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Malaria is a serious and, in some unfortunate cases, fatal disease caused by a parasite of the Plasmodium genus. It predominantly occurs in tropical areas where it is transmitted through the bite of an infected Anopheles mosquito. The pathogenesis of malaria is complex and incompletely elucidated. During blood-stage infection, in response to the presence of the parasite, the host’s immune system produces proinflammatory cytokines including IL-6, IL-8, IFN-γ, and TNF, cytokines which play a pivotal role in controlling the growth of the parasite and its elimination. Regulatory cytokines such as transforming growth factor- (TGF-) β and IL-10 maintain the balance between the proinflammatory and anti-inflammatory responses. However, in many cases, cytokines have a double role. On the one hand, they contribute to parasitic clearance, and on the other, they are responsible for pathological changes encountered in malaria. Cytokine-modulating strategies may represent a promising modern approach in disease management. In this review, we discuss the host immune response in malaria, analyzing the latest studies on the roles of pro- and anti-inflammatory cytokines.

Retinoblastoma (RB) is the most common type of intraocular malignant tumor that lowers the quality of life among children worldwide. Long noncoding RNAs (lncRNAs) are reported to play a dual role in tumorigenesis and development of RB. Autophagy is also reported to be involved in RB occurrence. Although several studies of autophagy-related lncRNAs in RB have been explored before, there are still unknown potential mechanisms in RB. In the present study, we mined dataset GSE110811 from the Gene Expression Omnibus database and downloaded autophagy-related genes from the Human Autophagy Database for further bioinformatic analysis. By implementing the differential expression analysis and Pearson correlation analysis on the lncRNA expression matrix and autophagy-related genes expression matrix, we identified four autophagy-related lncRNAs (namely, N4BP2L2-IT2, SH3BP5-AS1, CDKN2B-AS1, and LINC-PINT) associated with RB. We then performed differential expression analysis on microRNA (miRNA) from dataset GSE39105 for further analyses of lncRNA-miRNA-mRNA regulatory mechanisms. With the miRNA-lncRNA module on the StarBase 3.0 website, we predicted the differentially expressed miRNAs that could target the autophagy-related lncRNAs and constructed a potential lncRNA-miRNA-mRNA regulatory network. Furthermore, the functional annotations of these target genes in regulatory networks were presented using the Cytoscape and the Metascape annotation tool. Finally, the expression pattern of the four autophagy-related lncRNAs was evaluated via qRT-PCR. In conclusion, our findings suggest that the four autophagy-related lncRNAs could be critical molecules associated with the development of RB and affect the occurrence and development of RB through the lncRNA-miRNA-mRNA regulatory network. Genes (GRP13B, IFT88, EPHA3, GABARAPL1, and EIF4EBP1) may serve as potential novel therapeutic targets and biomarkers in RB.

Global change poses new challenges for pest management. Omnivorous predatory arthropods play an important role in pest management, yet their potential has not been fully explored. Not only do they consume prey, but their plant-feeding induces plant defences that decrease herbivores' performance, and increases production of volatiles that attract natural enemies. Growing evidence from different plant-arthropod systems indicates the generality of plant defence induction following omnivore plant-feeding. Furthermore, these responses appear to affect other organisms (e.g. plant viruses), altering multi-trophic interactions. Here, we review the dual role of omnivores (as predators and plant inducers), identify knowledge gaps and provide future perspectives to increase our understanding of omnivores' multiple functions, and how this can be applied to advance plant protection strategies.

The spread of Acinetobacter baumannii in clinical settings is a great concern at the time being, given the epidemic potential and the capacity to elude the effects of drugs of this bacterial species. How A. baumannii achieves its resistance determinants is not yet exactly understood, hence the need for new studies aimed at resolving its structure and functions. In this work, we employ Re-scan Confocal Microscopy (RCM), an emerging super-resolution technique, for investigating the morphology of this pathogen. Interestingly, about 1.5% of the imaged cells were found to be filamentous without internal division septa, in both logarithmic and stationary phases, which, to our knowledge, has not been previously reported. Since filamenting represents one of the first mechanisms adopted by bacteria to resist antibiotic effects, we also focus on evaluating the sensitivity of A. baumannii to colistin. For this, the LIVE/DEAD ratio is assessed by means of a fluorometric approach based on SYTO9 and KK114 dyes, two stains that we also used for RCM imaging. Their dual role demonstrated here can potentially be exploited in-tandem in multimodal systems for imaging and fluorometry.

Lipases play an important dual role in the dairy industry. Lipases improve quality but cause deterioration and changes in quality during the processing and storage of dairy products. Therefore, a rapid and sensitive method for determining lipase activity is needed. A new reagent, called a ‘Clarifying Buffer’, was developed for the clarification of opaque milk and the direct detection of lipase activity in milk using spectrophotometry. The present study successfully used a microplate-based method to analyze lipase activity in milk products. The lipase activities of raw milk samples subjected to different heat treatments were evaluated using the new method. The new method was sensitive to the activity of trace lipase in milk samples treated at 135 °C for 5, 10, and 30 s.

