Host Growth Rate Research Articles

IncC plasmid genome rearrangements influence the vertical and horizontal transmission tradeoff in Escherichia coli.

It has been shown that an evolutionary tradeoff between vertical (host growth rate) and horizontal (plasmid conjugation) transmissions contributes to global plasmid fitness. As conjugative IncC plasmids are important for the spread of multidrug resistance (MDR), in a broad range of bacterial hosts, we investigated vertical and horizontal transmissions of two multidrug-resistant IncC plasmids according to their backbones and MDR-region rearrangements, upon plasmid entry into a new host. We observed plasmid genome deletions after conjugation in three diverse natural Escherichia coli clinical strains, varying from null to high number depending on the plasmid, all occurring in the MDR region. The plasmid burden on bacterial fitness depended more on the strain background than on the structure of the MDR region, with deletions appearing to have no impact. Besides, we observed an increase in plasmid transfer rate, from ancestral host to new clinical recipient strains, when the IncC plasmid was rearranged. Finally, using a second set of conjugation experiments, we investigated the evolutionary tradeoff of the IncC plasmid during the critical period of plasmid establishment in E. coli K-12, by correlating the transfer rates of deleted or non-deleted IncC plasmids and their costs on the recipient strain. Plasmid deletions strongly improved conjugation efficiency with no negative growth effect. Our findings indicate that the flexibility of the MDR-region of the IncC plasmids can promote their dissemination, and provide diverse opportunities to capture new resistance genes. In a broader view, they suggest that the vertical-horizontal transmission tradeoff can be manipulated by the plasmid to improve its fitness.

Enhancing metabolic efficiency via novel constitutive promoters to produce protocatechuic acid in Escherichia coli

The antioxidant molecule protocatechuic acid (PCA) can also serve as a precursor for polymer building blocks. PCA can be produced in Escherichia coli overexpressing 3-dehydroshikimate dehydratase (DSD), an enzyme that catalyses the transformation of 3-dehydroshikimate to PCA. Nevertheless, optimizing the expression rate of recombinant enzymes is a key factor in metabolic engineering when producing biobased chemicals. In this study, a degenerate synthetic promoter approach was investigated to improve further the production of PCA. By limited screening of a randomized promoter library made using pSEVA221 plasmid in E. coli, three novel synthetic constitutive promoters were selected that increased the PCA yield from glucose by 10–21% compared to the inducible T7-promoter. RT-qPCR analysis showed that the DSD gene, regulated by the synthetic promoters, had high expression during the exponential phase, albeit the gene expression level dropped 250-fold during stationary phase. Besides the increased product yield, the synthetic promoters avoided the need for a costly inducer for gene expression. Screening of the entire promoter library is likely to provide more positive hits. The study also shows that E. coli transformed with the DSD gene on either pSEVA221 or pCDFDuet plasmids exhibit background PCA levels (~ 0.04 g/L) in the absence of a transcriptional regulatory element.Key points• Degenerate synthetic promoters are remarkable tools to produce protocatechuic acid.• The constitutive synthetic promoters did not affect the growth rate of the bacterial host.• The use of constitutive synthetic promoters avoids the need for the costly inducer.

Climatic variations and Fasciola: a review of impacts across the parasite life cycle.

Fasciolosis, caused by the liver fluke Fasciola spp., is a significant parasitic disease of livestock and humans worldwide. Fasciola transmission and life cycle are highly dependent on climatic conditions, especially temperature and humidity. This dependency has gained significance in the context of ongoing climate change. This literature review examined evidence on the effects of temperature variability on the developmental stages of Fasciola spp. and the snail intermediate hosts. We reviewed free larval stages of Fasciola spp. development, as well as snail intermediate hosts, while investigating the climate-related factors influencing each stage. We found that Fasciola spp. egg hatching and development were inhibited below 10 °C and optimal between 20 and 30 °C, miracidia hatching time decreased with higher temperatures and cercarial shedding by snail hosts accelerated around 27 °C. Further, metacercarial viability declined at higher temperatures but was prolonged by higher humidity. Snail intermediate host growth rates peaked at 25 °C, and their susceptibility to Fasciola infection depends on temperature, underscoring its importance in transmission dynamics. Overall, the Fasciola life cycle and snail host development exhibit stage-specific temperature thresholds, indicating a complex relationship between temperature fluctuations and parasite transmission potential. This research highlights the key role of temperature and humidity on Fasciola spp. and snail development, shedding light on the potential consequences of climate change on their survival, development, and disease transmission. Data limitations, primarily from the scarcity of high-resolution climate-related experiments, should drive future research to enhance predictive models and deepen our understanding of the impact of climate change on this parasitic disease.

