Phenotypic switching in cancer cells has been found to be present across tumor types. Recent studies on Glioblastoma report a remarkably common architecture of four well-defined phenotypes coexisting within high levels of intra-tumour genetic heterogeneity. Tumours grown from any cell type recapitulate the original phenotypic composition. Similar dynamics have been shown to occur in breast cancer, melanoma and likely across further cancer types. Given the adaptive potential of phenotypic switching (PHS) strategies, understanding how it drives tumour evolution and how to break down these architectures is a major priority. Here we model the ecological dynamics behind PHS. The model is able to reproduce experimental results, and specific conditions for cancer progression and clearance reveal novel features of plastic tumours and its direct consequences on therapy resistance. Following our results we discuss \textit{transition} therapy as a novel scheme to target not only combined cytotoxicity but also the rates of phenotypic switching.

Establishing macrometastases at distant organs is a highly challenging process for cancer cells, with extremely high attrition rates. A very small percentage of disseminated cells have the ability to dynamically adapt to their changing micro-environments through reversibly switching to another phenotype, aiding metastasis. Such plasticity can be exhibited along one or more axes – epithelial-mesenchymal plasticity (EMP) and cancer stem cells (CSCs) being the two most studied, and often tacitly assumed to be synonymous. Here, we review the emerging concepts related to EMP and CSCs across multiple cancers. Both processes are multi-dimensional in nature; for instance, EMP can be defined on morphological, molecular and functional changes, which may or may not be synchronized. Similarly, self-renewal, multi-lineage potential, and anoikis and/or therapy resistance may not all occur simultaneously in CSCs. Thus, arriving at rigorous functional definitions for both EMP and CSCs is crucial. These processes are dynamic, reversible, and semi-independent in nature; cells traverse the inter-connected high-dimensional EMP and CSC landscapes in diverse paths, each of which may exhibit a distinct EMP-CSC coupling. Our proposed model offers a potential unifying framework for elucidating the coupled decision-making along these dimensions and highlights a key set of open questions to be answered.

Background: Drought, N deficiency and herbivory are considered the most important stressors caused by climate change in the agro- and eco-systems and varied in space and time shaping a highly dynamic and heterogeneous stressful environments. This study aims to evaluate the to-mato morpho-physiological and metabolic responses to combined abiotic and herbivory at dif-ferent within-plant spatial levels and temporal scales. Methods: Leaf-level morphological, gas exchange traits and VOC profiles were measured in to-mato plants exposed to N deficiency and drought, T. absoluta larvae and their combination. Ad-ditive, synergistic or antagonistic effects of the single stress when combined were also evaluat-ed. Morpho-physiological traits and VOC profile were also measured on leaves located at three different positions along the shoot axes. Results: The combination of the abiotic and biotic stress has been more harmful than single stress with antagonistic and synergistic but non-additive effects for the morpho-physiological and VOC tomato responses, respectively. Combined stress also determined a high within-plant phenotypic plasticity of the morpho-physiological responses. Conclusions: These results suggest that the combined stress in tomato determined a “new stress state” and a higher within-plant phenotypic plasticity which could permit an efficient use of the growth and defence resources in the heterogeneous and multiple stressful environmental condi-tions.

Background: As cancer progresses, cells acquire traits that allow them to disperse and disseminate to distant locations in the body – a process known as metastasis. While in the vasculature, these cells are referred to as circulating tumour cells (CTCs) and can manifest either as single cells or clusters of cells (i.e., CTC clusters), with the latter being the most aggressive. The increased metastatic potential of CTC clusters is generally associated with cooperative group benefits in terms of survival, such as increased resistance to shear stress, anoikis, immune attacks and drugs. However, the adoption of a group phenotype poses a challenge when exiting the vasculature (extravasation) as the large size can hinder the passage through vessel walls. Despite their significant role in the metastatic process, the mechanisms through which CTC clusters extravasate remain largely unknown. Based on the observed in vivo association between CTC clusters and platelets, we hypothesized that cancer cells take advantage of the platelet-derived Transforming Growth Factor Beta 1 (TGF-β1) – a signalling factor that has been widely implicated in many aspects of cancer, to facilitate their own dissemination. To address this possibility, we evaluated the effect of exogenous TGF-β1 on an experimentally evolved non-small lung cancer cell line that we previously developed and used to investigate the biology of CTC clusters. Results: We found that exogenous TGF-β1 induced the dissociation of clusters into adherent single cells. Once adhered, cells released their own TGF-β1 and were able to individually migrate and invade in the absence of exogenous TGF-β1. Based on these findings we developed a model that involves a TGF-β1-mediated plastic switch between a cooperative phenotype and a single-celled stage that enables the extravasation of CTC clusters. Conclusions: This model allows for the possibility that therapies can be developed against TGF-β1 signalling components and/or TGF-β1 target genes to suppress the metastatic potential of CTC clusters. Considering the negative impact that metastasis has on cancer prognosis and the lack of therapies against this process, interfering with the ability of CTC clusters to switch between cooperative and individual behaviours could provide new strategies to improve patient survival.

Competition between cotton, winter, and summer crops is the greatest obstacle for plant breeders in Egypt. Breeders are thus seeking early maturing, high-yielding cultivars that are suited for planting following winter crops. This study was conducted during the 2016 and 2018 growing seasons at the Sakha agriculture research station, Egypt's agricultural research facility. This research used breeding material from the F2, F3, and F4 generations that resulted from crossing Giza 94 and Uzbekistan. During the 2016 growing season, the F2 population was cultivated, and the top 5% of the F2 population (75 plants) were chosen based on the selection criteria. In the summer of 2017, the F3 families were cultivated, and 5% of the superior F3 families were chosen to become the F4 fam-ilies, which were planted in the summer of 2018 at the single plant and bulk studies in a randomised full block design with three replications. The average performance of the characteristics boll weight, seed cotton yield, lint percentage, and lint index increased as generations passed from F2 to F4. In the meanwhile, the characteristic value of the first flower to open decreased, showing the accu-mulation of advantageous alleles. For all examined characteristics, the phenotypic coefficient of variance was greater than the genotypic coefficient of variation. In addition, the data demonstrated that heritability in a broad sense was greater in F4 populations than in F3 and F2 populations. With a few exceptions, the phenotypic and genotypic associations for all investigated characteristics were positive and very significant. According to the data, initial opening flowering and boll weight had a substantial impact on seed cotton output per feddan. In general, five superior families No. 9, 13, 18, 19, and 20 were chosen from the F4 population, which were more significant for yield and yield component than the commercial variety, and these genotypes may be promising for the breeding programme to develop new genotypes with superior yield.

Rice (Oryza sativa L.) is primary dietary source for half of the global population that comprising both essential nutrients and toxic heavy metal elements for human health. A number of nutrients are required within the diet and generally lacking in human diets, and need to biofortify into the rice grains, such as iron (Fe), zinc (Zn), calcium (Ca), potassium (K), sodium (Na), magnesium (Mg), phosphorus (P), copper (Cu), iodine (I), selenium (Se), and Sulphur (S). Meanwhile, some elements are toxic to human, including arsenic (As), cadmium (Cd), chromium (Cr), cobalt (Co), mercury (Hg), manganese (Mn), nickel (Ni), and lead (Pb) which need to be eliminated from the rice grains. This article reviews the aspects of phenotypic variation of grain elemental concentration in the diverse rice genotypes, relationship of environmental conditions and rice grain elemental accumulation, correlation between rice grain elemental content and others agronomic traits, and also genetic basis of grain elemental concentration in rice. All of these aspects are important to develop rice varieties with a balanced elemental nutrients and lower toxic heavy metal elements. Enhancing the concentration of essential mineral elements and reducing the accumulation of toxic elements in the rice grain are important to improve the rice quality for human health in addressing mineral deficiency and toxicity that could be accomplished by using plant breeding, agronomic, and genetic engineering approaches.

The notion that there is a one to one mapping from genotype to phenotype was overturned a long time ago. Along with genotype and environment, ‘non-genetic changes’ orchestrated by altered RNA and protein molecules also guide the development of phenotype. The idea that there is a route through which changes in phenotype can lead to changes in genotype impinges on several phenomena of molecular, developmental, evolutionary and applied interest. Phenotypic changes that do not alter the underlying DNA sequence have been studied across model systems (eg: DNA and histone modifications, RNA editing, prion formation) and are known to play an important role in short term adaptation. However, because of their transient nature and unstable inheritance, the role of such changes in long term evolution has remained controversial. I classify and review three ways in which non-genetic changes can influence genotype and impact cellular fitness across generations, with an emphasis on the enticing idea that they may act as stepping stones for genetic adaptation. I focus on work from microbial systems and attempt to highlight recent experiments and models that bear on this idea. Overall, I review evidence which suggests that non-genetic changes can impact phenotype via their influence on the genotype, and thus play a role in evolutionary change.

