Life in a fragment: Evolution of foraging strategies of translocated collared brown lemurs,Eulemur collaris,over an 18-year period

While the drivers of primate persistence in forest fragments have been often considered at the population level, the strategies to persist in these habitats have been little investigated at the individual or group level. Considering the rapid variation of fragment characteristics over time, longitudinal data on primates living in fragmented habitats are necessary to understand the key elements for their persistence. Since translocated animals have to cope with unfamiliar areas and face unknown fluctuations in food abundance, they offer the opportunity to study the factors contributing to successful migration between fragments. Here, we illustrated the evolution of the foraging strategies of translocated collared brown lemurs (Eulemur collaris) over an 18-year period in the Mandena Conservation Zone, south-east Madagascar. Our aim was to explore the ability of these frugivorous lemurs to adjust to recently colonized fragmented forests. Although the lemurs remained mainly frugivorous throughout the study period, over the years we identified a reduction in the consumption of leaves and exotic/pioneer plant species. These adjustments were expected in frugivorous primates living in a degraded area, but we hypothesize that they may also reflect the initial need to cope with an unfamiliar environment after the translocation. Since fragmentation is often associated with the loss of large trees and native vegetation, we suggest that the availability of exotic and/or pioneer plant species can provide an easy-to-access, nonseasonal food resource and be a key factor for persistence during the initial stage of the recolonization.     

The Influence of Changes in Magnetic Variations and Light–Dark Cycle on Life-History Traits of Daphnia magna

Day–night cycle is the main zeitgeber (time giver) for biological circadian rhythms. Recently, it was suggested that natural diurnal geomagnetic variation may also be utilized by organisms for the synchronization of these rhythms. In this study, life-history traits in Daphnia magna were evaluated after short-term and multigenerational exposure to 16 h day/8 h night cycle, 32 h day/16 h night cycle, diurnal geomagnetic variation of 24 h, simulated magnetic variation of 48 h, and combinations of these conditions. With short-term exposure, the lighting mode substantially influenced the brood to brood period and the lifespan in daphnids. The brood to brood period, brood size, and body length of crustaceans similarly depended on the lighting mode during the multigenerational exposure. At the same time, an interaction of lighting mode and magnetic variations affected to a lesser extent brood to brood period, brood size, and newborn's body length. The influence of simulated diurnal variation on life-history traits in daphnids appeared distinctly as effects of synchronization between periods of lighting mode and magnetic variations during the multigenerational exposure. Newborn's body length significantly depended on the lighting regime when the periods of both studied zeitgebers were unsynchronized, or on the interaction of light regime with magnetic variations when the periods were synchronized. These results confirm the hypothesis that diurnal geomagnetic variation is an additional zeitgeber for biological circadian rhythms. Possible mechanisms for these observed effects are discussed. Bioelectromagnetics. © 2020 Bioelectromagnetics Society     

A DNA‐promoted amyloid proteinopathy in Escherichia coli

Protein amyloids arise from the conformational conversion and assembly of a soluble protein into fibrilar aggregates with a crossed β‐sheet backbone. Amyloid aggregates are able to replicate by acting as a template for the structural transformation and accretion of further protein molecules. In physicochemical terms, amyloids arguably constitute the simplest self‐replicative macromolecular assemblies. Similarly to the mammalian proteins PrP and α‐synuclein, the winged‐helix dimerization (WH1) domain of the bacterial, plasmid‐encoded protein RepA can assemble into amyloid fibres upon binding to DNA in vitro. Here we report that a hyper‐amyloidogenic functional variant (A31V) of RepA, fused to a red fluorescent protein, causes an amyloid proteinopathy in Escherichia coli with the following features: (i) in the presence of multiple copies of the specific DNA sequence opsp, WH1(A31V) accumulates as cytoplasmatic inclusions segregated from the nucleoid; (ii) such aggregates are amyloid in nature; (iii) bacteria carrying the amyloid inclusions age, exhibiting a fivefold expanded generation time; (iv) before cytokinesis, small inclusions are assembled de novo and transferred to the daughter cells, in which transmission failures cure amyloidosis; and (v) in the absence of inducer DNA, purified cellular WH1(A31V) inclusions seed amyloid fibre growth in vitro from the soluble protein. RepA‐WH1 is a suitable bacterial model system for amyloid proteinopathies.     