Mutualism at the leading edge: insights into the eco-evolutionary dynamics of host-symbiont communities during range expansion.

The evolution of mutualism between host and symbiont communities plays an essential role in maintaining ecosystem function and should therefore have a profound effect on their range expansion dynamics. In particular, the presence of mutualistic symbionts at the leading edge of a host-symbiont community should enhance its propagation in space. We develop a theoretical framework that captures the eco-evolutionary dynamics of host-symbiont communities, to investigate how the evolution of resource exchange may shape community structure during range expansion. We consider a community with symbionts that are mutualistic or parasitic to various degrees, where parasitic symbionts receive the same amount of resource from the host as mutualistic symbionts, but at a lower cost. The selective advantage of parasitic symbionts over mutualistic ones is increased with resource availability (i.e. with host density), promoting mutualism at the range edges, where host density is low, and parasitism at the population core, where host density is higher. This spatial selection also influences the speed of spread. We find that the host growth rate (which depends on the average benefit provided by the symbionts) is maximal at the range edges, where symbionts are more mutualistic, and that host-symbiont communities with high symbiont density at their core (e.g. resulting from more mutualistic hosts) spread faster into new territories. These results indicate that the expansion of host-symbiont communities is pulled by the hosts but pushed by the symbionts, in a unique push-pull dynamic where both the host and symbionts are active and tightly-linked players.

Determination of Optimal Phage Load and Administration Time for Antibacterial Treatment.

Using phages as antibacterials is becoming a customary practice in Western countries. Nonetheless, successful treatments must consider the growth rate of the bacterial host and the degradation of the virions. Therefore, successful treatments require administering the right amount of phage (viral load, Vφ) at the right moment (administration time, Tφ). The present protocols implement a machine learning approach to determine the best combination of Vφ and Tφ to obtain the elimination of the target bacterium from a system. © 2024 The Authors. Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: One bacterium, one phage Alternate Protocol 1: One bacterium, one phage (wrapping function) Alternate Protocol 2: One bacterium, one phage (wrapping function, alternative growing model) Basic Protocol 2: Two bacteria, one phage Alternate Protocol 3: Two bacteria, one phage (launch from terminal).

The twin-arginine translocation system is vital for cell adhesion and uptake of iron in the cystic fibrosis pathogen Achromobacter xylosoxidans

ABSTRACT Background Achromobacter xylosoxidans is an emerging pathogen that causes airway infections in patients with cystic fibrosis. Knowledge of virulence factors and protein secretion systems in this bacterium is limited. Twin arginine translocation (Tat) is a protein secretion system that transports folded proteins across the inner cell membranes of gram-negative bacteria. Tat has been shown to be important for virulence and cellular processes in many different bacterial species. This study aimed to investigate the role of Tat in iron metabolism and host cell adhesion in A. xylosoxidans. Methods Putative Tat substrates in A. xylosoxidans were identified using the TatFind, TatP, and PRED-Tat prediction tools. An isogenic tatC deletion mutant (ΔtatC) was generated and phenotypically characterized. The wild-type and ΔtatC A. xylosoxidans were fractionated into cytosolic, membrane, and periplasmic fractions, and the expressed proteome of the different fractions was analyzed using liquid chromatography-mass spectrometry (LC-MS/MS). Results A total of 128 putative Tat substrates were identified in the A. xylosoxidans proteome. The ΔtatC mutant showed attenuated host cell adhesion, growth rate, and iron acquisition. Twenty predicted Tat substrates were identified as expressed proteins in the periplasmic compartment, nine of which were associated with the wild type. Conclusion The data indicate that Tat secretion is important for iron acquisition and host cell adhesion in A. xylosoxidans.

Targeted C-to-T and A-to-G dual mutagenesis system for RhtA transporter in vivo evolution.