Nanoparticles (NPs) are one of the most advanced technologies for combating the increased resistance of agriculture pests to current remedies. We report copper nanoparticles (CuNPs) as an efficient...

This study reviews the possible origins, functional roles, and diagnostic applications of 'extracellular genetic material' (EGM), a novel term introduced to cover DNA, RNA, and DNA/RNA-related molecules released from all types of cells into the extracellular region. The literature on EGMs shows them to play a dual role in diverse, fine-tuning mechanisms involved in both homeostasis and pathological events, including cancerogenesis and genometastasis. Recent developments in the next-generation technology have provided successful applications of low quantities of genomic materials into the diagnostic field, yielding high sensitivity and specificity in test results. Also, the successful application of EGMs into diagnostics has afforded promising outcomes for researchers and clinicians. This study of EGM provides a deeper understanding of the subject as an area of interest, especially cell-free DNA, aiming toward the eventual development of new therapeutic applications and diagnostic strategies.

Background Neurodegenerative diseases are debilitating conditions that diminish the quality of life and pose significant financial and social burdens. Therefore, strategies to relieve and control these diseases are urgently required, which will improve the quality of patients’ lives. Dysbacteriosis of gut microbiota has been shown to be a key component of neurodegenerative disease etiology. The homeostasis of gut microbiota and the balance of reactive oxygen species (ROS) in the gut can be altered by bioactive peptides derived from food sources. Therefore, biopeptides that improve neurodegenerative diseases by regulating gut microbiota have received considerable attention. Scope and approach The impact of gut microbiota on the brain through the gut-brain axis has been summarized. Additionally, the dual role of ROS in regulating the homeostasis of gut and gut microbiota and the function of bioactive peptides in ameliorating neurodegenerative diseases via the microbiota-gut-brain axis are discussed. Potential strategies for the production and modification of peptides to improve their bioactivity are also highlighted. Key findings and conclusions Increasing evidence supports that the gut microbiota modulates neurodegenerative diseases. Bioactive peptides that modulate the gut microbiota can be used as novel and strategic molecules to control and reduce neurodegenerative diseases. The bioactivity of the peptides can be dramatically influenced by different production and modification strategies. Strategies for further development of functional foods to ameliorate neurodegenerative diseases by regulating the gut microbiota are available. Future work should focus on the bioavailability and interactions of bioactive peptides and their impact on neurodegenerative diseases.

4-Androstenedione (4-AD) and progesterone (PG) are two of the most important precursors for synthesis of steroid drugs, however their current manufacturing processes suffer from low efficiency and severe environmental issues. In this study, we decipher a dual-role reductase (mnOpccR) in the phytosterols catabolism, which engages in two different metabolic branches to produce the key intermediate 20-hydroxymethyl pregn-4-ene-3-one (4-HBC) through a 4-e reduction of 3-oxo-4-pregnene-20-carboxyl-CoA (3-OPC-CoA) and 2-e reduction of 3-oxo-4-pregnene-20-carboxyl aldehyde (3-OPA), respectively. Inactivation or overexpression of mnOpccR in the Mycobacterium neoaurum can achieve exclusive production of either 4-AD or 4-HBC from phytosterols. By utilizing a two-step synthesis, 4-HBC can be efficiently converted into PG in a scalable manner (100 gram scale). This study deciphers a pivotal biosynthetic mechanism of phytosterol catabolism and provides very efficient production routes of 4-AD and PG.

Cardiovascular diseases (CVDs) remain the world’s leading cause of death. Cardiomyocyte autophagy helps maintain normal metabolism and functioning of the heart. Importantly, mounting evidence has revealed that autophagy plays a dual role in CVD pathology. Under physiological conditions, moderate autophagy maintains cell metabolic balance by degrading and recycling damaged organelles and proteins, and it promotes myocardial survival, but excessive or insufficient autophagy is equally deleterious and contributes to disease progression. Noncoding RNAs (ncRNAs) are a class of RNAs transcribed from the genome, but most ncRNAs do not code for functional proteins. In recent years, increasingly, various ncRNAs have been identified, and they play important regulatory roles in the physiological and pathological processes of organisms, as well as in autophagy. Thus, determining whether ncRNA-regulated autophagy plays a protective role in CVDs or promotes their progression can help us to develop ncRNAs as therapeutic targets in autophagy-related CVDs. In this review, we briefly summarize the regulatory roles of several important ncRNAs, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the autophagy of various CVDs to provide a theoretical basis for the etiology and pathogenesis of CVDs and develop novel therapies to treat CVDs., Graphical Abstract, Cardiovascular diseases (CVDs) remain the world’s leading cause of death. Mounting evidence has revealed that ncRNAs and autophagy play critical roles in CVD pathology. Determining whether ncRNA-regulated autophagy plays a protective role in CVDs or promotes their progression can help us to develop ncRNAs as therapeutic targets in autophagy-related CVDs.

