CEA), the main output station of the amygdala for conditioned fear responses. Thus, after extinction training, ITC cells could reduce the impact of conditioned-stimulus-related BLA inputs to the CEA by means of feed-forward inhibition. Here we test the hypothesis that ITC neurons mediate extinction by lesioning them with a toxin that selectively targets cells expressing micro-opioid receptors (microORs). Electron microscopic observations revealed that the incidence of microOR-immunoreactive synapses is much higher in ITC cell clusters than in the BLA or CEA and that microORs typically have a post-synaptic location in ITC cells. In keeping with this, bilateral infusions of the microOR agonist dermorphin conjugated to the toxin saporin in the vicinity of ITC neurons caused a 34% reduction in the number of ITC cells but no significant cell loss in surrounding nuclei. Moreover, ITC lesions caused a marked deficit in the expression of extinction that correlated negatively with the number of surviving ITC neurons but not CEA cells. Because ITC cells exhibit an unusual pattern of receptor expression, these findings open new avenues for the treatment of anxiety disorders.     

DNA-programmable nanoparticle crystallization

It was first shown more than ten years ago that DNA oligonucleotides can be attached to gold nanoparticles rationally to direct the formation of larger assemblies. Since then, oligonucleotide-functionalized nanoparticles have been developed into powerful diagnostic tools for nucleic acids and proteins, and into intracellular probes and gene regulators. In contrast, the conceptually simple yet powerful idea that functionalized nanoparticles might serve as basic building blocks that can be rationally assembled through programmable base-pairing interactions into highly ordered macroscopic materials remains poorly developed. So far, the approach has mainly resulted in polymerization, with modest control over the placement of, the periodicity in, and the distance between particles within the assembled material. That is, most of the materials obtained thus far are best classified as amorphous polymers, although a few examples of colloidal crystal formation exist. Here, we demonstrate that DNA can be used to control the crystallization of nanoparticle-oligonucleotide conjugates to the extent that different DNA sequences guide the assembly of the same type of inorganic nanoparticle into different crystalline states. We show that the choice of DNA sequences attached to the nanoparticle building blocks, the DNA linking molecules and the absence or presence of a non-bonding single-base flexor can be adjusted so that gold nanoparticles assemble into micrometre-sized face-centred-cubic or body-centred-cubic crystal structures. Our findings thus clearly demonstrate that synthetically programmable colloidal crystallization is possible, and that a single-component system can be directed to form different structures.     

Carbon nanotube and conducting polymer composites for supercapacitors

Composites of carbon nanotubes and conducting polymers can be prepared via chemical synthesis, electrochemical deposition on preformed carbon nanotube electrodes, or by electrochemical co-deposition. The composites combine the large pseudocapacitance of the conducting polymers with the fast charging/discharging double-layer capacitance and excellent mechanical properties of the carbon nanotubes. The electrochemically co-deposited composites are the most homogeneous and show an unusual interaction between the polymer and nanotubes, giving rise to a strengthened electron delocalisation and conjugation along the polymer chains. As a result they exhibit excellent electrochemical charge storage properties and fast charge/discharge switching, making them promising electrode materials for high Dower suDercapacitors.     

基于分子瓦自组装的DNA纳米管的制备与表征

利用DNA分子自组装技术可以构建从一维到三维不同形状的纳米结构,并且这些结构在微纳米电子学、纳米生物学等众多领域有许多潜在的用途.本文利用DNA分子瓦(tile)自组装技术,采用双交叉(DX)DNA分子瓦成功组装了一维DNA纳米管结构,聚丙烯酰胺凝胶电泳(native-PAGE)、透射电子显微镜(TEM)、荧光显微镜和原子力显微镜(AFM)对制得的DNA纳米管结构进行了表征,结果表明,组装成功的DNA纳米管直径在7～20nm之间,长度最长可以达到50μm以上.为了结构更加稳定,对分子瓦中每条DNA单链的5′末端进行磷酸化处理,自组装完成后利用T4DNA连接酶连接磷酸化修饰的DNA纳米管的缺口.AFM结果显示,使用T4DNA连接酶处理后的DNA纳米管更能保持完好的管状结构,表明连接处理后的DNA纳米管更加坚固,促进了DNA纳米管应用于微纳米领域的研究.     