T7 RNA polymerase (T7RNAP) has been fused with cytosine or adenine deaminase individually, enabling in vivo C-to-T or A-to-G transitions on DNA sequence downstream of T7 promoter, and greatly accelerated directed protein evolution. However, its base conversion type is limited. In this study, we created a dual-functional system for simultaneous C-to-T and A-to-G in vivo mutagenesis, called T7-DualMuta, by fusing T7RNAP with both cytidine deaminase (PmCDA1) and a highly active adenine deaminase (TadA-8e). The C-to-T and A-to-G mutagenesis frequencies of T7-DualMuta were 4.02 × 10-3 and 1.20 × 10-2, respectively, with 24 h culturing and distributed mutations evenly across the target gene. The T7-DualMuta system was used to in vivo directed evolution of L-homoserine transporter RhtA, resulting in efficient variants that carried the four types of base conversions by T7-DualMuta. The evolved variants greatly increased the host growth rates at L-homoserine concentrations of 8 g/L, which was not previously achieved, and demonstrated the great in vivo evolution capacity. The novel molecular device T7-DualMuta efficiently provides both C/G-to-T/A and A/T-to-G/C mutagenesis on target regions, making it useful for various applications and research in Enzymology and Synthetic Biology studies. It also represents an important expansion of the base editing toolbox.ImportanceA T7-DualMuta system for simultaneous C-to-T and A-to-G in vivo mutagenesis was created. The mutagenesis frequency was 4.02 × 107 fold higher than the spontaneous mutation, which was reported to be approximately 10-10 bases per nucleotide per generation. This mutant system can be utilized for various applications and research in Enzymology and Synthetic Biology studies.

Altered growth and death in dilution-based viral predation assays.

Viral lysis of phytoplankton is one of the most common forms of death on Earth. Building on an assay used extensively to assess rates of phytoplankton loss to predation by grazers, lysis rates are increasingly quantified through dilution-based techniques. In this approach, dilution of viruses and hosts are expected to reduce infection rates and thus increase host net growth rates (i.e., accumulation rates). The difference between diluted and undiluted host growth rates is interpreted as a measurable proxy for the rate of viral lytic death. These assays are usually conducted in volumes ≥ 1 L. To increase throughput, we implemented a miniaturized, high-throughput, high-replication, flow cytometric microplate dilution assay to measure viral lysis in environmental samples sourced from a suburban pond and the North Atlantic Ocean. The most notable outcome we observed was a decline in phytoplankton densities that was exacerbated by dilution, instead of the increased growth rates expected from lowered virus-phytoplankton encounters. We sought to explain this counterintuitive outcome using theoretical, environmental, and experimental analyses. Our study shows that, while die-offs could be partly explained by a 'plate effect' due to small incubation volumes and cells adhering to walls, the declines in phytoplankton densities are not volume-dependent. Rather, they are driven by many density- and physiology-dependent effects of dilution on predation pressure, nutrient limitation, and growth, all of which violate the original assumptions of dilution assays. As these effects are volume-independent, these processes likely occur in all dilution assays that our analyses show to be remarkably sensitive to dilution-altered phytoplankton growth and insensitive to actual predation pressure. Incorporating altered growth as well as predation, we present a logical framework that categorizes locations by the relative dominance of these mechanisms, with general applicability to dilution-based assays.

Theft of Host Transferrin Receptor-1 by Toxoplasma gondii is required for infection.

Nutrient acquisition by apicomplexan parasites is essential to drive their intracellular replication, yet the mechanisms that underpin essential nutrient acquisition are not defined. Using the apicomplexan model Toxoplasma gondii , we show that host cell proteins including the transferrin receptor 1, transferrin, ferritin heavy and light chains, and clathrin light chain are robustly taken up by tachyzoites. Tachyzoite acquisition of host cell protein was not related to host cell type or parasite virulence phenotypes. Bradyzoites possessed little capacity to acquire host cell proteins consistent with the cyst wall representing a barrier to host cell protein cargo. Increased trafficking of host cell transferrin receptor 1 and transferrin to endolysosomes boosted tachyzoite acquisition of host proteins and growth rate. Theft of host transferrin 1 and transferrin did not significantly affect iron levels in the tachyzoite. This study provides insight into essential functions associated with parasite theft of host iron sequestration and storage proteins.