For many drugs, the liver is the major site of metabolism. Uptake transporters from the solute carrier superfamily, cytochrome P450 enzymes, and efflux transporters from the adenosine triphosphate (ATP) binding cassette (ABC) transporters play major roles in systemic pharmacokinetics and drug-drug interactions. Solute carriers may facilitate drug passage from blood to the liver for further processing by metabolizing enzymes and efflux transporters. This chapter reviews the dual role of ABC transporters in drug metabolism and cancer multidrug resistance. It highlights the critical role of polymorphisms in treatment success. ABC transporter encoding genes are widely dispersed in the genome and show a high degree of sequence identity among eukaryotes. They translocate a wide range of substrates across cell or organelle membranes using the energy from ATP hydrolysis. The survival benefit of systemic chemotherapy in the treatment of liver cancer is only marginal at best.

E-cadherin is the main component of epithelial adherens junctions (AJs), which play a crucial role in the maintenance of stable cell–cell adhesion and overall tissue integrity. Down-regulation of E-cadherin expression has been found in many carcinomas, and loss of E-cadherin is generally associated with poor prognosis in patients. During the last decade, however, numerous studies have shown that E-cadherin is essential for several aspects of cancer cell biology that contribute to cancer progression, most importantly, active cell migration. In this review, we summarize the available data about the input of E-cadherin in cancer progression, focusing on the latest advances in the research of the various roles E-cadherin-based AJs play in cancer cell dissemination. The review also touches upon the “cadherin switching” in cancer cells where N- or P-cadherin replace or are co-expressed with E-cadherin and its influence on the migratory properties of cancer cells.

The Wnt pathway plays an essential role in the initiation and progression of various types of cancer. ROR1 and ROR2 are Wnt receptors that are critical for β-catenin-independent (non-canonical) pathways and have been linked to processes driving tumor development and progression, such as cell proliferation, survival, invasion, and therapy resistance. Both receptors have garnered interest as potential therapeutic targets since they are largely absent in adult tissue, are overexpressed in several cancers, and, as members of the receptor tyrosine kinase family, are easier to target than all other components of the pathway. Unlike ROR1 which always promotes tumorigenesis, ROR2 has a very complex role in cancer acting either to promote or inhibit tumor progression in different tumor types. In the present article, we summarize the findings on ROR2 expression in cancer patients and its impact on clinical outcome. Further, we review the biological processes and signaling pathways regulated by ROR2 that explain its dual role in cancer. Finally, we describe the ongoing strategies to target ROR2 in cancer.

It is shown that the Drosophila slp1 gene is a direct target of the Runt transcription factor. Interestingly, binding sites for Runt important for repression, but less so for activation by the slp1 DESE enhancer, clearly contribute to DESE-dependent activation in a composite reporter gene construct also containing the slp1 PESE enhancer.

Environment structure often shapes social interactions. Spatial attractors that draw multiple individuals may play a particularly important role in dispersed groups, where individuals must first encounter one another to interact. We use GPS data recorded simultaneously from five spotted hyenas (Crocuta crocuta) within a single clan to investigate how communal dens and daily ranging patterns shape fission-fusion dynamics (subgroup splits and merges). We introduce a species-general framework for identifying and characterizing dyadic fission-fusion events and describe a taxonomy of ten possible configurations of these events. Applying this framework to the hyena data illuminates the spatiotemporal structure of social interactions within hyenas’ daily routines. The most common types of fission-fusion events involve close approaches between individuals, do not involve co-travel together, and occur at the communal den. Comparison to permutation-based reference models suggests that den usage structures broad-scale patterns of social encounters, but that other factors influence how those encounters unfold. We discuss the dual role of communal dens in hyenas as physical and social resources, and suggest that dens are an example of a general “social piggybacking” process whereby environmental attractors take on social importance as reliable places to encounter conspecifics, causing social and spatial processes to become fundamentally intertwined.

In this review, we examine the multiple roles of ROS in the pathogenesis of melanoma, focusing on signal transduction and regulation of gene expression. In recent years, different studies have analyzed the dual role of ROS in regulating the redox system, with both negative and positive consequences on human health, depending on cell concentration of these agents. High ROS levels can result from an altered balance between oxidant generation and intracellular antioxidant activity and can produce harmful effects. In contrast, low amounts of ROS are considered beneficial, since they trigger signaling pathways involved in physiological activities and programmed cell death, with protective effects against melanoma. Here, we examine these beneficial roles, which could have interesting implications in melanoma treatment.

