Hydrology shapes microbial communities and microbiome-mediated growth of an Everglades tree island species

Plant-associated microbiomes can improve plant fitness by ameliorating environmental stress, providing a promising avenue for improving outplantings during restoration. However, the effects of water management on these microbial communities and their cascading effects on primary producers are unresolved for many imperiled ecosystems. One such habitat, Everglades tree islands, has declined by 54% in some areas, releasing excess nutrients into surrounding wetlands and exacerbating nutrient pollution. We conducted a factorial experiment, manipulating the soil microbiome and hydrological regime experienced by a tree island native, Ficus aurea, to determine how microbiomes impact growth under two hydrological management plans. All plants were watered to simulate natural precipitation, but plants in the “unconstrained” management treatment were allowed to accumulate water above the soil surface, while the “constrained” treatment had a reduced stage to avoid soil submersion. We found significant effects of the microbiomes on overall plant performance and aboveground versus belowground investment; however, these effects depended on hydrological treatment. For instance, microbiomes increased investment in roots relative to aboveground tissues, but these effects were 142% stronger in the constrained compared to unconstrained water regime. Changes in hydrology also resulted in changes in the prokaryotic community composition, including a >20 log₂fold increase in the relative abundance of Rhizobiaceae, and hydrology-shifted microbial composition was linked to changes in plant performance. Our results suggest that differences in hydrological management can have important effects on microbial communities, including taxa often involved in nitrogen cycling, which can in turn impact plant performance.     

Inoculation with native soil improves seedling survival and reduces non-native reinvasion in a grassland restoration

Losses of grasslands have been largely attributed to widespread land-use changes, such as conversion to row-crop agriculture. The remaining tallgrass prairie faces further losses due to biological invasions by non-native plant species, often with resultant ecosystem degradation. Of critical concern for conservation, restoration of native grasslands has been met with little success following eradication of non-native plants. In addition to the direct and indirect effects of non-native invasive plants on beneficial soil microbes, management practices targeting invasive species may also negatively affect subsequent restoration efforts. To assess mechanisms limiting germination and survival of native species and to improve native species establishment, we established six replicate plots of each of the following four treatments: (1) inoculated with freshly collected prairie soil with native seeds; (2) inoculated with steam-pasteurized soil with native seeds; (3) noninoculated with native seeds; or (4) noninoculated/nonseeded control. Inoculation with whole soil did not improve seed germination; however, addition of whole soil significantly improved native species survival, compared to pasteurized soil or noninoculated treatments. Inoculation with whole soil significantly decreased reestablishment of non-native invasive Bothriochloa bladhii (Caucasian bluestem); at the end of the growing season, plots receiving whole soil consisted of approximately 30% B. bladhii cover, compared to approximately 80% in plots receiving no soil inoculum. Our results suggest invasion and eradication efforts negatively affect arbuscular mycorrhizal hyphal and spore abundances and soil aggregate stability, and inoculation with locally adapted soil microbial communities can improve metrics of restoration success, including plant species richness and diversity, while decreasing reinvasion by non-native species.     

Smartphone repairability indexes in practice: Linking repair scores to industrial design features

Policymaking mediates the relationships between manufacturers and consumers, thus defining the boundaries for the philosophies of production set forth by major companies. Research states that policymaking falls short in addressing the waste issues, natural resources consumption, greenhouse gas emissions, and other negative impacts posed by premature obsolescence; only recently have the “right-to-repair” guidelines demanded by environmental organizations and communities of citizens been included in policymaking. The introduction of the Index of Repairability in France as information at the point of sale aims to inform consumers and support their decision-making in purchasing more repairable products. In this paper, we consider the two Indexes of Repairability publicly available to consumers—in the French legislation and iFixit—and assess their application to smartphones from three manufacturers. The study establishes links between the scores and the industrial design features that promote or hinder repairability, service factors and information for self-repair, authorized repair, and independent repair. Data collection considers the available information for consumers and citizens by using netnography and secondary data from manufacturers, policymakers, and communities of users. Our findings suggest that higher scores that indicate easier repairability are not limited to product architectures that follow design for disassembly guidelines. Smartphones that are difficult to repair can still score high, and thus be perceived as easier to repair, if manufacturers provide high quality and affordable service. This paper discusses the results of the ongoing development of repairability scores for smartphones, thus suggesting paths for future research to improve methods and policies to support a longer lifetime of products.     

