Gene duplication and subsequent diversification strongly affect phenotypic evolvability and robustness.

We study the effects of non-determinism and gene duplication on the structure of genotype-phenotype (GP) maps by introducing a non-deterministic version of the Polyomino self-assembly model. This model has previously been used in a variety of contexts to model the assembly and evolution of protein quaternary structure. Firstly, we show the limit of the current deterministic paradigm which leads to built-in anti-correlation between evolvability and robustness at the genotypic level. We develop a set of metrics to measure structural properties of GP maps in a non-deterministic setting and use them to evaluate the effects of gene duplication and subsequent diversification. Our generalized versions of evolvability and robustness exhibit positive correlation for a subset of genotypes. This positive correlation is only possible because non-deterministic phenotypes can contribute to both robustness and evolvability. Secondly, we show that duplication increases robustness and reduces evolvability initially, but that the subsequent diversification that duplication enables has a stronger, inverse effect, greatly increasing evolvability and reducing robustness relative to their original values

Volkov-Pankratov states in topological heterojunctions

We show that a smooth interface between two insulators of opposite topological Z2 indices possesses multiple surface states, both massless and massive. While the massless surface state is non-degenerate, chiral and insensitive to the interface potential, the massive surface states only appear for a sufficiently smooth heterojunction. The surface states are particle-hole symmetric and a voltage drop reveals their intrinsic relativistic nature, similarly to Landau bands of Dirac electrons in a magnetic field. We discuss the relevance of the massive Dirac surface states in recent ARPES and transport experiments

Gene duplication and subsequent diversification strongly affect phenotypic evolvability and robustness

We study the effects of non-determinism and gene duplication on the structure of genotype–phenotype (GP) maps by introducing a non-deterministic version of the Polyomino self-assembly model. This model has previously been used in a variety of contexts to model the assembly and evolution of protein quaternary structure. Firstly, we show the limit of the current deterministic paradigm which leads to built-in anti-correlation between evolvability and robustness at the genotypic level. We develop a set of metrics to measure structural properties of GP maps in a non-deterministic setting and use them to evaluate the effects of gene duplication and subsequent diversification. Our generalized versions of evolvability and robustness exhibit positive correlation for a subset of genotypes. This positive correlation is only possible because non-deterministic phenotypes can contribute to both robustness and evolvability. Secondly, we show that duplication increases robustness and reduces evolvability initially, but that the subsequent diversification that duplication enables has a stronger, inverse effect, greatly increasing evolvability and reducing robustness relative to their original values

Gene duplication and subsequent diversification strongly affect phenotypic evolvability and robustness

We study the effects of non-determinism and gene duplication on the structure of genotype–phenotype (GP) maps by introducing a non-deterministic version of the Polyomino self-assembly model. This model has previously been used in a variety of contexts to model the assembly and evolution of protein quaternary structure. Firstly, we show the limit of the current deterministic paradigm which leads to built-in anti-correlation between evolvability and robustness at the genotypic level. We develop a set of metrics to measure structural properties of GP maps in a non-deterministic setting and use them to evaluate the effects of gene duplication and subsequent diversification. Our generalized versions of evolvability and robustness exhibit positive correlation for a subset of genotypes. This positive correlation is only possible because non-deterministic phenotypes can contribute to both robustness and evolvability. Secondly, we show that duplication increases robustness and reduces evolvability initially, but that the subsequent diversification that duplication enables has a stronger, inverse effect, greatly increasing evolvability and reducing robustness relative to their original values

Synthesis of SWNTs and MWNTs by a molten salt (NaCl) method

International audienceA method to obtain the single-walled and multi-walled carbon nanotubes is presented. It consists of electrolytic conversion of graphite to carbon nanotubes in fused NaCl at 810 degreesC. The experimental conditions are given. The filling of the nanotubes is also possible if elements are added in the salt solution

Distribution and functional characterization of pituitary adenylate cyclase-activating polypeptide receptors in the brain of non-human primates.

International audienceThe distribution and density of pituitary adenylate cyclase-activating polypeptide (PACAP) binding sites have been investigated in the brain of the primates Jacchus callithrix (marmoset) and Macaca fascicularis (macaque) using [(125)I]-PACAP27 as a radioligand. PACAP binding sites were widely expressed in the brain of these two species with particularly high densities in the septum, hypothalamus and habenula. A moderate density of recognition sites was seen in all subdivisions of the cerebral cortex with a heterogenous distribution, the highest concentrations occurring in layers I and VI while the underlying white matter was almost devoid of binding sites. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed intense expression of the mRNAs encoding the short and hop-1 variants of pituitary adenylate cyclase-activating polypeptide-specific receptor (PAC1-R) in the cortex of both marmoset and macaque, whereas vasoactive intestinal polypeptide/pituitary adenylate cyclase-activating polypeptide mutual receptor, subtype 1 (VPAC1-R) and vasoactive intestinal polypeptide/pituitary adenylate cyclase-activating polypeptide mutual receptor, subtype 2 (VPAC2-R) mRNAs were expressed at a much lower level. In situ hybridization histochemistry showed intense expression of PAC1-R and weak expression of VPAC1-R mRNAs in layer IV of the cerebral cortex. Incubation of cortical tissue slices with PACAP induced a dose-dependent stimulation of cyclic AMP formation, indicating that PACAP binding sites correspond to functional receptors. Moreover, treatment of primate cortical slices with 100 nM PACAP significantly reduced the activity of caspase-3, a key enzyme of the apoptotic cascade. The present results indicate that PACAP should exert the same neuroprotective effect in the brain of primates as in rodents and suggest that PAC1-R agonists may have a therapeutic value to prevent neuronal cell death after stroke or in specific neurodegenerative diseases