Enterococcus spp. are one of the most frequent producers of bacteriocins (enterocins), which provides them with an advantage to compete in their natural environment, which is the gut of humans and many animals. The enterocins’ activity against microorganisms from different phylogenetic groups has raised interest in Enterococcus spp. in different contexts throughout the last decades, especially in the food industry. Nevertheless, some species can also cause opportunistic life-threatening infections and are frequently multidrug-resistant (MDR). Vancomycin-resistant Enterococcus (VRE), in particular, are an ongoing global challenge given the lack of therapeutic options. In this scenario, bacteriocins can offer a potential solution to this persistent threat, either alone or in combination with other antimicrobials. There are a handful of studies that demonstrate the advantages and applications of bacteriocins, especially against VRE. The purpose of this review is to present a current standpoint about the dual role of Enterococcus spp., from important producers to targets needed to be controlled, and the crucial role that enterocins may have in the expansion of enterococcal populations. Classification and distribution of enterocins, the current knowledge about the bacteriocinome of clinical enterococci, and the challenges of bacteriocin use in the fight against VRE infections are particularly detailed.

Autophagy, an essential biological process that affects immunity, is a powerful tool that host cells can use to defend against infections caused by pathogenic microorganisms. Autophagy can not only initiate innate immune responses but also degrade the cellular components that provide the conditions for removing the invaders. However, hyperactivated or inhibited autophagy leads to mitochondrial dysfunction, which is harmful to the host itself and is involved in many types of diseases. Mitochondria perform the functions of biological oxidation and energy exchange. In addition, mitochondrial functions are closely related to cell death, oxygen radical formation, and disease. Accumulation of mitochondrial metabolites affects survival of intracellular pathogens. In this mini-review, we focus on the crosstalk between autophagy and mitochondrial homeostasis during infection.

Endothelial-to-mesenchymal transition (EndMT) is the biological process through which endothelial cells transdifferentiate into mesenchymal cells. During embryo development, EndMT regulates endocardial cushion formation via TGFβ/BMP signaling. In adults, EndMT is mainly activated during pathological conditions. Hence, it is necessary to characterize molecular regulators cooperating with TGFβ signaling in driving EndMT, to identify potential novel therapeutic targets to treat these pathologies. Here, we studied YAP, a transcriptional co-regulator involved in several biological processes, including epithelial-to-mesenchymal transition (EMT). As EndMT is the endothelial-specific form of EMT, and YAP (herein referring to YAP1) and TGFβ signaling cross-talk in other contexts, we hypothesized that YAP contributes to EndMT by modulating TGFβ signaling. We demonstrate that YAP is required to trigger TGFβ-induced EndMT response, specifically contributing to SMAD3-driven EndMT early gene transcription. We provide novel evidence that YAP acts as SMAD3 transcriptional co-factor and prevents GSK3β-mediated SMAD3 phosphorylation, thus protecting SMAD3 from degradation. YAP is therefore emerging as a possible candidate target to inhibit pathological TGFβ-induced EndMT at early stages., Journal of Cell Science, 134 (15), ISSN:1477-9137, ISSN:0021-9533

Variation in floral displays, both between and within species, has been long known to be shaped by the mutualistic interactions that plants establish with their pollinators. However, increasing evidence suggests that abiotic selection pressures influence floral diversity as well. Here we analyze the genetic and environmental factors that underlie patterns of floral pigmentation in wild sunflowers. While sunflower inflorescences appear invariably yellow to the human eye, they display extreme diversity for patterns of ultraviolet pigmentation, which are visible to most pollinators. We show that this diversity is largely controlled by cis-regulatory variation at a single MYB transcription factor, HaMYB111, through accumulation of UV-absorbing flavonol glycosides. As expected, different patterns of ultraviolet pigments in flowers have a strong effect on pollinator preferences. However, variation for floral ultraviolet patterns is also associated with environmental variables, especially relative humidity, across populations of wild sunflowers. Larger ultraviolet patterns, which are found in drier environments, limit transpiration, therefore reducing water loss. The dual role of floral UV patterns in pollination attraction and abiotic responses reveals the complex adaptive balance underlying the evolution of floral traits.

Toll-like receptors (TLRs) are a class of pattern recognition receptors (PRRs) family that identify pathogen-associated molecular patterns derived from microbes and activate immune cell response. Following TLRs ligation, different adaptor and transcription molecules such as myeloid differentiation primary response gene 88 (MyD88) and nuclear factor kappa B (NF-kB) are recruited that initiate inflammatory signaling pathways. The human Toll-like receptor 10 (hTLR10) is a novel member of the PRRs family with a regulatory function of immune responses because of unique cytoplasmic domains which lead to induction of both inflammatory and anti-inflammatory properties. Recent studies have reported the association of TLR10 polymorphisms with many inflammatory diseases and human cancer. Engagement of TLR10 on the surface of the epithelium and macrophages leads to the production of proinflammatory cytokines and chemokines, while other studies have proven an anti-inflammatory role of TLR10. Accordingly, TLR10 suppresses proinflammatory cytokine production via negative regulation of MyD88 and the Akt (protein kinase B) and MAPK (mitogen-activated protein kinase) signaling pathways. This review aimed to provide answers for these conflicting findings (Inflammatory and anti-inflammatory properties of TLR10) to further identify distinct biological functions of TLR10.