退火时间对二维DNA晶体自组装的影响

DNA自组装的过程,不仅需要合适的缓冲液,还需要适当的退火时间.本文利用DNA自组装技术,以反向平行双交叉(double-crossover,DX)DNA分子瓦(DNAtile)作为建筑模块,带有互补黏性末端(sticky-ends)的分子瓦依据Watson-Crick碱基互补配对原则配对连接,成功制备出二维晶体结构.比较不同退火时间下形成的DNA分子瓦结构,采用非变性聚丙烯酰胺凝胶电泳(non-denaturing PAGE)表征.结果表明,退火时间为2.5h时形成的分子瓦的结构较稳定.等量混合此条件下形成的不同分子瓦,分别从50,37和25℃退火至室温,利用原子力显微镜(AFM)对退火后的结构进行表征,结果表明,起始退火温度为37℃时得到的DNA二维晶体较平整.     

颗粒间作用力影响颗粒体系流变性能的研究进展

悬浮颗粒体系在许多工业中都能见到踪影, 比如矿物加工、水和废水处理、陶瓷加工、造纸、食品加工工业等. 对于胶体颗粒悬浮体系, 颗粒间的相互作用力是控制体系的剪切流变性能、密实化性能和沉积性能的关键因素^[1,2]. 当颗粒间的作用力为排斥力时(排斥性颗粒体系), 颗粒不易“抱团”, 颗粒体系在溶液中处于稳定的分散状态. 而由于布朗热运动的作用, 颗粒的沉降速度很小. 不过, 对于这样的体系, 一旦颗粒最终都沉降下来形成颗粒网络就很密实; 而且即使在较低的外压下被压缩, 沉积层也很容易达到较高的固体体积比率(含水量少). 排斥性颗粒体系的黏度很低, 剪切流变抗力很小. 反之, 如果颗粒间的作用力是吸引力(吸引性颗粒体系), 颗粒就极易形成团块. 团块一般包含很多单个颗粒, 质量较大, 因此团块的沉降速度比单个颗粒快得多. 由此形成的颗粒网络的性质完全与排斥性颗粒体系相反: 它的密度低、含水量高, 需要更高的外压力才能密实化; 而且颗粒网络的黏度高, 剪切流变抗力较高^[3].     

A nuclear Argonaute promotes multigenerational epigenetic inheritance and germline immortality

Epigenetic information is frequently erased near the start of each new generation. In some cases, however, epigenetic information can be transmitted from parent to progeny (multigenerational epigenetic inheritance). A particularly notable example of this type of epigenetic inheritance is double-stranded RNA-mediated gene silencing in Caenorhabditis elegans. This RNA-mediated interference (RNAi) can be inherited for more than five generations. To understand this process, here we conduct a genetic screen for nematodes defective in transmitting RNAi silencing signals to future generations. This screen identified the heritable RNAi defective 1 (hrde-1) gene. hrde-1 encodes an Argonaute protein that associates with small interfering RNAs in the germ cells of progeny of animals exposed to double-stranded RNA. In the nuclei of these germ cells, HRDE-1 engages the nuclear RNAi defective pathway to direct the trimethylation of histone H3 at Lys?9 (H3K9me3) at RNAi-targeted genomic loci and promote RNAi inheritance. Under normal growth conditions, HRDE-1 associates with endogenously expressed short interfering RNAs, which direct nuclear gene silencing in germ cells. In hrde-1- or nuclear RNAi-deficient animals, germline silencing is lost over generational time. Concurrently, these animals exhibit steadily worsening defects in gamete formation and function that ultimately lead to sterility. These results establish that the Argonaute protein HRDE-1 directs gene-silencing events in germ-cell nuclei that drive multigenerational RNAi inheritance and promote immortality of the germ-cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to regulate important biological processes.