Phenotypical screening is a widely used approach in drug discovery for the identification of small molecules with cellular activities. However, functional annotation of identified hits often poses a challenge. The development of small molecules with narrow or exclusive target selectivity such as chemical probes and chemogenomic (CG) libraries, greatly diminishes this challenge, but non-specific effects caused by compound toxicity or interference with basic cellular functions still poses a problem to associate phenotypic readouts with molecular targets. Hence, each compound should ideally be comprehensively characterized regarding its effects on general cell functions. Here, we report an optimized live-cell multiplexed assay that classifies cells based on nuclear morphology, presenting an excellent indicator for cellular responses such as early apoptosis and necrosis. This basic readout in combination with the detection of other general cell damaging activities of small molecules such as changes in cytoskeletal morphology, cell cycle and mitochondrial health provides a comprehensive time-dependent characterization of the effect of small molecules on cellular health in a single experiment. The developed high-content assay offers multi-dimensional comprehensive characterization that can be used to delineate generic effects regarding cell functions and cell viability, allowing an assessment of compound suitability for subsequent detailed phenotypic and mechanistic studies.

During the 1970s, Tunisian durum wheat landraces were replaced progressively by modern cultivars. These landraces are nowadays maintained by smallholder farmers in some ecological niches and are threatened gradually by extinction resulting on the narrowing of the genetic diversity. This study aims to investigate patterns of phenotypic variability using twelve quantitative traits in a panel of 189 durum wheat landraces and seven checks, based on farmer’s population name attribution and genetic structure. Our results showed high phenotypic variability among and within landraces and checks for the majority of the studied traits. The principal components analysis showed similar grouping using farmers name attribution and genetic structure using K = 6, which confirmed the identification of a new gene pool in the oases of Tunisia, represented by the sub-population Jenah Zarzoura and the robustness and high relationships between phenotypic and genome-wide genetic structure using DArTseq method. These findings will enhance the conservation efforts of these landraces and their use in breeding efforts at national and international levels to adapt to dry conditions.

Disruptive selection arises when extreme phenotypes have a fitness advantage compared to more intermediate phenotypes. Theory and evidence suggest that intraspecific resource competition is a key driver of disruptive selection. However, while competition can be indirect (exploitative) or direct (interference), the role of interference competition in disruptive selection has not been tested, and most models of disruptive selection assume exploitative competition. We experimentally investigated whether the type of competition affects the outcome of competitive interactions using a system where disruptive selection is common: Mexican spadefoot toads (Spea multiplicata). Spea tadpoles develop into alternative resource-use phenotypes: carnivores, which consume fairy shrimp and other tadpoles, and omnivores, which feed on algae and detritus. Tadpoles intermediate in phenotype have low fitness when competition is intense, as they are outcompeted by the specialized tadpoles. Our experiments revealed that the presence of carnivores significantly decreased foraging behavior in intermediate tadpoles, and that intermediate tadpoles had significantly lower growth rates in interference competition treatments with carnivores but not with omnivores. Interference competition may therefore be important in driving disruptive selection. As carnivore tadpoles are also cannibalistic, the ‘fear’ effect may have a greater impact on intermediate tadpoles than exploitative competition alone, similarly to non-consumptive effects in predator-prey or intraguild relationships.