Dorsal-ventral patterning of the Drosophila embryo depends on the NFκB superfamily transcription factor Dorsal (Dl). Toll receptor activation signals for degradation of the IκB inhibitor Cactus (Cact), leading to a ventral-to-dorsal nuclear Dl gradient. Cact is critical for Dl nuclear import, as it binds to and prevents Dl from entering the nuclei. Quantitative analysis of cact mutants revealed an additional Cact function to promote Dl nuclear translocation in ventral regions of the embryo. To investigate this dual Cact role, we developed a predictive model based on a reaction-diffusion regulatory network. This network distinguishes non-uniform Toll-dependent Dl nuclear import and Cact degradation, from the Toll-independent processes of Cact degradation and reversible nuclear-cytoplasmic Dl flow. In addition, it incorporates translational control of Cact levels by Dl. Our model successfully reproduces wild-type data and emulates the Dl nuclear gradient in mutant dl and cact allelic combinations. Our results indicate that the dual role of Cact depends on the dynamics of Dl-Cact trimers along the dorsal-ventral axis: In the absence of Toll activation, free Dl-Cact trimers retain Dl in the cytoplasm, limiting the flow of Dl into the nucleus; in ventral-lateral regions, Dl-Cact trimers are recruited by Toll activation into predominant signaling complexes and promote Dl nuclear translocation. Simulations suggest that the balance between Toll-dependent and Toll-independent processes are key to this dynamics and reproduce the full assortment of Cact effects. Considering the high evolutionary conservation of these pathways, our analysis should contribute to understanding NFκB/c-Rel activation in other contexts such as in the vertebrate immune system and disease., Author summary In Drosophila, Toll pathway establishes spatially distinct gene expression territories that define the embryonic dorsal-ventral axis. Toll activation leads to degradation of the IκB inhibitor Cactus, releasing the NFκB superfamily transcription factor Dorsal for nuclear entry. Recently, quantitative analysis of cact mutants revealed that Cact displays an additional function to promote Dl nuclear translocation in ventral regions of the embryo. To understand this novel activity, we developed a predictive theoretical model that shows that the kinetics of Dorsal-Cactus complex formation prior to their recruitment to Toll-signaling complexes is an essential regulatory hub. Cactus controls the balance between the recruitment of these complexes by active Toll receptor and association-dissociation events that generate free Dorsal for direct nuclear import.

The Ki67 protein is proposed to have two conformations; one which segregates chromosomes before anaphase, and the other which results in chromosome condensation after cell division to exclude large cytosolic components from the reforming nuclei of daughter cells.

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.

Multiple studies have shown that cancer‐associated fibroblasts (CAFs) play an important role in tumour progression, including carcinogenesis, invasion, metastasis and the chemoresistance of cancer cells. Immune cells, including macrophages, natural killer cells, dendritic cells and T cells, play a dual role in the tumour microenvironment. Although increasing research has focused on studying interactions between distinct cells in the tumour microenvironment, the complex relationships between CAFs and immune cells remain unclear and need further study. Here, we summarize our current understanding of crosstalk between CAFs and immune cells, which may help clarify their diagnostic and therapeutic value in tumour progression.

Tau is an axonal protein known to form abnormal aggregates and is the biomarker of Alzheimer's disease. Metal-based therapeutics for inhibition of Tau aggregation is limited and rarely reported in contemporary science. Here, we report the first example of rationally designed molecular cobalt(II)-complexes for effective inhibition of Tau and disaggregation of preformed Tau fibrils. The mechanistic studies reveal that prevention of Tau aggregation by cobalt-based metal complexes (CBMCs) is concentration-dependent and Tau seldom exhibits conformational changes. Interestingly, CBMCs play dual role in causing disassembly of preformed aggregates as well as inhibition of complete Tau aggregation. Furthermore, CBMCs were nontoxic and maintained the tubulin network intact. CBMCs also prevented okadaic acid-induced toxicity in SH-SY5Y cells thus, preventing hyperphosphorylation of Tau. We believe that this unprecedented finding by the newly developed molecular complexes has a potential toward metal-based therapeutics for Alzheimer's disease.

15 pages, 3 tables, 3 figures, Interferon-gamma (IFN-ϒ) is probably one of the most relevant cytokines orchestrating the immune response in vertebrates. Although the activities mediated by this molecule are well known in mammals, several aspects of the IFN-ϒ system in teleosts remain a riddle to scientists. Numerous studies support a potentially similar role of the fish IFN-ϒ signalling pathway in some well-described immunological processes induced by this cytokine in mammals. Nevertheless, the existence in some teleost species of duplicated ifng genes and an additional gene derived from ifng known as interferon-γ-related (ifngrel), among other things, raises new interesting questions about the mode of action of these various molecules in fish. Moreover, certain IFN-ϒ-mediated activities recently observed in mammals are still fully unknown in fish. Another attractive but mainly unexplored curious property of IFN-ϒ in vertebrates is its potential dual role depending on the type of pathogen. In addition, some aspects mediated by this molecule could favour the resolution of a bacterial infection but be harmful in the context of a viral disease, and vice versa. This review collects old and new aspects of IFN-ϒ research in teleosts and discusses new questions and pathways of investigation based on recent discoveries in mammals, This work was funded by the project BIO2017-82851-C3-1-R from the Spanish Ministerio de Economía y Competitividad and IN607B 2016/12 from Consellería de Economía, Emprego e Industria (GAIN), Xunta de Galicia. Patricia Pereiro wishes to thank the Axencia Galega de Innovación (GAIN, Xunta de Galicia) for her postdoctoral contract (IN606B-2018/010)

