Cat Dilemma: Too Protected To Escape Trophy Hunting?

Trophy hunting is one of the most controversial issues in the field of biodiversity conservation. In particular, proponents and opponents debate fiercely over whether it poses a threat to hunted populations. Here, we show that trophy hunting constitutes a greater menace to threatened species than previously realized. Because humans value rarity, targeted species that are threatened are likely to be disproportionately hunted, thereby becoming even more vulnerable, which could eventually push them to extinction. With the ten felid species currently hunted for their trophies, we present evidence that (1) the number of killed individuals increases with time, in several cases exponentially, despite population declines, (2) the price of trophies is strongly dependent on species protection status, (3) changes of protection status coincide with counter-intuitive changes of hunting pressures: protection intensification with augmented hunting effort, and protection relaxation with lower effort. This suggests an over-exploitation of trophy-hunted felids and the necessity of a better quota system coupled with reconsidered protection methods.     

Deletion of UL21 causes a delay in the early stages of the herpes simplex virus 1 replication cycle

The herpes simplex virus 1 (HSV-1) U(L)21 gene encodes a 62-kDa tegument protein with homologs in the alpha-, beta-, and gammaherpesvirus subfamilies. In the present study, we characterized a novel U(L)21-null virus and its genetic repair to determine whether this protein plays a role in early stages of the HSV-1 replication cycle. Single-step growth analyses, protein synthesis time courses, and mRNA quantifications indicated that the absence of U(L)21 results in a delay early in the HSV-1 replication cycle.     

The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function in the rat

The influence of manganese deficiency on liver trace element concentration, MnSOD activity, and mitochondrial structure and function during postnatal development was determined in rats. In both normal and manganese-deficient animals, liver manganese concentration increased with time, but in deficient rats liver manganese was lower than in controls at all ages measured. At 9 mo of age, liver manganese concentration in the deficient rats was only 20% that of controls. The developmental pattern observed for MnSOD paralleled that of liver manganese concentration in normal and deficient rats; it was lower than in controls on days 20 and 60. However, at 9 mo of age, MnSOD levels were similar in the two groups. Although there were no differences at 9 mo of age in MnSOD activity between the groups, manganese-deficient rats showed mitochondrial abnormalities in liver. Despite mitochondrial abnormalities, however, oxygen uptake and P/O ratios were normal. We suggest that the mitochondrial damage apparent at 9 mo of age is, at least in part, the result of lower than normal MnSOD activity occurring earlier. The functional significance of the abnormalities remains to be established.     

In situ immunoassays for gene translation products in phage plaques and bacterial colonies

A series of simple, in situ immunoassays have been developed which can be used in screening for translation products of genes cloned in vitro recombination experiments with either phage or plasmid vectors. Antigen-antibody complex formation occurring within a vector-phage plaque can be used to detect the production of a specific protein from an amplified gene. Immunoassays of colonies lysed in situ either by λ prophage induction or by biochemical means afford a much higher level of sensitivity than the plaque assay probably adequate to detect the production of a few molecules of protein per cell.     

Functional characterization of the common c.-32-13T>G mutation of GAA gene: identification of potential therapeutic agents

Glycogen storage disease type II is a lysosomal storage disorder due to mutations of the GAA gene, which causes lysosomal alpha-glucosidase deficiency. Clinically, glycogen storage disease type II has been classified in infantile and late-onset forms. Most late-onset patients share the leaky splicing mutation c.-32-13T>G. To date, the mechanism by which the c.-32-13T>G mutation affects the GAA mRNA splicing is not fully known. In this study, we demonstrate that the c.-32-13T>G mutation abrogates the binding of the splicing factor U2AF65 to the polypyrimidine tract of exon 2 and that several splicing factors affect exon 2 inclusion, although the only factor capable of acting in the c.-32-13 T>G context is the SR protein family member, SRSF4 (SRp75). Most importantly, a preliminary screening using small molecules described to be able to affect splicing profiles, showed that resveratrol treatment resulted in a significant increase of normal spliced GAA mRNA, GAA protein content and activity in cells transfected with a mutant minigene and in fibroblasts from patients carrying the c-32-13T>G mutation. In conclusion, this work provides an in-depth functional characterization of the c.-32-13T>G mutation and, most importantly, an in vitro proof of principle for the use of small molecules to rescue normal splicing of c.-32-13T>G mutant alleles.     

New directions in management strategy evaluation through cross-fertilization between fisheries science and terrestrial conservation

On 1 and 2 June 2010, an international meeting was held at the University of Paris Sud XI, France, organized within the framework of the EU FP7 consortium project HUNT, to bring together fisheries and conservation scientists to discuss a unified framework for the future of management strategies for harvested species.