The triple-negative breast cancer (TNBC) subtype is one of the most aggressive forms of breast cancer that has poor clinical outcome and still remains as an unmet clinical challenge. Accumulating evidence suggests that intratumoral heterogeneity or the presence of phenotypically heterogeneous cell populations within a tumor plays a crucial role in chemoresistance, tumor progression and metastasis. Increased understanding of the molecular regulators of intratumoral heterogeneity will enable the development of effective therapeutic strategies in TNBC. We have identified a molecular mediator involved in intratumoral heterogeneity in breast cancer using an unbiased approach. We isolated two heterogeneous tumor cell populations from the 4T1 TNBC tumor model and phenotypic characterization revealed that the cells are distinct in terms of their morphology, proliferation and self-renewal ability in vitro; as well as primary tumor formation and metastatic potential in vivo. Further, RNA sequencing on both cell populations was performed to identify the molecular mediators underlying this heterogeneity. Bioinformatic analysis performed on the differentially expressed genes along with the Kaplan-Meier survival analysis in TNBC patients identified Metastasis associated colon cancer 1 (Macc1) as the top candidate gene mediating the aggressive phenotype. The role of Macc1 in regulating the proliferative phenotype was validated using siRNA mediated gene knockdown. The role of Macc1 in the aggressive cancer cell phenotypes and disease progression is being studied further using a small molecule transcriptional inhibitor of Macc1 in cell line and animal models, thus increasing our understanding of the molecular underpinnings of intratumoral heterogeneity in breast cancer that is critical to the improvement in the treatment of women currently living with the highly aggressive TNBC subtype.

The current and projected climate change that is represented by increasing temperatures, humidity levels and irregular rainfall patterns, promotes the occurrence of preharvest sprouting (PHS) in wheat. PHS results in significant economic losses, globally, which necessitates the need for high-yielding cultivars with increased PHS tolerance, hence this study was conducted. The current study evaluated two doubled-haploid (DH) wheat populations of Tugela-Dn × Elands and Elands × Flamink across six environments in the Free State Province of South Africa to select genotypes with increased PHS tolerance and further map the underlying loci. Significant effects of DH lines (194) and environments (6) were observed for PHS tolerance. The results of this study validate previous findings that PHS is only expressed when environmental conditions are conducive. Quantitative trait loci (QTL) mapping using single nucleotide polymorphism (SNP) and silicoDArT markers revealed three additive QTL with major effects on chromosomes 5B and 7B, and these QTL were detected more than once, when conditions were favourable. These QTL explained a phenotypic variation (PVE) varying between 10.08% and 20.30% (LOD = 2.73 – 3.11). About 16.50% of DH lines performed to the level of Elands (the PHS-tolerant parent) and are recommended for further selection in a pre-breeding or breeding programme. The findings of the study are expected to facilitate the on-going breeding efforts for PHS tolerance in winter wheat.

Rice varieties such as Mahsuri Mutan and Basmati 370 are categorized as specialty rice with kernel elongation ratio exceeding 1.6 and 2.0, respectively. Ageing treatment in rice could affect the physical and chemical properties of rice such as grain size and shape, quality and taste of the cooked rice. The main objective of this study was to determine the effects of ageing treatment on the physicochemical properties of Mahsuri Mutan, Basmati 370 and MR219 rice varieties. The three rice varieties were subjected to heat treatment at 90ºC using the oven for 3 hours. After the heat treatment, the samples were cooled at room temperature (25ºC) for 1 hour. Physicochemical properties such as alkali digestion value, water uptake ratio (WUR), solids in cooking water (SCW), high kernel elongation (HKE) ratio and amylose contents were determined. Data collected on physicochemical traits and ageing vs non-ageing treatments were subjected to analysis of variance (ANOVA) using SAS software version 9.4. Phenotypic correlation coefficient indicated that there was a high positive correlation between HKE and water uptake ratio. The ageing treatment also showed significant difference in all the physicochemical traits of the varieties studied. Observation under electron microscope showed that the ageing samples had more cracks on the tissue structure compared to normal rice samples. The hexagon structure in Mahsuri Mutan gave more elongation effect on its kernel. The findings from this study could be useful to breeders in selection and development of new high kernel elongation rice variety.

Background: Advancements in the next-generation sequencing (NGS) techniques have allowed for efficient genetic variant detection at reduced costs. Methods: We describe an ad hoc NGS-based custom designed resequencing gene panel to identify genetic variants in 8 patients with dementing disorders. Results: We found variants of TREM2 and APP genes in three patients; these have been previously identified as pathogenic or likely pathogenic and, therefore, considered as “Disease Causing”. In the remaining subjects, the pathogenicity was evaluated on the in silico analysis, according to the guidelines of the American College of Medical Genetics. In one patient, the p.R205W variant was causative of the disease, thus considered as “Possibly Disease Causing”. The variants found from the other four subjects in the CSF1R, SERPINI1, GRN, and APP genes revealed discordant in silico results and, therefore, it was not possible to assign a definitive pathogenicity. Conclusions: Notwithstanding the limitations of a customized panel, we detected some rare genetic variants with a probable disease association. The future application of NGS techniques and the further replication of these experimental data will replace the so-called “gene by gene” approach with a “panel of genes” strategy, that offers promising perspectives in the diagnosis and management of neurodegenerative disorders.