Root gravitropism is one of the most important processes allowing plant adaptation to the land environment. Auxin plays a central role in mediating root gravitropism, but how auxin contributes to gravitational perception and the subsequent response are still unclear. Here, we showed that the local auxin maximum/gradient within the root apex, which is generated by the PIN directional auxin transporters, regulates the expression of three key starch granule synthesis genes, SS4, PGM and ADG1, which in turn influence the accumulation of starch granules that serve as a statolith perceiving gravity. Moreover, using the cvxIAA-ccvTIR1 system, we also showed that TIR1-mediated auxin signaling is required for starch granule formation and gravitropic response within root tips. In addition, axr3 mutants showed reduced auxin-mediated starch granule accumulation and disruption of gravitropism within the root apex. Our results indicate that auxin-mediated statolith production relies on the TIR1/AFB-AXR3-mediated auxin signaling pathway. In summary, we propose a dual role for auxin in gravitropism: the regulation of both gravity perception and response.

The light-harvesting 1 reaction center (LH1-RC) complex in the purple sulfur bacterium Thiorhodovibrio (Trv.) strain 970 cells exhibits its LH1 Qy transition at 973 nm, the lowest-energy Qy absorpt...

A large number of reviews have discussed many aspects of oxidative burst due to plant exposure to biotic and abiotic stresses, including the dual role of reactive oxygen species (ROS) as both signaling and toxic compounds, and the strategies developed by plants to cope with this oxidative imbalance. In this review, we have concentrated on fresh new information and other promising and emerging topics of oxidative stress and antioxidant mechanisms in plants, giving particular attention to genotoxicity, transgenerational alterations and quantitative trait loci (QTL) associated with enhancements in the plant tolerance to stresses. Furthermore, besides the discussion of the “classical” enzymatic and non-enzymatic components of plant defense, novel aspects about the components of the antioxidant machinery, which now includes sugars, annexins and dehydrins, are also presented, along with a final section on future directions in this field.

Reactive Oxygen Species (ROS) play an essential dual role in living systems. Healthy levels of ROS modulate several signaling pathways, but at the same time, when they exceed normal physiological amounts, they work in the opposite direction, playing pivotal functions in the pathophysiology of multiple severe medical conditions (i.e., cancer, diabetes, neurodegenerative and cardiovascular diseases, and aging). Therefore, the research for methods to detect their levels via light-sensitive fluorescent probes has been extensively studied over the years. However, this is not the only link between light and ROS. In fact, the modulation of ROS mediated by light has been exploited already for a long time. In this review, we report the state of the art, as well as recent developments, in the field of photostimulation of oxidative stress, from photobiomodulation (PBM) mediated by naturally expressed light-sensitive proteins to the most recent optogenetic approaches, and finally, we describe the main methods of exogenous stimulation, in particular highlighting the new insights based on optically driven ROS modulation mediated by polymeric materials.

A nursery pollinator system comprises a plant and an insect pollinator which uses the reproductive structures of the plant to guard its eggs and serve it as food for the larvae. This kind of systems usually includes a third party, one or more species of parasitoids, that inject their eggs inside the larvae of the pollinating-seed predator to feed on them from the inside out. Here we build a model based on differential equations that replicates this system, first by showing the dual role of the pollinating-seed predator, which behaves both as a mutualist and as antagonist for the plant. We show that the system is more stable with the presence of the parasitoids; the stationary solutions with them significantly favor the plant population size with minor effects for the population of the pollinating-seed predator. By modeling both sexes of the nursery pollinator separately, we also highlight the role that male adults can have to compensate the costs and benefits of the interaction with plants, and thus to contribute to the stability of such mutualisms.

