Prevalence of Candidatus Erwinia dacicola in wild and laboratory olive fruit fly populations and across developmental stages

The microbiome of the olive fruit fly, Bactrocera oleae (Gmelin), a worldwide pest of olives (Olea europaea L.), has been examined for >100 yr as part of efforts to identify bacteria that are plant pathogens vectored by the fly or are beneficial endosymbionts essential for the fly's survival and thus targets for possible biological control. Because tephritid fruit flies feed on free-living bacteria in their environment, distinguishing between the transient, acquired bacteria of their diet and persistent, resident bacteria that are vertically transmitted endosymbionts is difficult. Several culture-dependent and -independent studies have identified a diversity of species in the olive fruit fly microbiome, but they have not distinguished the roles of the microbes. Candidatus Erwinia dacicola, has been proposed to be a coevolved endosymbiont of the olive fruit fly; however, this was based on limited samples from two Italian populations. Our study shows that C. Erwinia dacicola was present in all New and Old World populations and in the majority of individuals of all life stages sampled in 2 yr. Olive fruit flies reared on olives in the laboratory had frequencies of C. Erwinia dacicola similar to that of wild populations; however, flies reared on artificial diets containing antibiotics in the laboratory rarely had the endosymbiont. The relative abundance of C. Erwinia dacicola varied across development stages, being most abundant in ovipositing females and larvae. This uniform presence of C. Erwini dacicola suggests that it is a persistent, resident endosymbiont of the olive fruit fly.     

Genetic signatures of a demographic collapse in a large-bodied forest dwelling primate (Mandrillus leucophaeus)

It is difficult to predict how current climate change will affect wildlife species adapted to a tropical rainforest environment. Understanding how population dynamics fluctuated in such species throughout periods of past climatic change can provide insight into this issue. The drill (Mandrillus leucophaeus) is a large-bodied rainforest adapted mammal found in West Central Africa. In the middle of this endangered monkey's geographic range is Lake Barombi Mbo, which has a well-documented palynological record of environmental change that dates to the Late Pleistocene. We used a Bayesian coalescent-based framework to analyze 2,076 base pairs of mitochondrial DNA across wild drill populations to infer past changes in female effective population size since the Late Pleistocene. Our results suggest that the drill underwent a nearly 15-fold demographic collapse in female effective population size that was most prominent during the Mid Holocene (approximately 3-5 Ka). This time period coincides with a period of increased dryness and seasonality across Africa and a dramatic reduction in forest coverage at Lake Barombi Mbo. We believe that these changes in climate and forest coverage were the driving forces behind the drill population decline. Furthermore, the warm temperatures and increased aridity of the Mid Holocene are potentially analogous to current and future conditions faced by many tropical rainforest communities. In order to prevent future declines in population size in rainforest-adapted species such as the drill, large tracts of forest should be protected to both preserve habitat and prevent forest loss through aridification.     

Function and evolution of 'green' GSK3/Shaggy-like kinases

Glycogen synthase kinase 3 (GSK3) proteins, also known as SHAGGY-like kinases, have many important cell signalling roles in animals, fungi and amoebae. In particular, GSK3s participate in key developmental signalling pathways and also regulate the cytoskeleton. GSK3-encoding genes are also present in all land plants and in algae and protists, raising questions about possible ancestral functions in eukaryotes. Recent studies have revealed that plant GSK3 proteins are actively implicated in hormonal signalling networks during development as well as in biotic and abiotic stress responses. In this review, we outline the mechanisms of Arabidopsis GSK3 action, summarize GSK3 functions in dicot and monocot flowering plants, and speculate on the possible functions of GSK3s in the earliest-evolving land plants.     