Drug discovery utilizes high-throughput screening (HTS) methods applying target and cell-based assays. This review discusses the challenges and benefits associated with these assays in HTS. Discussed the strategies that can be applied for the development of screening assays through primary and secondary screens for target identification. Further discussion on identify-ing the most efficacious drugs following these approaches in cancer. Even though various drugs have been identified to treat cancer, there is high demand of more relevant phenotypic assays to produce desired diseased phenotype to only highlighting the specific targets instead of off-targets. Hopefully, the new developing strategies could provide innovative drugs to treat cancer patients to reduce mortality rate.

This review highlights normal and tumor tissue vasculature, immunological changes, and phenotypic alterations (VIP model) as fundamental in abscopal interaction. In the stereotactic body radiotherapy (SBRT) and immunotherapy era, we are moving toward “immunological radiation planning,” i.e., radiation scheduling with abscopal effect as a vital endpoint as well. Towards this end, this manuscript presents specific diagrammatic tumor models to optimize the outcome of abscopal response in SBRT, based on the principle of the four R’s - Repair, Redistribution, Repopulation, and Reoxygenation of radiotherapy. The article highlights the importance of restricting the dose of SBRT to < 10 Gy per fraction, appropriate use of dose painting, and concomitant/delayed SBRT boost potential. Current literature indicates that immunotherapy should not precede but follow SBRT within seven days. Included is the review of integrating “cyclical” antiangiogenics, immune adjuvants/immune-metabolites as abscopal effect enhancers with SBRT. The importance of proton, carbon-ion SBRT is dealt with briefly. Proposed six fundamental requirements for augmentation of the abscopal cascade are listed. The existing exploratory results need to develop a definitive strategy amidst complex interactions in SBRT, immunotherapy, immune-adjuvants, & abscopal effects. We now have enough literature evidence to convert “abscopal by chance” to “abscopal by design” by harmonized combinatorial approach.

This review aimed at defining and classifying extended spectrum β-lactamases, ESBLs and carbapenemases, summarizing the different phenotypic methods used to detect production of these enzymes in clinically significant gram negative bacteria and also describing the methods that discourse challenges mostly encountered during detection of these enzymes in microbiology laboratories with the purpose of formulating recommendations on best practice to screen for these enzymes. We conclude that the modified double disk synergy, MDDS is not only suitable for the confirmation of ESBL production after screening isolates with the cephalosporin/clavulanate combination disc diffusion or broth micro-dilution methods but also distinguishes ESBL production and over-expression of AmpC-derepressed mutants and as well serves as an indicator for AmpC screening. Furthermore, we suggest cefotaxime, ceftazidime and cefpodoxime (for testing using a single drug) as indicator antibiotics of choice for ESBL detection. The MDDS and cefoxitin/AmpC inhibitor combination disc method, using cloxacillin and phenylboronic acid can be used as screening tests for AmpC production and either the AmpC disc test, the disc approximation test or the modified three dimensional extract test as confirmatory tests for AmpC production. We also suggest that confirmation of carbapenemase production be done with the modified hodge test, using Klebsiella pneumoniae ATCC 700603 as the indicator organism or the modified carbapenem inactivation method. However, to differentiate between the different classes of carbapenemases, boronic acid and EDTA based methods (double-disk synergy tests and combined-disk tests) using imipenem, meropenem and ertapenem, in combination with 3-aminophenylboronic acid and ethylene diamine tetra acetic acid be used.