The distinction between mechanisms that generate biological variation and mechanisms that modify it has been important in contemporary Biology, especially since the establishment of the Evolutionary Synthesis (ES) in the first part of the twentieth century. In the ES, and in its subsequent legacy to evolutionary biology, the focus was directed at mechanisms that modify biological variation. In recent years, evo-devo (Evolutionary Developmental Biology) emerged as an area of knowledge that proposes to extend the ES in many forms. In this sense, given that evo-devo integrates different areas of Biology, different types of mechanisms can be found. In order to understand evo-devo mechanisms, as well as its relation with the ES, we analyzed the role that evo-devo mechanisms play with respect to biological variation. The main question in our analysis was: do evo-devo mechanisms have a function of generators and/or modifiers of biological variation? We focused on three evo-devo mechanisms: environmental induction, hypervariability/somatic selection and developmental bias. Our analysis showed a different characterization of the action of evo-devo mechanisms. This heterogeneity in the role of evo-devo mechanisms shows that, in general, the distinction is maintained but there is a mechanism that presents a dual role. Our analysis indicates that, at least with respect to mechanisms, evo-devo extends and departs from what was proposed in the evolutionary synthesis. Fil: Folguera, Guillermo. Universidad de Buenos Aires. Facultad de Filosofía y Letras. Instituto de Filosofía "Dr. Alejandro Korn"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Lavagnino, Nicolas Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Ecología, Genética y Evolución de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Ecología, Genética y Evolución de Buenos Aires; Argentina

PURPOSE OF THE REVIEW: In this review, we discuss recent advances into delineating the dual role of intestinal phagocytes in health and during intestinal disease. We further discuss the key role of gut-resident macrophages in recognition of bacterial and fungal microbiota in the gut. RECENT FINDINGS: Inflammatory bowel disease (IBD) commonly manifests with pathologic changes in the composition of gut bacterial and fungal microbiota. Intestinal macrophages are key regulators of the balance between tolerogenic immunity and inflammation. Recent studies have highlighted the role of resident intestinal macrophages in the control of commensal fungi and bacteria in the steady state and during dysbiosis. The dual role of these cells in maintaining intestinal homeostasis and responding to microbiota dysbiosis during inflammation is being increasingly studied. SUMMARY: It is becoming increasingly clear that an aberrant pro-inflammatory response to microbiota by infiltrating monocytes plays a role in the development of intestinal inflammation. Intestinal mononuclear phagocytes with characteristics of macrophages play an important role in limiting fungal and bacterial overgrowth under these conditions, but can be influenced by the inflammatory environment to further propel inflammation. Better understanding of the interaction of intestinal macrophages with host microbiota including commensal fungi and bacteria, provides an opportunity for the development of more targeted therapies for Inflammatory Bowel Disease.

Persuasion is a crucial component of the courtship ritual needed to overcome contact aversion. In fruit flies, it is well established that the male courtship song prompts receptivity in female flies, in part by causing sexually mature females to slow down and pause, allowing copulation. Whether the above receptivity behaviours require the suppression of contact avoidance or escape remains unknown. Here we show, through genetic manipulation of neurons we identified as required for female receptivity, that male song induces avoidance/escape responses that are suppressed in wild type flies. First, we show that silencing 70A09 neurons leads to an increase in escape, as females increase their walking speed during courtship together with an increase in jumping and a reduction in pausing. The increase in escape response is specific to courtship, as escape to a looming threat is not intensified. Activation of 70A09 neurons leads to pausing, confirming the role of these neurons in escape modulation. Finally, we show that the escape displays by the female result from the presence of a courting male and more specifically from the song produced by a courting male. Our results suggest that courtship song has a dual role, promoting both escape and pause in females and that escape is suppressed by the activity of 70A09 neurons, allowing mating to occur.

The prion-like self-perpetuating conformational conversion is involved in both transmissible neurodegenerative diseases and non-Mendelian inheritance traits. The transmissibility of amyloid-like aggregates is dependent on the stoichiometry of chaperones such as heat shock proteins. To provide the mechanistic underpinning of the generation and persistence of prefibrillar amyloid seeds that are critical for the prion-like propagation, we studied the effect of Hsp104 disaggregase on the assembly mechanism of a yeast prion determinant of Saccharomyces cerevisiae Sup35. At low sub-stoichiometric concentrations, Hsp104 exhibits a dual role and considerably accelerates the formation of seeding-competent prefibrillar amyloids by shortening the lag phase but also prolongs their persistence by introducing unusual kinetic halts and delaying their conversion into matured fibers. Hsp104-mediated amyloid species comprise a more ordered packing and display an enhanced autocatalytic self-templating ability compare to amyloids formed without Hsp104. Our findings underscore the key functional and pathological roles of sub-stoichiometric chaperones in prion-like propagation.

The ability to maintain a high core body temperature is a defining characteristic of all mammals, yet their diverse habitats present disparate thermal challenges that have led to specialized adaptations. Marine mammals inhabit a highly conductive environment. Their thermoregulatory capabilities far exceed our own despite having limited avenues of heat transfer. Additionally, marine mammals must balance their thermoregulatory demands with those associated with diving (i.e. oxygen conservation), both of which rely on cardiovascular adjustments. This review presents the progress and novel efforts in investigating marine mammal thermoregulation, with a particular focus on the role of peripheral perfusion. Early studies in marine mammal thermal physiology were primarily performed in the laboratory and provided foundational knowledge through in vivo experiments and ex vivo measurements. However, the ecological relevance of these findings remains unknown because comparable efforts on free-ranging animals have been limited. We demonstrate the utility of biologgers for studying their thermal adaptations in the context in which they evolved. Our preliminary results from freely diving northern elephant seals (Mirounga angustirostris) reveal blubber’s dynamic nature and the complex interaction between thermoregulation and the dive response due to the dual role of peripheral perfusion. Further exploring the potential use of biologgers for measuring physiological variables relevant to thermal physiology in other marine mammal species will enhance our understanding of the relative importance of morphology, physiology, and behavior for thermoregulation and overall homeostasis.