Dead or alive: carbon as a currency to integrate disease and ecosystem ecology theory

Death is a common outcome of infection, but most disease models do not track hosts after death. Instead, these hosts disappear into a void. This assumption lacks critical realism, because dead hosts can alter host–pathogen dynamics. Here, we develop a theoretical framework of carbon‐based models combining disease and ecosystem perspectives to investigate the consequences of feedbacks between living and dead hosts on disease dynamics and carbon cycling. Because autotrophs (i.e. plants and phytoplankton) are critical regulators of carbon cycling, we developed general model structures and parameter combinations to broadly reflect disease of autotrophic hosts across ecosystems. Analytical model solutions highlight the importance of disease–ecosystem coupling. For example, decomposition rates of dead hosts mediate pathogen spread, and carbon flux between live and dead biomass pools are sensitive to pathogen effects on host growth and death rates. Variation in dynamics arising from biologically realistic parameter combinations largely fell along a single gradient from slow to fast carbon turnover rates, and models predicted higher disease impacts in fast turnover systems (e.g. lakes and oceans) than slow turnover systems (e.g. boreal forests). Our results demonstrate that a unified framework, including the effects of pathogens on carbon cycling, provides novel hypotheses and insights at the nexus of disease and ecosystem ecology.

The role of host refuge and strong Allee effects in a host–parasitoid system

We propose and study a discrete host–parasitoid model of difference equations with a spatial host refuge where hosts in the refuge patch are free from parasitism but undergo a demographic strong Allee effect. If the growth rate of hosts in the non-refuge patch is less than one, a host Allee threshold is derived below which both populations become extinct. It is proven that both populations can persist indefinitely if the host growth rate in the non-refuge patch exceeds one and the maximum reproductive number of parasitoids is greater than one. Numerical simulations reveal that the host refuge can either stabilize or destabilize the host–parasitoid interactions, depending on other model parameters. A large number of parasitoid turnover from a parasitized host may be detrimental to the parasitoids due to Allee effects in the hosts within the refuge patch. Moreover, it is demonstrated numerically that if the host growth rate is not small, the population level of parasitoids may suddenly drop to a small value as some parameters are varied.

Growth rate determines prokaryote-provirus network modulated by temperature and host genetic traits

BackgroundProkaryote-virus interactions play key roles in driving biogeochemical cycles. However, little is known about the drivers shaping their interaction network structures, especially from the host features. Here, we compiled 7656 species-level genomes in 39 prokaryotic phyla across environments globally and explored how their interaction specialization is constrained by host life history traits, such as growth rate.ResultsWe first reported that host growth rate indicated by the reverse of minimal doubling time was negatively related to interaction specialization for host in host-provirus network across various ecosystems and taxonomy groups. Such a negative linear growth rate-specialization relationship (GrSR) was dependent on host optimal growth temperature (OGT), and stronger toward the two gradient ends of OGT. For instance, prokaryotic species with an OGT ≥ 40 °C showed a stronger GrSR (Pearson’s r = −0.525, P < 0.001). Significant GrSRs were observed with the presences of host genes in promoting the infection cycle at stages of adsorption, establishment, and viral release, but nonsignificant with the presence of immune systems, such as restriction-modification systems and CRISPR-Cas systems. Moreover, GrSR strength was increased with the presence of temperature-dependent lytic switches, which was also confirmed by mathematical modeling.ConclusionsTogether, our results advance our understanding of the interactions between prokaryotes and proviruses and highlight the importance of host growth rate in interaction specialization during lysogenization.-HizC61KJzNQvhhU_7paSqVideo

Disease‐mediated nutrient dynamics: Coupling host–pathogen interactions with ecosystem elements and energy

AbstractAutotrophs play an essential role in the cycling of carbon and nutrients, yet disease‐ecosystem relationships are often overlooked in these dynamics. Importantly, the availability of elemental nutrients like nitrogen and phosphorus impacts infectious disease in autotrophs, and disease can induce reciprocal effects on ecosystem nutrient dynamics. Relationships linking infectious disease with ecosystem nutrient dynamics are bidirectional, though the interdependence of these processes has received little attention. We introduce disease‐mediated nutrient dynamics (DND) as a framework to describe the multiple, concurrent pathways linking elemental cycles with infectious disease. We illustrate the impact of disease–ecosystem feedback loops on both disease and ecosystem nutrient dynamics using a simple mathematical model, combining approaches from classical ecological (logistic and Droop growth) and epidemiological (susceptible and infected compartments) theory. Our model incorporates the effects of nutrient availability on the growth rates of susceptible and infected autotroph hosts and tracks the return of nutrients to the environment following host death. While focused on autotroph hosts here, the DND framework is generalizable to higher trophic levels. Our results illustrate the surprisingly complex dynamics of host populations, infection patterns, and ecosystem nutrient cycling that can arise from even a relatively simple feedback between disease and nutrients. Feedback loops in disease‐mediated nutrient dynamics arise via effects of infection and nutrient supply on host stoichiometry and population size. Our model illustrates how host growth rate, defense, and tissue chemistry can impact the dynamics of disease–ecosystem relationships. We use the model to motivate a review of empirical examples from autotroph–pathogen systems in aquatic and terrestrial environments, demonstrating the key role of nutrient–disease and disease–nutrient relationships in real systems. By assessing existing evidence and uncovering data gaps and apparent mismatches between model predictions and the dynamics of empirical systems, we highlight priorities for future research intended to narrow the persistent disciplinary gap between disease and ecosystem ecology. Future empirical and theoretical work explicitly examining the dynamic linkages between disease and ecosystem ecology will inform fundamental understanding for each discipline and will better position the field of ecology to predict the dynamics of disease and elemental cycles in the context of global change.

