Impacts of Mesopredator Control on Conservation of Mesopredators and Their Prey

Declining large carnivore populations, increased habitat fragmentation, declining interests in fur trapping, and other anthropogenic factors can all lead to increased mesopredator populations and these may negatively impact biodiversity. Lethal mesopredator control potentially mitigates some of these effects but can be controversial, largely because impacts on mesopredator populations have not been evaluated. Estimating these impacts may reduce controversies while increasing our understanding of when lethal control may be beneficial. Therefore, we analyzed published mesopredator removal data to determine if mesopredator removal rates changed over time. Removals of medium,(e.g., raccoons (Procyon lotor) or red foxes (Vulpes vulpes), and large, i.e., bobcats (Lynx rufus) or coyotes (Canis latrans), mesopredators were consistent from year to year and over the duration of study (i.e., number removed during the first and last years of studies were similar). In contrast, removals of small mesopredators, e.g., weasels (Mustela spp.) or spotted skunks (Spilogale putorius), declined over the duration of study. Study area size, number of species targeted for removal, and duration of removal effort were poor predictors of removal rates. Our analyses suggest that: (1) control, as typically implemented, is unlikely to cause negative long-term impacts on populations of medium and large mesopredators but may negatively impact small mesopredators, (2) if mesopredator control benefits prey, recurring removals will generally be needed to maintain benefits, and (3) timing of removals will be important to achieve management goals. We suggest that mesopredator control efforts are frequently spatially structured harvests from continuously distributed populations. This may explain (1) why removal of small mesopredators declined over time; whereas, medium and large mesopredator removals remained consistent, and (2) why some prey failed to respond to mesopredator control efforts.     

Direct Interference on Competition in a Chemostat

Thispaperstudiestheglobaldynamicsofcompetitioninchemostatinwhichtwopopulationsofmicrooganismscompeteexploitativelyforasingle,essential,nonreproducing,growth-limitingsubstrateandthereisadirectinterferencebetweencompetitors.Inordertounderstandthedifferencesintheeffectsofintraspecificandinterspecificinterference,thebothcasesareconsideredrespectively.Keywords:##4Populationdynamicsecology;;chemostat;;competition;;interference;;interspecific;;intraspecific;;principalofcompetitiveexclusion     

Impact of Population Substructure on Trend Tests for Genetic Case–Control Association Studies

Summary .  Hidden population substructure in case–control data has the potential to distort the performance of Cochran–Armitage trend tests (CATTs) for genetic associations. Three possible scenarios that may arise are investigated here: (i) heterogeneity of genotype frequencies across unidentified subpopulations (PSI), (ii) heterogeneity of genotype frequencies and disease risk across unidentified subpopulations (PSII), and (iii) cryptic correlations within unidentified subpopulations. A unified approach is presented for deriving the bias and variance distortion under the three scenarios for any CATT in a general family. Using these analytical formulas, we evaluate the excess type I errors of the CATTs numerically in the presence of population substructure. Our results provide insight into the properties of some proposed corrections for bias and variance distortion and show why they may not fully correct for the effects of population substructure.     

Effects of High Levels of DNA Adenine Methylation on Methyl-Directed Mismatch Repair in ESCHERICHIA COLI

Two methods were used in an attempt to increase the efficiency and strand selectivity of methyl-directed mismatch repair of bacteriophage lambda heteroduplexes in E. coli. Previous studies of such repair used lambda DNA that was only partially methylated as the source of methylated chains. Also, transfection was carried out in methylating strains. Either of these factors might have been responsible for the incompleteness of the strand selectivity observed previously. In the first approach to increasing strand selectivity, heteroduplexes were transfected into a host deficient in methylation, but no changes in repair frequencies were observed. In the second approach, heteroduplexes were prepared using DNA that had been highly methylated in vitro with purified DNA adenine methylase as the source of methylated chains. In heteroduplexes having a repairable cI/+ mismatch, strand selectivity was indeed enhanced. In heteroduplexes with one chain highly methylated and the complementary chain unmethylated, the frequency of repair on the unmethylated chain increased to nearly 100%. Heteroduplexes with both chains highly methylated were not repaired at a detectable frequency. Thus, chains highly methylated by DNA adenine methylase were refractory to mismatch repair by this system, regardless of the methylation of the complementary chain. These results support the hypothesis that methyl-directed mismatch repair acts to correct errors of replication, thus lowering the mutation rate.     

Apoptosis in lactating and involuting mouse mammary tissue demonstrated by nick-end DNA labelling

Mammary involution after cessation of milk removal is associated with extensive loss of secretory epithelial cells. Ultrastructural changes and the appearance of oligonucleosomal DNA laddering in ethidium bromide-stained gels indicates that cell loss during involution occurs by apoptosis. In this study, a technique for nick end-labelling of genomic DNA with radiolabelled deoxynucleotide has been used to monitor the induction of programmed cell death in mice after litter removal at peak lactation. This technique proved more sensitive than conventional ethidium bromide staining, and results suggested that apoptosis was induced rapidly by milk stasis, before extensive tissue re-modelling had begun. Oligonucleosomal DNA laddering on agarose gels was detected within 24 h of milk stasis, and increased progressively for at least 4 days. Nick-end labelling also detected laddering before litter removal, suggesting that programmed cell death is a normal feature of the lactating tissue. The DNA end-labelling technique was also adapted for in situ visualisation of apoptotic cells in tissue sections. By this criterion, apoptotic cells were identified in both the secretory epithelium lining the alveoli of the gland and, increasingly with prolonged milk stasis, amongst those sloughed into the alveolar lumen. The results demonstrate the utility of these techniques for study of mammary cell death and suggest that, whilst apoptosis is rapidly induced by milk stasis, it is also a normal physiological event in the lactating mammary gland.