In this week's PNAS Early Edition, a team led by investigators at Cardiff University shows that "combining disease 'risk' variants in add-back assays yielded six-fold higher hemolytic activity compared with 'protective' variants" in their investigations of age-related macular degeneration. The team says its results "introduce the concept of a functional complotype — combination of polymorphisms — defining complement activity in an individual, thereby influencing susceptibility to AP [alternative pathway]-driven disease."
An international team led by researchers at the University of California, San Diego, this week reports "genomic insights into the physiology and ecology of the marine filamentous cyanobacterium Lyngbya majuscula." Using a combination of Sanger and 454 approaches, the team sequenced the genome of a Caribbean strain of L. majuscula; in its comparative analysis, the researchers report on a "large suite of Lyngbya metabolites" that they say could be "strain specific and may be useful in species delineation."
Investigators at the University of North Carolina at Chapel Hill along with their international colleagues show that, when compared with mice heterozygous for the Akita diabetogenic mutation and those homozygous for the D257A mutation in mitochondrial DNA polymerase gamma, male mice with both mutations show a decrease in symptoms of diabetes as they aged to 9 months. Male mice with both mutations also show a decrease in food intake, met with an increase in plasma leptin and a decrease plasma ghrelin, as well as a reduction in hypothalamic expression of the orexic gene, neuropeptide Y, and an increase in expression of the anorexic gene, proopiomelanocortin. In its PNAS paper, the Chapel Hill-led team traces the root of reduced diabetic symptoms of these particular mice to "appetite suppression triggered by decreased testosterone associated with damage to the Leydig cells of the testis."
Julius Lucks and his colleagues at the University of California, Berkeley, present "versatile RNA-sensing transcriptional regulators for engineering genetic networks." Lucks et al. describe in PNAS how they overcame the requirement that proteins propagate regulatory signals in intracellular networks and expanded "the RNA synthetic biology toolkit by engineering three unique features of the plasmid pT181 antisense-RNA-mediated transcription attenuation mechanism." Taken together, the Berkeley team says that when applied within a single RNA-based regulatory mechanism, these three features have "the potential to simplify the design and construction of genetic networks by directly propagating signals as RNA molecules."