Using the zebrafish neural tube as a model, we uncover thein vivomechanisms allowing the generation of two opposing apical epithelial surfaces within the centre of an initially unpolarised, solid organ. We show that NOK/Pals1/Mpp5a and Rab11a play a dual role in coordinating the generation of ipsilateral junctional belts whilst simultaneously releasing contralateral adhesions across the centre of the tissue. We show that Nok and Rab11a mediated resolution of cell-cell adhesions are both necessary for midline lumen opening and contribute to later maintenance of epithelial organisation. We propose these roles for both Nok and Rab11a operate through the transmembrane protein Crumbs. In light of a recent conflicting publication, we also clarify that the junction remodelling role of Nok is not specific to dividing cells.

Using the zebrafish neural tube as a model, we uncover the in vivo mechanisms allowing the generation of two opposing apical epithelial surfaces within the centre of an initially unpolarised, solid organ. We show that Mpp5a and Rab11a play a dual role in coordinating the generation of ipsilateral junctional belts whilst simultaneously releasing contralateral adhesions across the centre of the tissue. We show that Mpp5a- and Rab11a-mediated resolution of cell-cell adhesions are both necessary for midline lumen opening and contribute to later maintenance of epithelial organisation. We propose that these roles for both Mpp5a and Rab11a operate through the transmembrane protein Crumbs. In light of a recent conflicting publication, we also clarify that the junction-remodelling role of Mpp5a is not specific to dividing cells.

The female mammal produces, stores and ejects milk from the mammary gland to nourish her offspring. Calcium plays a dual role, both as an essential nutrient in milk and in signal transduction. This perspective covers exciting new insights on calcium and cellular connectivity in this essential organ.

The Insulin signal cascade is one of the best studied metabolic circuits, and shows a remarkable high molecular and functional conservation across the animal kingdom. Insulin-producing cells respond directly to nutritional cues in circulation and receive modulatory input from connected neuronal networks. Neuronal control is rapid and integrates a wide range of variables including dietary change or environmental temperature. However, despite various detailed studies that demonstrated the potential of neuronal regulation the physiological relevance of this circuit remains elusive.In Drosophila, Insulin-like peptide 7 (dIlp7)-producing neurons are wired with Insulin-producing cells. We found a dual role for this neuronal subset: a.) activated dilp7-producing neurons are required to facilitate development at high temperatures, and if confronted with calorie-rich food that represses neuronal activity b.) their product, dIlp7, regulates Insulin signalling levels. Our work shows that Insulin-producing cells not simply integrate signals from circulating nutritional cues and neuronal inputs, but switch to neuronal control in response to dietary composition.

Animals continuously encounter microorganisms that are essential for health or cause disease. They are thus challenged to control harmful microbes while allowing acquisition of beneficial microbes. This challenge is likely especially important for social insects with respect to microbes in food, as they often store food and exchange food among colony members. Here we show that formicine ants actively swallow their antimicrobial, highly acidic poison gland secretion. The ensuing acidic environment in the stomach, the crop, limits establishment of pathogenic and opportunistic microbes ingested with food and improves survival of ants when faced with pathogen contaminated food. At the same time, crop acidity selectively allows acquisition and colonization by Acetobacteraceae, known bacterial gut associates of formicine ants. This suggests that swallowing of the poison gland secretion acts as a microbial filter in formicine ants and indicates a potentially widespread but so far underappreciated dual role of antimicrobials in host-microbe interactions.

A unique feature in the organization of the olfactory system is the dual role of the odorant receptors: they detect odors in the nasal epithelium and they play an instructive role in the convergence of olfactory sensory neuron axons in specific loci, ie, glomeruli, in the olfactory bulb. The dual role is corroborated by the expression of the odorant receptors in 2 specific locations of the olfactory sensory neurons: the cilia that protrude in the nostril, where the odorant receptors interact with odors, and the axon terminal, a suitable location for a potential axon guidance molecule. The mechanism of activation and function of the odorant receptors expressed at the axon terminal remained unknown for almost 20 years. A recent study identified the first putative ligand of the axonal odorant receptors, phosphatidylethanolamine-binding protein1, a molecule expressed in the olfactory bulb. The distinctive mechanisms of activation of the odorant receptors expressed at the opposite locations in sensory neurons, by odors, at the cilia, and by molecules expressed in the olfactory bulb, at the axon terminal, explain the dual role of the odorant receptors and link the specificity of odor perception with its internal representation, in the topographic map.