The use of an enzymatic kit to measure plasma creatinine in the mouse and three other species

Plasma creatinine concentrations were determined in mice, rats, dogs and humans using a kinetic alkaline picrate method and an enzymatic method with a centrifugal analyser. Lower creatinine values were obtained for all four species using the enzymatic method, but the differences between methods were greater for mice and rats. Removal of creatininase from the enzymatic method reagents gave proportionally higher values for non-creatinine chromogens in mice and rats. A single enzymatic method was not specific for creatinine when used for these species.     

Replisome pausing in mutagenesis

E. coli cells containing a temperature-sensitivednaE mutation, in the α-subunit of holoenzyme DNA polymerase III, do not survive at the restrictive temperature. Such cells may survive in the presence of thepcbA1 mutation, an allele of thegyrB gene. Such survival is dependent on an active DNA polymerase I. Evidence indicates that DNA polymerase I interacts directly in the replisome (REP·A). Despite normal survival for cells using thepcbA replication pathway after some type of DNA damage, we have noted a failure of damage-induced mutagenesis. Here we present evidence supporting a model of replisome pausing in cells dependent upon thepcbA replication pathway. The model argues that the (REP·A) complex pauses longer at the site of the lesion, allowing excision repair to occur completely. In the normal replication pathway (REP·E) bypass of the lesion occurs, fixing the mutation.     

Two novel loci underlie natural differences in Caenorhabditis elegans abamectin responses

Parasitic nematodes cause a massive worldwide burden on human health along with a loss of livestock and agriculture productivity. Anthelmintics have been widely successful in treating parasitic nematodes. However, resistance is increasing, and little is known about the molecular and genetic causes of resistance for most of these drugs. The free-living roundworm Caenorhabditis elegans provides a tractable model to identify genes that underlie resistance. Unlike parasitic nematodes, C. elegans is easy to maintain in the laboratory, has a complete and well annotated genome, and has many genetic tools. Using a combination of wild isolates and a panel of recombinant inbred lines constructed from crosses of two genetically and phenotypically divergent strains, we identified three genomic regions on chromosome V that underlie natural differences in response to the macrocyclic lactone (ML) abamectin. One locus was identified previously and encodes an alpha subunit of a glutamate-gated chloride channel (glc-1). Here, we validate and narrow two novel loci using near-isogenic lines. Additionally, we generate a list of prioritized candidate genes identified in C. elegans and in the parasite Haemonchus contortus by comparison of ML resistance loci. These genes could represent previously unidentified resistance genes shared across nematode species and should be evaluated in the future. Our work highlights the advantages of using C. elegans as a model to better understand ML resistance in parasitic nematodes.     

Japanese barberry seed predation by Rhagoletis meigenii fruit flies harboring Wolbachia endosymbionts

The phytophagous fruit fly Rhagoletis meigenii harbors the bacterium Wolbachia pipientis and, together with Japanese barberry, form a tri-partite symbiosis. R. meigenii is a seed predator of invasive Japanese barberry plants and is dependent on this insect-plant interaction for reproductive success. The endosymbiotic bacterium W. pipientis is a reproductive parasite known to alter the sex ratios of offspring and the fitness of infected host insects. We investigated Japanese barberry fruit for the degree of infestation by R. meigenii and characterized the Wolbachia strain infecting R. meigenii. Densities of R. meigenii in four naturalized stands of Japanese barberry revealed low numbers of fruit flies with high variability in the population densities observed among individual plants. Overall, R. meigenii infested roughly 10–20 % of the Japanese barberry fruits analyzed; fruit with two seeds (vs. one seed) were the most frequently infested. Approximately, 90 % of the R. meigenii tested positive for Wolbachia infection via PCR amplification of the Wolbachia surface protein (wsp) gene. No bacterial strain diversity was observed when comparing multi-locus sequence typing (MLST) profiles within or among five R. meigenii populations in Maine, although the MLST profile obtained from R. meigenii differed from three co-occurring Rhagoletis. The Wolbachia endosymbiont of R. meigenii is a member of the Wolbachia supergroup A and the ST-13 cluster complex.     

The Evolution of Resistance to Simian Immunodeficiency Virus (SIV): A Review

Examining how pathogens cross species boundaries, spread within species, and persist within their hosts is an essential part of understanding the factors that underpin the evolution of virulence and host resistance. Here, we review current knowledge about the genetic diversity, molecular epidemiology, prevalence, and pathogenicity of simian immunodeficiency viruses (SIVs). SIVs have crossed species boundaries from simian hosts to humans on at least 12 separate occasions, one of which led to the global HIV–AIDS crisis. Though SIVs infect a wide range of primates, scientists have only recently begun to describe the natural history of SIV infection in their natural hosts. Several new studies reveal how both viral and host factors are responsible for the transmission to, and adaptation in, new hosts. These studies also suggest that the spread of the virus may be affected by host-specific traits, including social structure, mating system and demographic history. These studies challenge the traditional view that SIV is relatively benign in its natural host, and instead suggest that a highly dynamic relationship exists between SIV and its simian hosts.