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Summary After a period of heavy emphasis on negative interactions, such as predation and competition, the past two decades have seen an explosion of literature on the role of positive interactions in ecological communities. Such positive interactions can take many forms. One possibility is that amelioration of environmental stress by plants or sessile animals enhances growth, reproduction and survival of others, but many more intricate patterns exist. Importantly such positive interactions may contribute to creating a positive feedback. For instance, biomass can lead to improved environmental conditions causing better growth and therefore leading to more biomass. A positive feedback is a necessary (but not sufficient) condition for the emergence of alternative stable states at the community scale. However, the literature on positive interactions in plant and animal communities rarely addresses this connection. Here, we address this gap, asking the question of when positive interactions may lead to alternative stable states, and hence set the stage for catastrophic transitions at tipping points in ecosystems. We argue that, although there are a number of now classical examples in the literature for which positive interactions are clearly the main actors of positive feedback loops, more empirical and theoretical research scaling up from the individual‐level interactions to the community and the ecosystem scale processes is needed to further understand under which conditions positive interactions can trigger positive feedback loops, and thereby alternative stable states. Lay Summary

• Anthocyanin and proanthocyanidin (PA) accumulation is regulated by both myeloblastosis (MYB) activators and repressors, but little information is available on hierarchical interactions between the positive and negative regulators. Here, we report on a R2R3-MYB repressor in peach, designated PpMYB18, which acts as a negative regulator of anthocyanin and PA accumulation. • PpMYB18 can be activated by both anthocyanin- and PA-related MYB activators, and is expressed both at fruit ripening and juvenile stages when anthocyanins or PAs, respectively, are being synthesized. • The PpMYB18 protein competes with MYB activators for binding to basic Helix Loop Helixes (bHLHs), which develops a fine-tuning regulatory loop to balance PA and anthocyanin accumulation. In addition, the bHLH binding motif in the R3 domain and the C1 and C2 repression motifs in the C-terminus of PpMYB18 both confer repressive activity of PpMYB18. • Our study also demonstrates a modifying negative feedback loop, which prevents cells from excess accumulation of anthocyanin and PAs, and serves as a model for balancing secondary metabolite accumulation at the transcriptional level.

TaVrn1, encoding a MADS-box transcription factor (TF), is the central regulator of wheat vernalization-induced flowering. Considering that the MADS-box TF usually works by forming hetero- or homodimers, we conducted yeast-two-hybrid screening and identified an SVP-like MADS-box protein TaVrt2 interacting with TaVrn1. However, the specific function of TaVrt2 and the biological implication of its interaction with TaVrn1 remained unknown. We validated the function of TaVrt2 and TaVrn1 by wheat transgenic experiments and their interaction through multiple protein-binding assays. Population genetic analysis also was used to display their interplay. Transcriptomic sequencing and chromatin immunoprecipitation assays were performed to identify their common targets. TaVrt2 and TaVrn1 are flowering promoters in the vernalization pathway and interact physically in vitro, in planta and in wheat cells. Additionally, TaVrt2 and TaVrn1 were significantly induced in leaves by vernalization, suggesting their spatio-temporal interaction during vernalization. Genetic analysis indicated that TaVrt2 and TaVrn1 had significant epistatic effects on flowering time. Furthermore, native TaVrn1 was up-regulated significantly in TaVrn1-OE (overexpression) and TaVrt2-OE lines.Moreover, TaVrt2 could bind with TaVrn1 promoter directly. A TaVrt2-mediated positive feedback loop of TaVrn1 during vernalization was proposed, providing additional understanding on the regulatory mechanism underlying vernalization-induced flowering.

Type I interferons (IFN) induce powerful antiviral and innate immune responses via the transcription factor, IFN‐stimulated gene factor (ISGF3). However, in some pathological contexts, type I IFNs are responsible for exacerbating inflammation. Here, we show that a high dose of IFN‐β also activates an inflammatory gene expression program in contrast to IFN‐λ3, a type III IFN, which elicits only the common antiviral gene program. We show that the inflammatory gene program depends on a second, potentiated phase in ISGF3 activation. Iterating between mathematical modeling and experimental analysis, we show that the ISGF3 activation network may engage a positive feedback loop with its subunits IRF9 and STAT2. This network motif mediates stimulus‐specific ISGF3 dynamics that are dependent on ligand, dose, and duration of exposure, and when engaged activates the inflammatory gene expression program. Our results reveal a previously underappreciated dynamical control of the JAK–STAT/IRF signaling network that may produce distinct biological responses and suggest that studies of type I IFN dysregulation, and in turn therapeutic remedies, may focus on feedback regulators within it. Synopsis The dose and duration of type I interferon exposure is interpreted by a signaling module that contains a stimulus‐contingent positive feedback loop to specify ISGF3 activation dynamics. A secondary, potentiated phase of ISGF3 activates a pro‐inflammatory gene expression program. High‐dose IFN‐β activates a pro‐inflammatory gene program in epithelial cells. IFN‐β, but not IFN‐λ3, induces a second, potentiated phase in ISGF3 activity. ISGF3 induces its subunits to form a stimulus‐contingent positive feedback loop. The positive feedback motif is required for the pro‐inflammatory gene program. Graphical Abstract The dose and duration of type I interferon exposure is interpreted by a signaling module that contains a stimulus‐contingent positive feedback loop to specify ISGF3 activation dynamics. A secondary, potentiated phase of ISGF3 activates a pro‐inflammatory gene expression program.