Second messenger and protein phosphorylation mechanisms underlying opiate addiction: Studies in the rat locus coeruleus

We have studied the role of second messenger and protein phosphorylation pathways in mediating changes in neuronal function associated with opiate addiction in the rat locus coeruleus. We have found that chronic opiates increase levels of the G-protein subunits Gi and Go, adenylate cyclase, cyclic AMP-dependent protein kinase, and a number of phosphoproteins (including tyrosine hydroxylase) in this brain region. Electrophysiological data have provided direct support for the view that this up-regulation of the cyclic AMP system contributes to opiate tolerance, dependence, and withdrawal exhibited by these neurons. As the adaptations in G-proteins and the cyclic AMP system appear to occur at least in part at the level of gene expression, current efforts are aimed at identifying the mechanisms, at the molecular level, by which opiates regulate the expression of these intracellular messenger proteins in the locus coeruleus. These studies will lead to an improved understanding of the biochemical basis of opiate addiction.Special issue dedicated to Dr. Paul Greengard     

Drug resistance in rat colon cancer cell lines is associated with minor changes in susceptibility to cytotoxic cells

The development of resistance to anticancer drugs urges the search for different treatment modalities. Several investigators have reported the concomitant development of drug resistance and resistance to natural killer (NK), lymphokine-activated killer (LAK) or monocyte/macrophage cell lysis, while others described unchanged or even increased susceptibility. We investigated this subject in the rat colon carcinoma cell line, CC531-PAR, which is intrinsically multidrug-resistant (MDR), and in three sublines derived from this parental cell line: a cell line with an increased MDR phenotype (CC531-COL), a revertant line from CC531-COL (CC531-REV), which demonstrates enhanced sensitivity to anticancer drugs of the MDR phenotype, and an independently developed cisplatin-resistant line (CC531-CIS). In a 4-h⁵¹Cr-release assay we found no difference in susceptibility to NK cell lysis. No significant differences in lysability by adherent LAK (aLAK) cells were observed in a 4-h assay. In a prolonged 20-h⁵¹Cr-release assay an enhanced sensitivity to aLAK-cell-mediated lysis was observed in the revertant, P-glycoprotein-negative cell line and in the cisplatin-resistant cell line (CC531-CIS). None of the cell lines was completely resistant to lysis by aLAK cells. Therefore, a role for immunotherapy in the treatment of drug-resistant tumors remains a realistic option.     

Loss of DNA repair mechanisms in cardiac myocytes induce dilated cardiomyopathy

Cardiomyopathy is a progressive disease of the myocardium leading to impaired contractility. Genotoxic cancer therapies are known to be potent drivers of cardiomyopathy, whereas causes of spontaneous disease remain unclear. To test the hypothesis that endogenous genotoxic stress contributes to cardiomyopathy, we deleted the DNA repair gene Ercc1 specifically in striated muscle using a floxed allele of Ercc1 and mice expressing Cre under control of the muscle-specific creatinine kinase (Ckmm) promoter or depleted systemically (Ercc1^−/D mice). Ckmm-Cre^+/−;Ercc1^−/fl mice expired suddenly of heart disease by 7 months of age. As young adults, the hearts of Ckmm-Cre^+/−;Ercc1^−/fl mice were structurally and functionally normal, but by 6-months-of-age, there was significant ventricular dilation, wall thinning, interstitial fibrosis, and systolic dysfunction indicative of dilated cardiomyopathy. Cardiac tissue from the tissue-specific or systemic model showed increased apoptosis and cardiac myocytes from Ckmm-Cre^+/-;Ercc1^−/fl mice were hypersensitive to genotoxins, resulting in apoptosis. p53 levels and target gene expression, including several antioxidants, were increased in cardiac tissue from Ckmm-Cre^+/−;Ercc1^−/fl and Ercc1^−/D mice. Despite this, cardiac tissue from older mutant mice showed evidence of increased oxidative stress. Genetic or pharmacologic inhibition of p53 attenuated apoptosis and improved disease markers. Similarly, overexpression of mitochondrial-targeted catalase improved disease markers. Together, these data support the conclusion that DNA damage produced endogenously can drive cardiac disease and does so mechanistically via chronic activation of p53 and increased oxidative stress, driving cardiac myocyte apoptosis, dilated cardiomyopathy, and sudden death.