Intratumoral heterogeneity can exist along multiple axes: Cancer Stem Cells (CSCs)/non-CSCs, drug-sensitive/drug-tolerant states and a spectrum of epithelial-hybrid-mesenchymal phenotypes. Further, these diverse cell-states can switch reversibly among one another, thereby posing a major challenge to therapeutic efficacy. Therefore, understanding the origins of phenotypic plasticity and heterogeneity remains an active area of investigation. While genomic components (mutations, chromosomal instability) driving heterogeneity have been well-studied, recent reports highlight the role of non-genetic mechanisms in enabling both phenotypic plasticity and heterogeneity. Here, we discuss various processes underlying phenotypic plasticity such as stochastic gene expression, chromatin reprogramming, asymmetric cell division and the presence of multiple “attractors”. These processes can facilitate a dynamically evolving cell population such that a subpopulation of (drug-tolerant) cells can survive lethal drug exposure and recapitulate population heterogeneity on drug withdrawal, leading to relapse. These drug-tolerant cells can be both pre-existing and also induced by the drug itself through cell-state reprogramming. The dynamics of cell-state transitions both in absence and presence of the drug can be quantified through mathematical models. Such a dynamical systems approach to elucidating patterns of intratumoral heterogeneity by integrating longitudinal experimental data with mathematical models can help design effective combinatorial and/or sequential therapies for better clinical outcomes.

Despite identical genetic constitution, a cancer cell population can exhibit phenotypic variations termed as non-genetic/non-mutational heterogeneity. Such heterogeneity – a ubiquitous nature of biological systems – has been implicated in metastasis, therapy resistance and tumour relapse. Here, we review the evidence for existence, sources and implications of non-genetic heterogeneity in multiple cancer types. Stochasticity/ noise in transcription, protein conformation and/or external microenvironment can underlie such heterogeneity. Moreover, the existence of multiple possible cell states (phenotypes) as a consequence of the emergent dynamics of gene regulatory networks may enable reversible cell-state transitions (phenotypic plasticity) that can facilitate adaptive drug resistance and higher metastatic fitness. Finally, we highlight how computational and mathematical models can drive a better understanding of non-genetic heterogeneity and how a systems-level approach integrating mathematical modelling and in vitro/in vivo experiments can map the diverse phenotypic repertoire, and identify therapeutic vulnerabilities of an otherwise clonal cell population.

Bacterial conjugation, also referred to as bacterial sex, is a major horizontal gene transfer mechanism where the DNA is transferred from a donor to a recipient bacterium by direct contact. Conjugation is universally conserved among bacteria and occurs in a wide range of environments (soil, plant surfaces, water, sewage, biofilms and host-associated bacterial communities). Within these habitats, conjugation drives the rapid evolution and adaptation of bacterial strains by mediating the propagation of various metabolic properties, including symbiotic life-style, virulence, biofilm formation, or resistance to heavy metals and, most importantly, resistance to antibiotics. These properties make of conjugation a fundamentally important process at the center of extensive study. Here, we review the key steps of conjugation by following the life-cycle of the F plasmid during transfer from the donor to the recipient cell. We also discuss our current knowledge of the extent and impact of conjugation within an environmentally and clinically relevant bacterial habitat, bacterial biofilms.

The majority of Candida species are known as non-pathogenic yeasts and rarely involved in human diseases. However, recently case reports of human infections caused by non-albicans Candida species have increased, mostly in immunocompromised hosts. Our study aimed to describe and caracterise as thoroughly as possible, a new species of the Candida genus, named here Candida massiliensis (PMML0037), isolated from a clinical sample of human sputum. We compared genetic data based on the sequences of four genetic regions: "Internal Transcribed Spacers" of rRNA, D1/D2 domains (28S large subunit rRNA) and part of the genes encoding Translation Elongation Factor 1-α and β-tubulin2, to morphological characters, from scanning electron microscopy (TM 4000 Plus, SU5000), physiological, including the results of oxidation and assimilation tests of different carbon sources by the Biolog system, and chemical mapping by Energy-Dispersive X-ray Spectroscopy. Lastly, the in vitro antifungal susceptibility profile was performed using the E-testTM exponential gradient method. The multilocus analysis supported the genetic position of Candida massiliensis (PMML0037) as a new species of the genus Candida, and the phenotypic analysis highlighted its unique morphological and chemical profile when compared to other Candida species included in the study.

