Large electronic bandwidth in solution-processable pyrene crystals: The role of close-packed crystal structure

We examine the interdependence of structural and electronic properties of two substituted pyrene crystals by means of combined spectroscopic probes and density-functional theory calculations. One derivative features n-hexyl side groups, while the other one contains branched silanyl groups. Both derivatives form triclinic crystal structures when grown from solution, but the electronic dispersion behavior is significantly different due to differences in $\pi$-$\pi$ overlap along the $a$ crystal axis. Both systems display dispersion of 0.40-0.45 eV in the valence band, suggesting a high intrinsic hole mobility. However, the dispersion is primarily along the a-axis in the silanyl-substituted derivative, but less aligned with this crystal axis in the hexyl-substituted material. This is a direct consequence of the diferences in co-facial $\pi$ electron overlap revealed by the crystallographic studies. We find that photophysical defects, ascribed to excimer-like states, point to the importance of localized trap states. Substituted pyrenes are useful model systems to unravel the interplay of crystal structure and electronic properties in organic semiconductors.Comment: 25 pages, 8 figure

The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome

<p>Abstract</p> <p>Background</p> <p>Pseudoautosomal regions (PAR1 and PAR2) in eutherians retain homologous regions between the X and Y chromosomes that play a critical role in the obligatory X-Y crossover during male meiosis. Genes that reside in the PAR1 are exceptional in that they are rich in repetitive sequences and undergo a very high rate of recombination. Remarkably, murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome.</p> <p>Results</p> <p>We now report that the SNF2-type chromatin remodeling protein ATRX controls the expression of eutherian ancestral PAR1 genes that have translocated to autosomes in the mouse. In addition, we have identified two potentially novel mouse PAR1 orthologs.</p> <p>Conclusion</p> <p>We propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression.</p

Genome-wide location analysis and expression studies reveal a role for p110 CUX1 in the activation of DNA replication genes

Proteolytic processing of the CUX1 transcription factor generates an isoform, p110 that accelerates entry into S phase. To identify targets of p110 CUX1 that are involved in cell cycle progression, we performed genome-wide location analysis using a promoter microarray. Since there are no antibodies that specifically recognize p110, but not the full-length protein, we expressed physiological levels of a p110 isoform with two tags and purified chromatin by tandem affinity purification (ChAP). Conventional ChIP performed on synchronized populations of cells confirmed that p110 CUX1 is recruited to the promoter of cell cycle-related targets preferentially during S phase. Multiple approaches including silencing RNA (siRNA), transient infection with retroviral vectors, constitutive expression and reporter assays demonstrated that most cell cycle targets are activated whereas a few are repressed or not affected by p110 CUX1. Functional classes that were over-represented among targets included DNA replication initiation. Consistent with this finding, constitutive expression of p110 CUX1 led to a premature and more robust induction of replication genes during cell cycle progression, and stimulated the long-term replication of a plasmid bearing the oriP replicator of Epstein Barr virus (EBV).The pc3oriPE plasmid and helpful advices were kindly provided by Dr Lori Frappier. A.N. is the recipient of a scholarship from the Fonds de la Recherche en Sante´ du Québec. C.V. is the recipient of a studentship from the McGill University Cancer Consortium Training Grant in Cancer Research (sponsored by CIHR). F.R. holds a new investigator award from the CIHR. This research was supported by grant No. 014288 from the Canadian Cancer Society to A.N. and a grant from Genome Canada/ Génome Québec to F.R and A.N. Funding to pay the Open Access publication charges for this article was provided by grant No. 014288 from the Canadian Cancer Society to A.N

Effects of a healthy meal course on spontaneous energy intake, satiety and palatability

