Long-term increases in clutch size in common snapping turtles (Chelydra serpentina) and diamondback terrapins (Malaclemys terrapin)

Clutch size (CS) is a well-studied life history characteristic, and optimal egg size theory predicts that CS should correlate positively with reproductive investment. Turtles are good subjects for studies of reproductive strategies because few turtle species exhibit parental care; therefore quantifying their short-term reproductive investment is mostly limited to measuring egg size and number. Clutch size is usually reported as an average value for each turtle population, and where CS variation is noted, it is usually attributable to variation in adult body size. In two long-term studies of ecologically dissimilar species we detected a dramatic increase in CS in a common snapping turtle (Chelydra serpentina) population and in a diamondback terrapin (Malaclemys terrapin) population. It is unknown whether these changes are due to either variation in adult body size or resource availability; but the temporal patterns we observed have apparently never been reported previously. These trends remain unexplained and should be explored further.     

Conflict Pattern Analysis: Preparing the Ground for Participation in Policy Implementation

The participation of non-state actors in implementation processes is often understood as a means to increase compliance efficiency. But the implementation of spatial policies frequently focuses on pre-established goals, processes and instruments and thus renders difficult open discourse and shared decision-making. This paper introduces conflict pattern analysis (CPA) as a tool that supports the analysis of the actual actor constellation in order to define efficient approaches that avoid common problems of participatory processes. CPA is a semi-formalised method that helps to identify key-actors, their relations and interaction amongst each other as well as their core beliefs, interests and resources. It aggregates this information to interaction patterns that can be compared, classified and linked to different participatory methods on a theoretically informed basis. Particularly on the local and regional level, this could be the first step for successful (participatory) implementation strategies.     

Genomic surveys by methylation-sensitive SNP analysis identify sequence-dependent allele-specific DNA methylation

Allele-specific DNA methylation (ASM) is a hallmark of imprinted genes, but ASM in the larger nonimprinted fraction of the genome is less well characterized. Using methylation-sensitive SNP analysis (MSNP), we surveyed the human genome at 50K and 250K resolution, identifying ASM as recurrent genotype call conversions from heterozygosity to homozygosity when genomic DNAs were predigested with the methylation-sensitive restriction enzyme HpaII. Using independent assays, we confirmed ASM at 16 SNP-tagged loci distributed across various chromosomes. At 12 of these loci (75%), the ASM tracked strongly with the sequence of adjacent SNPs. Further analysis showed allele-specific mRNA expression at two loci from this methylation-based screen--the vanin and CYP2A6-CYP2A7 gene clusters--both implicated in traits of medical importance. This recurrent phenomenon of sequence-dependent ASM has practical implications for mapping and interpreting associations of noncoding SNPs and haplotypes with human phenotypes.     

The interaction of angiotensin with a binding factor in plasma

Résumé La liaison de l'angiotensine par les protéines plasmatiques est démontrée par dialyse équilibrée. L'angiotensine radioactive liée ne put être déplacée par l'angiotensine non radioactive, ce qui diminue la signification physiologique de cette liaison.

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Supported in part by the Michigan Heart Association.     

The knockout mouse project

Mouse knockout technology provides a powerful means of elucidating gene function in vivo, and a publicly available genome-wide collection of mouse knockouts would be significantly enabling for biomedical discovery. To date, published knockouts exist for only about 10% of mouse genes. Furthermore, many of these are limited in utility because they have not been made or phenotyped in standardized ways, and many are not freely available to researchers. It is time to harness new technologies and efficiencies of production to mount a high-throughput international effort to produce and phenotype knockouts for all mouse genes, and place these resources into the public domain.     

A gene expression atlas of the central nervous system based on bacterial artificial chromosomes

The mammalian central nervous system (CNS) contains a remarkable array of neural cells, each with a complex pattern of connections that together generate perceptions and higher brain functions. Here we describe a large-scale screen to create an atlas of CNS gene expression at the cellular level, and to provide a library of verified bacterial artificial chromosome (BAC) vectors and transgenic mouse lines that offer experimental access to CNS regions, cell classes and pathways. We illustrate the use of this atlas to derive novel insights into gene function in neural cells, and into principal steps of CNS development. The atlas, library of BAC vectors and BAC transgenic mice generated in this screen provide a rich resource that allows a broad array of investigations not previously available to the neuroscience community.     

Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect

Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor. Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 x 10(-6)) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes. Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease (P = 1.55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier.