Dam promotes downriver functional homogenization of phytoplankton in a transitional river-reservoir system in Amazon

Limnology - Dams disrupt the longitudinal gradient and decrease the natural connectivity of lotic systems and change the physical, chemical, and biological compartments of the river environment....     

Virtual special issue: Social-ecological systems research in tropical ecosystems

Biodiversity is declining globally, primarily due to anthropogenic threats. Therefore, effective conservation efforts must integrate human and environmental components. Social-ecological systems research is increasingly being adopted as a means of studying complex relationships between people and the environment. I assess how researchers are employing social-ecological systems approaches or frameworks to the study of tropical ecosystems. I reviewed articles published in Biotropica from 2010 through 2022 searching for research on social-ecological systems. A broad keyword search revealed only 2 articles using a variation of social-ecological systems, human-environment systems, or coupled human and natural systems. This contrasts with a growing number of articles published with these search terms in other conservation-related journals, primarily led by environmental scientists. After reviewing titles for all 1298 research articles published during this period, I selected 12 articles for inclusion in the virtual special issue “Social-Ecological Systems Research in Topical Ecosystems”. These articles cover a broad range of geographical locations, ecosystem types, species, and conservation themes. Social-ecological systems frameworks offer an integrated way to study complex relationships between humans and nature, yet this type of research appears under-utilized by authors in Biotropica. I offer seven guidelines for authors interested in pursuing this research such as developing collaborations between social and environmental scientists.     

Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii

GPIs isolated from Toxoplasma gondii, as well as a chemically synthesized GPI lacking the lipid moiety, activated a reporter gene in Chinese hamster ovary cells expressing TLR4, while the core glycan and lipid moieties cleaved from the GPIs activated both TLR4- and TLR2-expressing cells. MyD88, but not TLR2, TLR4, or CD14, is absolutely needed to trigger TNF-alpha production by macrophages exposed to T. gondii GPIs. Importantly, TNF-alpha response to GPIs was completely abrogated in macrophages from TLR2/4-double-deficient mice. MyD88(-/-) mice were more susceptible to death than wild-type (WT), TLR2(-/-), TLR4(-/-), TLR2/4(-/-), and CD14(-/-) mice infected with the ME-49 strain of T. gondii. The cyst number was higher in the brain of TLR2/4(-/-), but not TLR2(-/-), TLR4(-/-), and CD14(-/-), mice, as compared with WT mice. Upon infection with the ME-49 strain of T. gondii, we observed no decrease of IL-12 and IFN-gamma production in TLR2-, TLR4-, or CD14-deficient mice. Indeed, splenocytes from T. gondii-infected TLR2(-/-) and TLR2/4(-/-) mice produced more IFN-gamma than cells from WT mice in response to in vitro stimulation with parasite extracts enriched in GPI-linked surface proteins. Together, our results suggest that both TLR2 and TLR4 receptors may participate in the host defense against T. gondii infection through their activation by the GPIs and could work together with other MyD88-dependent receptors, like other TLRs or even IL-18R or IL-1R, to obtain an effective host response against T. gondii infection.     

Studies on the antioxidant activity of the essential oil and methanol extract of Marrubium globosum subsp. globosum (lamiaceae) by three different chemical assays

This study is designed to examine the chemical composition and in vitro antioxidant activity of the essential oil and sub-fractions of the methanol extract of Marrubium globosum subsp. globosum. The GC and GC-MS analysis of the essential oil were resulted in the determination of 84 components representing 88.2% of the oil. The major constituents of the oil were spathulenol (15.8%), beta-caryophyllene (9.0%), caryophyllene oxide (7.9%), germacrene D (6.5%), and bicyclogermacrene (3.1%). Antioxidant activities of the samples were determined by three different test systems namely DPPH, beta-carotene/linoleic acid and reducing power assay. In DPPH system, the weakest radical scavenging activity was exhibited by the essential oil (1203.38+/-7.18 microg ml(-1)). Antioxidant activity of the polar sub-fraction of methanol extract was superior to the all samples tested with an EC(50) value of 157.26+/-1.12 microg ml(-1). In the second case, the inhibition capacity (%) of the polar sub-fraction of methanol extract (97.39%+/-0.84) was found the strongest one, which is almost equal to the inhibition capacity of positive control BHT (97.44%+/-0.74). In the case of reducing power assay, a similar activity pattern was observed as given in the first two systems. Polar sub-fraction was the strongest radical reducer when compared with the non-polar one, with an EC(50) value of 625.63+/-1.02 microg ml(-1). The amount of the total phenolics was highest in polar sub-fraction (25.60+/-0.74 microg/mg). A positive correlation was observed between the antioxidant activity potential and total phenolic level of the extracts. On the other hand, total flavonoid content was found equal for the both sub-fractions.     