Purpose The usage of additive manufacturing (AM) technology in industries has reached up to 50 per cent as prototype or end-product. However, for AM products to be directly used as final products, AM product should be produced through advanced quality control process, which has a capability to be able to prove and reach their desire repeatability, reproducibility, reliability and preciseness. Therefore, there is a need to review quality-related research in terms of AM technology and guide AM industry in the future direction of AM development. Design/methodology/approach This paper overviews research progress regarding the QC in AM technology. The focus of the study is on manufacturing quality issues and needs that are to be developed and optimized, and further suggests ideas and directions toward the quality improvement for future AM technology. This paper is organized as follows. Section 2 starts by conducting a comprehensive review of the literature studies on progress of quality control, issues and challenges regarding quality improvement in seven different AM techniques. Next, Section 3 provides classification of the research findings, and lastly, Section 4 discusses the challenges and future trends. Findings This paper presents a review on quality control in seven different techniques in AM technology and provides detailed discussions in each quality process stage. Most of the AM techniques have a trend using in-situ sensors and cameras to acquire process data for real-time monitoring and quality analysis. Procedures such as extrusion-based processes (EBP) have further advanced in data analytics and predictive algorithms-based research regarding mechanical properties and optimal printing parameters. Moreover, compared to others, the material jetting progresses technique has advanced in a system integrated with closed-feedback loop, machine vision and image processing to minimize quality issues during printing process. Research limitations/implications This paper is limited to reviewing of only seven techniques of AM technology, which includes photopolymer vat processes, material jetting processes, binder jetting processes, extrusion-based processes, powder bed fusion processes, directed energy deposition processes and sheet lamination processes. This paper would impact on the improvement of quality control in AM industries such as industrial, automotive, medical, aerospace and military production. Originality/value Additive manufacturing technology, in terms of quality control has yet to be reviewed.

Circadian clocks coordinate organisms’ activities with daily cycles in their environment. Parasites are subject to daily rhythms in the within-host environment, resulting from clock-control of host activities, including immune responses. Parasites also exhibit rhythms in their activities: the timing of within-host replication by malaria parasites is coordinated to host feeding rhythms. Precisely which host feeding-related rhythm(s) parasites align with and how this is achieved are unknown. Understanding rhythmic replication in malaria parasites matters because it underpins disease symptoms and fuels transmission investment. We test if rhythmicity in parasite replication is coordinated with the host’s feeding-related rhythms and/or rhythms driven by the host’s canonical circadian clock. We find that parasite rhythms coordinate with the time of day that hosts feed in both wild-type and clockmutant hosts, whereas parasite rhythms become dampened in clock-mutant hosts that eat continuously. Our results hold whether infections are initiated with synchronous or with desynchronized parasites. We conclude that malaria parasite replication is coordinated to rhythmic host processes that are independent of the core-clock proteins PERIOD 1 and 2; most likely, a periodic nutrient made available when the host digests food. Thus, novel interventions could disrupt parasite rhythms to reduce their fitness, without interference by host clock-controlled homeostasis.

Evolutionary biology and ecology have a strong theoretical underpinning, and this has fostered a variety of modeling approaches. A major challenge of this theoretical work has been to unravel the tangled feedback loop between ecology and evolution. This has prompted the development of two main classes of models. While quantitative genetics models jointly consider the ecological and evolutionary dynamics of a focal population, a separation of timescales between ecology and evolution is assumed by evolutionary game theory, adaptive dynamics, and inclusive fitness theory. As a result, theoretical evolutionary ecology tends to be divided among different schools of thought, with different toolboxes and motivations. My aim in this synthesis is to highlight the connections between these different approaches and clarify the current state of theory in evolutionary ecology. Central to this approach is to make explicit the dependence on environmental dynamics of the population and evolutionary dynamics, thereby materializing the eco-evolutionary feedback loop. This perspective sheds light on the interplay between environmental feedback and the timescales of ecological and evolutionary processes. I conclude by discussing some potential extensions and challenges to our current theoretical understanding of eco-evolutionary dynamics.