In the last decades, intensive crop management has involved excessive use of pesticides or fertilizers, compromising environmental integrity and public health. Accordingly, there has been worldwide pressure to find an eco-friendly and safe strategy to ensure agricultural productivity. Recently, Plant Growth-Promoting (PGP) rhizobacteria are receiving increasing attention as suitable biocontrol agents against agricultural pests. In the present study, 22 spore-forming bacteria were selected among a salt-pan rhizobacteria collection for their PGP traits and their antagonistic activity against the plant pathogen fungus Macrophomina phaseolina. Based on the higher antifungal activity, strain RHFS10, identified as Bacillus vallismortis, was furtherly examined and cell-free supernatants assays, column purification, and tandem mass spectrometry employed to purify and preliminarily identify the antifungal metabolites. Interestingly, the minimum inhibitory concentration assessed for the fractions active against M. phaseolina, resulted 10 times lower and more stable than the one estimated for the commercial fungicide pentachloronitrobenzene. These results suggest the use of B. vallismortis strain RHFS10 as a potential Plant Growth Promoting Rhizobacteria to efficiently control phytopathogenic fungus M. phaseolina, in alternative to chemical pesticides.

Biological invasions have reached an unprecedented level and the number of introduced species is still increasing worldwide. Despite major advances in invasion science, the determinants of success of introduced species, the magnitude and dimensions of their impact, and the mechanisms sustaining successful invasions are still debated. Empirical studies show divergent impacts of non-native populations on ecosystems and contrasting effects of biotic and abiotic factors on the dynamics of non-native populations; this is hindering the emergence of a unified theory of biological invasions. We propose a synthesis that merges perspectives from population, community, and ecosystem levels. Along a timeline of ecosystem transformation driven by non-native species, from historical to human-modified ecosystems, we order invasion concepts and theories to clarify their chaining and relevance during each step of the invasion process. This temporal sorting of invasion concepts shows that each concept is relevant at a specific stage of the invasion. Concepts and empirical findings on non-native species may appear contradictory. However, we suggest that, when mapped onto an invasion timeline, they may be combined in a complementary way. An overall scheme is proposed to summarise the theoretical dynamics of ecosystems subjected to invasions. For any given case study, this framework provides a guide through the maze of theories and should help choose the appropriate concepts according to the stage of invasion.

The focus of recent research shifts towards complex ‘whole organism’ responses (i.e., in multiple functional traits) in adaptation to or to defend against stressors under complex environmental conditions. This increasing complexity is challenging to analyse and demands sophisticated tools to drive meaningful conclusions from those data. Trait-based regression models, multivariate analyses, like principal component analyses, and plasticity indices can be used to tackle challenges with those complex investigations. But those methods have substantial limitations, like the need for high sample size, multi-dimensionality of results or the need for trait coordination in high-dimensional space, or the calculation on the population level, which might buffer or cover the de facto occurring individual effects. To improve and simplify studies on ‘whole organism’ responses, analyses, and their interpretation, we developed the Index for Adaptive Responses. This straightforward framework can unite all traits of an organism in one number. A newly developed transformation method, included in this framework, comprises a normalisation and standardisation to a baseline or control without changing the data or variance structure of the original data. We assessed the performance and accuracy of the framework with an application in an extensive predator-prey case study, with simulations and application examples using literature data. We show that the Index for Adaptive Responses respects adaptations as well as maladaptations and outperforms established approaches. The framework is robust against outliers and non-gaussian distribution. We further show that the qualitative prediction of the adaptiveness of included traits is highly accurate, even under challenging conditions, e.g., low replicate numbers. Functions and algorithms of the framework are provided with an R package but can easily be translated into other programming languages. The Index for Adaptive Responses will simplify future research on complex adaptive responses and improves our understanding of these responses’ ecological as well as evolutionary implications.

A few empirical examples document fixed alternative male mating strategies in animals. Here we focus on the polymorphism of male mating strategies in the ruff (Calidris pugnax, Aves Charadriiformes). In ruffs, three fixed alternative male mating strategies coexist and are signaled by extreme plumage polymorphism. We first present relevant data on the biology of the species. Then we review the available knowledge of the behavioral ecology of ruffs during the breeding season and we detail the characteristics of each of the three known fixed male mating strategies. We next turn to the exceptional quality results accumulated on both the structural and functional genomics of the ruff over the past few years. We show how much these genomic data can shed a new, mechanistic light on the evolution and maintenance of the three fixed alternative male mating strategies. We then look if there are sufficient indication to support frequency-dependent selection as key mechanism in maintaining these three strategies. Specifically, we search for evidences of equal fitness among individuals using each of the three strategies. Finally, we propose three lines of research avenues that will help to understand the eco-evolutionary dynamics of phenotypic differences within natural populations of this iconic model species.