Genetic mapping of seed shape in three populations of recombinant inbred lines of soybean (Glycine max L. Merr.)

Round soybean seeds are sought-after for food-type soybean. Also the genetic control of seed geometry is of scientific interest. The objectives of this study were to estimate heritability and map quantitative trait loci (QTLs) responsible for seed shape traits. Three densely mapped recombinant inbred populations each with 192 segregants were used, Minsoy × Archer, Minsoy × Noir1, and Noir1 × Archer. A two rep two location experiment was conducted in Los Andes, Chile, and East Lansing, MI, USA. Seed height (SH), width (SW), length (SL), and seed volume (SV) as width × height × length were measured to determine seed shape. Heritability was estimated by variance component analysis. A total of 19 significant QTLs (LOD ≥ 3.7) in ten linkage groups (LG) were detected for all the traits. Only one QTL was stable across populations and environments and six were stable in at least two populations in both environments. The amount of phenotypic variation explained by a single QTL varied from 7.5% for SH, to 18.5% for SW and at least 30% of the genetic variation for the traits is controlled by four QTL or less. All traits were highly correlated with each other in all populations with values ranging from 0.5 to 0.9, except for SL and SW that were not significantly correlated or had a low correlation in all populations. Narrow sense heritabilities for all traits ranged from 0.42 to 0.88. We note that LG u9, u11, and u14 are hot points of the genome for QTLs for various traits. The number and genomic distribution of the QTLs confirms the complex genetic control of seed shape. Transgressive segregation was observed for all traits suggesting that careful selection of parents with similar phenotypes but different genotypes using molecular markers can result in desirable transgressive segregants.     

Multiple Functions of Human Papillomavirus Type 16 E6 Contribute to the Immortalization of Mammary Epithelial Cells

The E6 proteins from cervical cancer-associated human papillomavirus (HPV) types such as HPV type 16 (HPV-16) induce proteolysis of the p53 tumor suppressor protein through interaction with E6-AP. We have previously shown that human mammary epithelial cells (MECs) immortalized by HPV-16 E6 display low levels of p53. HPV-16 E6 as well as other cancer-related papillomavirus E6 proteins also binds the cellular protein E6BP (ERC-55). To explore the potential functional significance of these interactions, we created and analyzed a series of E6 mutants for their ability to interact with E6-AP, p53, and E6BP in vitro. While there was a similar pattern of binding among these E6 targets, a subset of mutants differentiated E6-AP binding, p53 binding, and p53 degradation activities. These results demonstrated that E6 binding to E6-AP is not sufficient for binding to p53 and that E6 binding to p53 is not sufficient for inducing p53 degradation. The in vivo activity of these HPV-16 E6 mutants was tested in MECs. In agreement with the in vitro results, most of these p53 degradation-defective E6 mutants were unable to reduce the p53 level in early-passage MECs. Interestingly, several mutants that showed severely reduced ability for interacting with E6-AP, p53, and E6BP in vitro efficiently immortalized MECs. These immortalized cells exhibited low p53 levels at late passage. Furthermore, mutants defective for p53 degradation but able to immortalize MECs were also identified, and the immortal cells retained normal levels of p53 protein. These results imply that multiple functions of HPV-16 E6 contribute to MEC immortalization.