Background Feedback loops in gene regulatory networks play pivotal roles in governing functional dynamics of cells. Systems approaches demonstrated characteristic dynamical features, including multistability and oscillation, of positive and negative feedback loops. Recent experiments and theories have implicated highly interconnected feedback loops (high-feedback loops) in additional nonintuitive functions, such as controlling cell differentiation rate and multistep cell lineage progression. However, it remains challenging to identify and visualize high-feedback loops in complex gene regulatory networks due to the myriad of ways in which the loops can be combined. Furthermore, it is unclear whether the high-feedback loop structures with these potential functions are widespread in biological systems. Finally, it remains challenging to understand diverse dynamical features, such as high-order multistability and oscillation, generated by individual networks containing high-feedback loops. To address these problems, we developed HiLoop, a toolkit that enables discovery, visualization, and analysis of several types of high-feedback loops in large biological networks. Results HiLoop not only extracts high-feedback structures and visualize them in intuitive ways, but also quantifies the enrichment of overrepresented structures. Through random parameterization of mathematical models derived from target networks, HiLoop presents characteristic features of the underlying systems, including complex multistability and oscillations, in a unifying framework. Using HiLoop, we were able to analyze realistic gene regulatory networks containing dozens to hundreds of genes, and to identify many small high-feedback systems. We found more than a 100 human transcription factors involved in high-feedback loops that were not studied previously. In addition, HiLoop enabled the discovery of an enrichment of high feedback in pathways related to epithelial-mesenchymal transition. Conclusions HiLoop makes the study of complex networks accessible without significant computational demands. It can serve as a hypothesis generator through identification and modeling of high-feedback subnetworks, or as a quantification method for motif enrichment analysis. As an example of discovery, we found that multistep cell lineage progression may be driven by either specific instances of high-feedback loops with sparse appearances, or generally enriched topologies in gene regulatory networks. We expect HiLoop’s usefulness to increase as experimental data of regulatory networks accumulate. Code is freely available for use or extension at https://github.com/BenNordick/HiLoop .

Background The Antarctic krill Euphausia superba is a keystone species in the Southern Ocean ecosystem. This crustacean has an ancestral clock whose main components have been identified and characterized in the past few years. However, the second feedback loop, modulating clock gene expression through two transcription factors, VRI and PDP1, has yet to be described. The presence of this second regulatory mechanism is suggested by the identification of its negative component, vrille , at the transcriptional level. Results Here, we describe the second feedback loop of krill by identifying the positive component, pdp1 , and functionally characterizing both pdp1 and vrille . Starting from the online transcriptome database KrillDB 2 , we identified and cloned three putative pdp1 sequences which were subsequently analyzed for tissue expression and functional activity using luciferase assays, individually and in combination with two vrille isoforms. Among the pdp1 isoforms , Espdp1 _3 displayed higher expression levels in relevant circadian districts than the other two. Furthermore, Es PDP1_3 and Es VRI_2 exhibited the expected positive and negative regulation of the V/P-box in our in vitro system. Finally, Espdp1 _3 and Esvrille also showed rhythmic expression in light–dark cycles, supporting their involvement in the regulation of the main circadian clock of the Antarctic krill. Conclusions This study expands our knowledge about the molecular architecture of the Antarctic krill circadian clock by defining the components that take part in the modulation of clock expression, establishing a second feedback loop.

The circadian clock is based on a transcriptional feedback loop with an essential time delay before feedback inhibition. Previous work has shown that PERIOD (PER) proteins generate circadian time cues through rhythmic nuclear accumulation of the inhibitor complex and subsequent interaction with the activator complex in the feedback loop. Although this temporal manifestation of the feedback inhibition is the direct consequence of PER’s cytoplasmic trafficking before nuclear entry, how this spatial regulation of the pacemaker affects circadian timing has been largely unexplored. Here we show that circadian rhythms, including wake-sleep cycles, are lengthened and severely unstable if the cytoplasmic trafficking of PER is disrupted by any disease condition that leads to increased congestion in the cytoplasm. Furthermore, we found that the time delay and robustness in the circadian clock are seamlessly generated by delayed and collective phosphorylation of PER molecules, followed by synchronous nuclear entry. These results provide clear mechanistic insight into why circadian and sleep disorders arise in such clinical conditions as metabolic and neurodegenerative diseases and aging, in which the cytoplasm is congested.