Effects of the Expression of Random Sequence Clones on Growth and Transcriptome Regulation in Escherichia coli.

Comparative genomic analyses have provided evidence that new genetic functions can emerge out of random nucleotide sequences. Here, we apply a direct experimental approach to study the effects of plasmids harboring random sequence inserts under the control of an inducible promoter. Based on data from previously described experiments dealing with the growth of clones within whole libraries, we extracted specific clones that had shown either negative, neutral or positive effects on relative cell growth. We analyzed these individually with respect to growth characteristics and the impact on the transcriptome. We find that candidate clones for negative peptides lead to growth arrest by eliciting a general stress response. Overexpression of positive clones, on the other hand, does not change the exponential growth rates of hosts, and they show a growth advantage over a neutral clone when tested in direct competition experiments. Transcriptomic changes in positive clones are relatively moderate and specific to each clone. We conclude from our experiments that random sequence peptides are indeed a suitable source for the de novo evolution of genetic functions.

Some Finite Difference Methods to Model Biofilm Growth and Decay: Classical and Non-Standard

The study of biofilm formation is undoubtedly important due to micro-organisms forming a protected mode from the host defense mechanism, which may result in alteration in the host gene transcription and growth rate. A mathematical model of the nonlinear advection–diffusion–reaction equation has been studied for biofilm formation. In this paper, we present two novel non-standard finite difference schemes to obtain an approximate solution to the mathematical model of biofilm formation. One explicit non-standard finite difference scheme is proposed for biomass density equation and one property-conserving scheme for a coupled substrate–biomass system of equations. The nonlinear term in the mathematical model has been handled efficiently. The proposed schemes maintain dynamical consistency (positivity, boundedness, merging of colonies, biofilm annihilation), which is revealed through experimental observation. In order to verify the accuracy and effectiveness of our proposed schemes, we compare our results with those obtained from standard finite difference schemes and earlier known results in the literature. The proposed schemes (NSFD1 and NSFD2) show good performance. The NSFD2 scheme reveals that the processes of biofilm formation and nutritive substrate growth are intricately linked.

Evolution of phenotypic fluctuation under host-parasite interactions.

Robustness and plasticity are essential features that allow biological systems to cope with complex and variable environments. In a constant environment, robustness, i.e., insensitivity of phenotypes, is expected to increase, whereas plasticity, i.e., the changeability of phenotypes, tends to diminish. Under a variable environment, existence of plasticity will be relevant. The robustness and plasticity, on the other hand, are related to phenotypic variances. As phenotypic variances decrease with the increase in robustness to perturbations, they are expected to decrease through the evolution. However, in nature, phenotypic fluctuation is preserved to a certain degree. One possible cause for this is environmental variation, where one of the most important "environmental" factors will be inter-species interactions. As a first step toward investigating phenotypic fluctuation in response to an inter-species interaction, we present the study of a simple two-species system that comprises hosts and parasites. Hosts are expected to evolve to achieve a phenotype that optimizes fitness. Then, the robustness of the corresponding phenotype will be increased by reducing phenotypic fluctuations. Conversely, plasticity tends to evolve to avoid certain phenotypes that are attacked by parasites. By using a dynamic model of gene expression for the host, we investigate the evolution of the genotype-phenotype map and of phenotypic variances. If the host-parasite interaction is weak, the fittest phenotype of the host evolves to reduce phenotypic variances. In contrast, if there exists a sufficient degree of interaction, the phenotypic variances of hosts increase to escape parasite attacks. For the latter case, we found two strategies: if the noise in the stochastic gene expression is below a certain threshold, the phenotypic variance increases via genetic diversification, whereas above this threshold, it is increased mediated by noise-induced phenotypic fluctuation. We examine how the increase in the phenotypic variances caused by parasite interactions influences the growth rate of a single host, and observed a trade-off between the two. Our results help elucidate the roles played by noise and genetic mutations in the evolution of phenotypic fluctuation and robustness in response to host-parasite interactions.

