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Facilitation by nurse plants increases understorey diversity and supports ecological communities. In turn, biodiversity shapes ecological networks and enhances ecosystem functioning. However, whether and how facilitation and increased biodiversity jointly influence community structure and ecosystem functioning remains unclear.We performed a field experiment disentangling the relative contribution of nurse plants and increasing understorey plant diversity in driving pollination interactions. Both the presence of nurse shrubs as well as increased understorey plant diversity increased pollinator diversity and visitation rates. While nurse and understorey diversity effects on pollinator visitation rates did not interact, the effects of increasing understorey plant diversity on pollinator diversity were stronger in the absence than in the presence of shrubs, meaning that nurse shrubs attenuated the effects of high understorey diversity and buffered the effects of low understorey diversity.We also found positive complementarity effects among understorey species as well as complementarity between nurse plants and understorey species at high diversity. Results also indicate negative selection effects, suggesting that species with generally few pollinators benefit the most in the polyculture, while a species (possibly the nurse plant) with generally lots of pollinators does not. The corresponding changes in pollination networks with the experimental treatments were due to both changes in the frequency of visits and turnover in pollinator community composition.Synthesis Plant–plant facilitative systems, where a nurse plant increases understorey plant diversity, are common in stressful environments. Here, we show that these facilitative systems positively influence mutualistic interactions with pollinators via both direct nurse effects and indirect positive effects of increasing plant diversity.Conserving and supporting nurse plant systems is crucial not only for maintaining plant diversity but also for supporting ecosystem functions and services.

Contact networks can provide useful insights into animal behaviour and have the potential to quantify the spread of disease. Successful control of livestock diseases requires an understanding of how they spread amongst animals and between premises. Whilst movement records can provide valuable data on potential between-farm spread, the within-group dynamics of livestock are not well quantified; without this knowledge it is difficult to fully exploit knowledge about one-to-one transmission (such as insights gained from small scale experiments). Here the physical contact structure of domestic sheep (Ovis Aries) flocks is determined for different stages in the breeding cycle. Three observational studies were carried out on conventionally managed flocks, consisting of approximately thirty Dorset/cross sheep grazing a large paddock: a flock with young (newborn) lambs and their mothers; the flock when the lambs were older (nearly weaned); and a flock of ewes outside of the lambing season. Networks were constructed and key centrality measures calculated for all direct physical and proximal contacts. Proximity networks with conventional sheep flocks appear to be dense, but physical contacts have a more complex structure with strong variations determined by stages in the breeding cycle. There was a significant difference in the level of physical contact within those flocks with lambs and those without, and also as a result of the age of lambs. A clear reduction in between-ewe contact was observed amongst individuals with young, but there was an overall increase in connectivity in such flocks as a result of contacts involving lambs. Results are considered applicable to different sized flocks, given the known social behaviour of sheep and the experimental protocol used.

Importance Although seroepidemiological studies indicate that greater than 50% of the population has been infected with John Cunningham virus (JCV), the sites of JCV persistence remain incompletely characterized. Objective To determine sites of JCV persistence in immunologically healthy individuals. Design, Setting, and Participants Tissue specimens from multiple sites including brain, renal, and nonrenal tissues were obtained at autopsy performed in the Department of Pathology at the University of Kentucky from 12 immunologically healthy patients between February 9, 2011, and November 27, 2012. Quantitative polymerase chain reaction was performed on the tissue specimens and urine. Serum JCV antibody status was determined by enzyme-linked immunosorbent assay. Main Outcomes and Measures The detection and quantification of JCV from the tissues by quantitative polymerase chain reaction illuminated sites of viral persistence. These results were correlated with JCV antibody levels. Results Autopsies were performed on 12 individuals, 10 men and 2 women, ranging in age from 25 to 75 years (mean, 55.3 years). Seven of 12 individuals were JCV antibody seropositive based on absorbance units. Serostatus was associated with amounts of JCV DNA in urine and its tissue distribution. John Cunningham virus DNA was found in 75% of genitourinary tissue samples from donors (18 of 24) with high JCV antibody levels, 13.3% of donors with low levels i(4 of 30), and 0% of seronegative persons (0 of 32). In nongenitourinary tissues, JCV DNA was detected in 45.1% of tissue samples of donors (32 of 71) with high JCV, 2.2% of donors with low JCV serostatus (2 of 93), and 0% of seronegative persons (0 of 43). Genitourinary tissues had higher copy numbers than other sites. John Cunningham virus DNA was detected in urine of seronegative individuals in a research-grade assay. Conclusions and Relevance Persistent (latent or actively replicating) JCV infection mostly predominates in genitourinary tissues but distributes in other tissues at low copy number. The distribution and copy numbers of the virus appear to correlate with urinary JCV shedding and serostatus.

Infection of glial cells by the human polyomavirus JC (JCV) causes progressive multifocal leukoencephalopathy (PML). JCV Encephalopathy (JCVE) is a newly identified disease characterized by JCV infection of cortical pyramidal neurons. The virus JCVCPN associated with JCVE contains a unique 143 base pair deletion in the agnogene. Contrary to most JCV brain isolates, JCVCPN has an archetype-like regulatory region (RR) usually found in kidney strains. This provided us with the unique opportunity to determine for the first time how each of these regions contributed to the phenotype of JCVCPN. We characterized the replication of JCVCPN compared to the prototype virus JCVMad-1 in kidney, glial and neuronal cell lines. We found that JCVCPN is capable of replicating viral DNA in all cell lines tested, but is unable to establish persistent infection seen with JCVMad-1. JCVCPN does not have an increased ability to replicate in the neuronal cell line tested. To determine whether this phenotype results from the archetype-like RR or the agnogene deletion, we generated chimeric viruses between JCVCPN of JCVMad-1. We found that the deletion in the agnogene is the predominant cause of the inability of the virus to maintain a persistent infection, with the introduction of a full length agnogene, either with or without agnoprotein expression, rescues the replication of JCVCPN. Studying this naturally occurring pathogenic variant of JCV provides a valuable tool for understanding the functions of the agnogene and RR form in JCV replication.

Although scientists have provided mounting evidence in the past few years that new neurons can be produced in some areas of the adult brain, the neocortex--the region most concerned with such higher brain functions as memory and learning--did not seem capable of such regeneration. Now, in the 22 June issue of Nature, neuroscientists report that when they induced certain neurons in the neocortex of adult mice to self-destruct, the loss triggered the formation of replacement neurons by brain stem cells. If similar regeneration of brain neurons can be triggered in humans, the findings could open the door for treatments that might restore memory in Alzheimer9s disease, for example, or undo the damage wreaked by spinal cord injury.