Many food components can influence satiety or energy intake. Combined together, these food components could represent an interesting dietary strategy in the prevention and treatment of obesity. The aims of this study were: 1) to determine the effect of a functional food in the form of a healthy meal course on subsequent energy intake and satiety; 2) to verify if it is possible to maintain palatability while preserving the satiating effects of the test meal. Thirteen subjects were invited to eat two lunch sessions: healthy and control meal courses (2090 kJ/meal). Anthropometric and ad libitum food intake measurements, and visual analogue scales (VAS) were performed during the two lunch sessions. The healthy main course acutely decreased energy intake during the rest of the meal ( − 744 kJ, P ≤ 0·0001) and lipid ( − 6 %, P ≤ 0·0001) compared with the control meal. VAS ratings during the course of the testing showed a meal effect for hunger, desire to eat and prospective food consumption (P ≤ 0·05) and a time effect for all appetite sensations (P ≤ 0·0001). VAS scores on hunger ratings were lower for the healthy meal (P ≤ 0·05), whereas fullness ratings were higher shortly after the healthy main course (P ≤ 0·05). The healthy meal produced a slightly higher palatability rating but this effect was not statistically significant. These results suggest that it is possible to design a healthy meal that decreases spontaneous energy intake and hunger without compromising palatability

A first record of Pestalotiopsis clavispora in Argan mass cutting propagation: Prevalence, prevention and consequences for plant production

A trial involving the mass propagation of Argania spinosa cuttings was established following two protocols: in mini-bouturathèques without mist and in a greenhouse under mist. Symptoms of petiole necrosis, foliar yellowing and abundant black acervuli were observed under both protocols. These symptoms were responsible for a 90% mortality rate in the mini-bouturathèques while under the mist treatment premature fatal necrosis of the apical buds resulted in 100% mortality. The disease’s causal agent, Pestalotiopsis clavispora, was identified on the basis of its morphological characteristics and by molecular analysis. Alternating weekly treatments of systemic and contact fungicides resulted in a 41% success rate in controlling this pathogen, described for the first time on argan cuttings.Deux approches différentes de bouturage de masse d’Argania spinosa ont été utilisées. La première consistait à enraciner les boutures dans des mini-bouturathèques sans brumisation, tandis que la deuxième consistait à utiliser une serre dotée d’un brumisateur. Des symptômes de nécrose des pétioles et de jaunissement des feuilles ainsi qu’une production abondante d’acervules noires ont été observés dans les deux protocoles. Dans les mini-bouturathèques, ces symptômes ont entraîné un taux de mortalité de 90 % des boutures, alors que sous brumisateur la nécrose précoce et fatale des bourgeons apicaux a engendré 100 % de mortalité. L’agent causal de la maladie, Pestalotiopsis clavispora, décrit pour la première fois sur les boutures d’arganier, a été identifié à partir de ses caractères morphologiques et par analyse moléculaire. Un traitement hebdomadaire à base de fongicide systémique et de fongicide de contact utilisés en alternance a permis de maîtriser cet agent pathogène avec un taux de réussite de 41 %

Loss of ATRX in Chondrocytes Has Minimal Effects on Skeletal Development

BACKGROUND:Mutations in the human ATRX gene cause developmental defects, including skeletal deformities and dwarfism. ATRX encodes a chromatin remodeling protein, however the role of ATRX in skeletal development is currently unknown. METHODOLOGY/PRINCIPAL FINDINGS:We induced Atrx deletion in mouse cartilage using the Cre-loxP system, with Cre expression driven by the collagen II (Col2a1) promoter. Growth rate, body size and weight, and long bone length did not differ in Atrx(Col2cre) mice compared to control littermates. Histological analyses of the growth plate did not reveal any differences between control and mutant mice. Expression patterns of Sox9, a transcription factor required for cartilage morphogenesis, and p57, a marker of cell cycle arrest and hypertrophic chondrocyte differentiation, was unaffected. However, loss of ATRX in cartilage led to a delay in the ossification of the hips in some mice. We also observed hindlimb polydactily in one out of 61 mutants. CONCLUSIONS/SIGNIFICANCE:These findings indicate that ATRX is not directly required for development or growth of cartilage in the mouse, suggesting that the short stature in ATR-X patients is caused by defects in cartilage-extrinsic mechanisms