Non-surgical uterine flushing for the recovery of preimplantation embryos in rhesus monkeys: Lack of seasonal infertility

A non-surgical uterine flushing technique was employed to recover rhesus monkey preimplantation embryos during April–-September, a period thought to be associated with reduced fertility. A total of 22 females of proven fertility, maintained indoors under strict light and temperature control, were employed for the study in which 72 menstrual cycles were monitored. The average length of their menstrual cycle was 27.9 ± 3.8 days. The percentages of cycles that showed normal cyclic patterns of estrogen, LH, and sex-skin color were 84.7%, 91.7%, and 90.3%, respectively. Following natural mating, uterine flushing was performed on days 4–7 of pregnancy. Of 58 attempts, 27 (46.6%) resulted in the recovery of embryonic materials. Two recoveries produced unfertilized oocytes; 20 yielded embryos which were morphologically normal, and 7 yielded damaged and/or degenerate embryos. Luteal function in cycles involving uterine flushings was evaluated by examining ovaries by laparoscopy, ovulation being confirmed in 34 of 35 examinations. Serum progesterone was > 2 ng/ml in 39 of 45 cycles. The conception rate of 46.6% noted in this study was similar (P > 0.4) to those observed from other natural matings in our colony, either during the same period (49.3%; n = 67) or during October–-March (46.9%; n = 113). These results show that rhesus monkeys, maintained under appropriate environmental conditions, can experience normal fertile menstrual cycles throughout the summer months, and extend previous observations to demonstrate, for the first time, that preimplantation embryos can be recovered from this species year-round. © 1993 Wiley-Liss, Inc.     

A neonatal polyvisceral failure linked to a de novo homoplasmic mutation in the mitochondrially encoded cytochrome b gene

Mutations within the mitochondrially encoded cytochrome b (MTCYB) gene are heteroplasmic and lead to severe exercise intolerance. We describe an unusual clinical presentation secondary to a novel homoplasmic mutation within MTCYB. The m.15635T > C transition (S297P) was carried by a newborn who presented with a polyvisceral failure. This mutation was responsible for a complex III deficiency. It was homoplasmic in all tissues tested and was undetectable in patient’s mother. Functional analyses, including studies on patient’s cybrid cell lines, demonstrate the pathogenicity of this variant. Our data show that mutations within MTCYB can be responsible for severe phenotype at birth.     

Abeta42 mutants with different aggregation profiles induce distinct pathologies in Drosophila

Aggregation of the amyloid-beta-42 (Abeta42) peptide in the brain parenchyma is a pathological hallmark of Alzheimer's disease (AD), and the prevention of Abeta aggregation has been proposed as a therapeutic intervention in AD. However, recent reports indicate that Abeta can form several different prefibrillar and fibrillar aggregates and that each aggregate may confer different pathogenic effects, suggesting that manipulation of Abeta42 aggregation may not only quantitatively but also qualitatively modify brain pathology. Here, we compare the pathogenicity of human Abeta42 mutants with differing tendencies to aggregate. We examined the aggregation-prone, EOFAD-related Arctic mutation (Abeta42Arc) and an artificial mutation (Abeta42art) that is known to suppress aggregation and toxicity of Abeta42 in vitro. In the Drosophila brain, Abeta42Arc formed more oligomers and deposits than did wild type Abeta42, while Abeta42art formed fewer oligomers and deposits. The severity of locomotor dysfunction and premature death positively correlated with the aggregation tendencies of Abeta peptides. Surprisingly, however, Abeta42art caused earlier onset of memory defects than Abeta42. More remarkably, each Abeta induced qualitatively different pathologies. Abeta42Arc caused greater neuron loss than did Abeta42, while Abeta42art flies showed the strongest neurite degeneration. This pattern of degeneration coincides with the distribution of Thioflavin S-stained Abeta aggregates: Abeta42Arc formed large deposits in the cell body, Abeta42art accumulated preferentially in the neurites, while Abeta42 accumulated in both locations. Our results demonstrate that manipulation of the aggregation propensity of Abeta42 does not simply change the level of toxicity, but can also result in qualitative shifts in the pathology induced in vivo.