Subcellular Distribution of Two Spin Trapping Agents in Rat Heart: Possible Explanation for Their Different Protective Effects Against Doxorubicin-Induced Cardiotoxicity

Previous investigations, performed on isolated rat atria, showed that the lipophylic spin-trapping agent N-tert-butyl-alpha-phenylnitrone (PBN) is able to prevent the acute cardiotoxic effects produced by doxorubicin (DXR), whereas the hydrophylic compound 5,5-dimethyl-pyrroline-N-oxide (DMPO) is inactive. The present study was designed to ascertain whether differences in the pharmacological effects of the two spin traps are related to their different subcellular distribution. Langendorff rat hearts were perfused for 60 minutes with [^I4C]-DXR and either PBN or DMPO. The subcellular mapping of the three compounds was performed by measuring DXR by liquid scintillation counting, PBN by GC/MS, and DMPO by HPLC in the following isolated fractions: nuclei, mitochondria, sarcoplasmic reticulum, sarcolemma, cytosol. DMPO was shown to accumulate in the cytosolic compartment; both PBM and DXR are taken up by nuclei and mitochondria, while only trace amounts of DXR were detected in the sarcoplasmic reticulum. These results suggest that mitochondrial (and not sarcoplasmic) enzymes are mainly involved in DXR-induced free radical production, which is thought to cause the acute cardiotoxic effects of DXR. An involvement of DXR-induced free radical generation in the nuclear compartment seems unlikely in the short-term “in vitro” effects observed with the experimental model adopted for these studies, although it may play a role in the delayed pathology.     

Functional interaction between information processing pathways in Escherichia coli and the nature of Δ-H+ (redox)-sensing

Glucose taxis and O₂-taxis in Escherichia coli signal to flagella via a pathway that includes PTS^glc and adenylate cyclase. Information from a number of attractants and repellents is focused at the level of methy-accepting chemotaxis proteins (MCPs) and information is passed to flagella by a separate pathway. Mutants defective in adenylate cyclase (Δcya) had a residual taxis to glucose that was eliminated by preincubating the cells with MCP attractants, or by depleting the -CH₃ donor. A methyltransferase mutant had a decreased sensitivity to MCP repellents and this response was completely blocked by preincubating the cells with glucose. Likewise, the response of cells, depleted for -CH₃, towards repellents, was blocked if bacteria carried a pts mutation. It is concluded that PTS and MCP pathways exchange information. In cya cells, O₂ taxis was restored in the presence of maltose, an MCPII attractat. It is suggested that MCPII is an additional protonmotive force (pmf) sensor.     

Cloned mouse mammary tumor virus DNA is biologically active in transfected mouse cells and its expression is stimulated by glucocorticoid hormones

We have cloned circular unintegrated mouse mammary tumor virus (MMTV) DNA from infected rat hepatoma cells in bacteriophage lambda. Seven independent clones containing MMTV DNA of homogeneous length of 9 kb (five) or 10 kb (two) were identified. The five 9 kb clones had identical restriction maps consistent with that of 9 kb unintegrated DNA; the other two were aberrant. MMTV DNA inserts were purified, ligated and used for cotransfection of Ltk^? cells together with a plasmid containing the thymidine kinase gene of herpes simplex virus. All Tk⁺ cell clones acquired new MMTV sequences and those transfected with the 9 kb MMTV DNA synthesized normal viral RNA and proteins. Viral gene expression was increased by the addition of dexamethasone.     

Reprogramming Substrate and Catalytic Promiscuity of Tryptophan Prenyltransferases

Prenylation is a process widely prevalent in primary and secondary metabolism, contributing to functionality and chemical diversity in natural systems. Due to their high regio- and chemoselectivities, prenyltransferases are also valuable tools for creation of new compounds by chemoenzymatic synthesis and synthetic biology. Over the last ten years, biochemical and structural investigations shed light on the mechanism and key residues that control the catalytic process, but to date crucial information on how certain prenyltransferases control regioselectivity and chemoselectivity is still lacking. Here, we advance a general understanding of the enzyme family by contributing the first structure of a tryptophan C5-prenyltransferase 5-DMATS. Additinally, the structure of a bacterial tryptophan C6-prenyltransferase 6-DMATS was solved. Analysis and comparison of both substrate-bound complexes led to the identification of key residues for catalysis. Next, site-directed mutagenesis was successfully implemented to not only modify the prenyl donor specificity but also to redirect the prenylation, thereby switching the regioselectivity of 6-DMATS to that of 5-DMATS. The general strategy of structure-guided protein engineering should be applicable to other related prenyltransferases, thus enabling the production of novel prenylated compounds.     

Conjugation of phosphonoacetic acid to nucleobase promotes a mechanism-based inhibition

Small molecule inhibitors have a powerful blocking action on viral polymerases. The bioavailability of the inhibitor, nevertheless, often raise a significant selectivity constraint and may substantially limit the efficacy of therapy. Phosphonoacetic acid has long been known to possess a restricted potential to block DNA biosynthesis. In order to achieve a better affinity, this compound has been linked with natural nucleotide at different positions. The structural context of the resulted conjugates has been found to be crucial for the acquisition by DNA polymerases. We show that nucleobase-conjugated phosphonoacetic acid is being accepted, but this alters the processivity of DNA polymerases. The data presented here not only provide a mechanistic rationale for a switch in the mode of DNA synthesis, but also highlight the nucleobase-targeted nucleotide functionalization as a route for enhancing the specificity of small molecule inhibitors.