Determining investment size and local embeddedness under host market uncertainty and growth rates

This study employs a growth options perspective to examine how multinational corporations (MNCs) design their investment attributes under the influence of host market uncertainty and growth rates. It specifically examines MNCs’ decisions on investment size and local embeddedness under host market conditions. Using data on Korean overseas manufacturing subsidiaries, we find that MNCs choose either more-local-embedded small investments or less-locally-embedded large investments under high demand uncertainty and GDP growth rates. We also find that this choice is moderated by host market political risk and competition. Our findings imply that MNCs consider both uncertainty-driven flexibility and growth rate-induced commitment when selecting international investment modes. This consideration allows MNCs to gain flexibility as well as an enhanced ability to expand in the future. This study contributes to the literature on real options and entry modes in the international business area by showing how host market conditions and investment decisions are related.

The Evolution of Plasmid Transfer Rate in Bacteria and Its Effect on Plasmid Persistence.

AbstractPlasmids are extrachromosomal segments of DNA that can transfer genes between bacterial cells. Many plasmid genes benefit bacteria but cause harm to human health by granting antibiotic resistance to pathogens. Transfer rate is a key parameter for predicting plasmid dynamics, but observed rates are highly variable, and the effects of selective forces on their evolution are unclear. We apply evolutionary analysis to plasmid conjugation models to investigate selective pressures affecting plasmid transfer rate, emphasizing host versus plasmid control, the costs of plasmid transfer, and the role of recipient cells. Our analyses show that plasmid-determined transfer rates can be predicted with three parameters (host growth rate, plasmid loss rate, and the cost of plasmid transfer on growth) under some conditions. We also show that low-frequency genetic variation in transfer rate can accumulate, facilitating rapid adaptation to changing conditions. Furthermore, reduced transfer rates due to host control have limited effects on plasmid prevalence until low enough to prevent plasmid persistence. These results provide a framework to predict plasmid transfer rate evolution in different environments and demonstrate the limited impact of host mechanisms to control the costs incurred when plasmids are present.

Evolutionarily Stable Coevolution Between a Plastic Lytic Virus and Its Microbial Host.

Hosts influence and are influenced by viral replication. Cell size, for example, is a fundamental trait for microbial hosts that can not only alter the probability of viral adsorption, but also constrain the host physiological processes that the virus relies on to replicate. This intrinsic connection can affect the fitness of both host and virus, and therefore their mutual evolution. Here, we study the coevolution of bacterial hosts and their viruses by considering the dependence of viral performance on the host physiological state (viral plasticity). To this end, we modified a standard host-lytic phage model to include viral plasticity, and compared the coevolutionary strategies emerging under different scenarios, including cases in which only the virus or the host evolve. For all cases, we also obtained the evolutionary prediction of the traditional version of the model, which assumes a non-plastic virus. Our results reveal that the presence of the virus leads to an increase in host size and growth rate in the long term, which benefits both interacting populations. Our results also show that viral plasticity and evolution influence the classic host quality-quantity trade-off. Poor nutrient environments lead to abundant low-quality hosts, which tends to increase viral infection time. Conversely, richer nutrient environments lead to fewer but high-quality hosts, which decrease viral infection time. Our results can contribute to advancing our understanding of the microbial response to changing environments. For instance, both cell size and viral-induced mortality are essential factors that determine the structure and dynamics of the marine microbial community, and therefore our study can improve predictions of how marine ecosystems respond to environmental change. Our study can also help devise more reliable strategies to use phage to, for example, fight bacterial infections.

Impact of the facultative parasitic weed Rhamphicarpa fistulosa (Hochst.) Benth. on photosynthesis of its host Oryza sativa L.

Rhamphicarpa fistulosa is a facultative root parasitic annual forb, of the family Orobanchaceae that is native to sub-Saharan Africa. Parasitism results in yield reductions by the host plants but it is not known how exactly R. fistulosa affects its host or how the host responds physiologically. In three pot experiments, we investigated whether and when the parasite affects photosynthesis of rice, whether the level of impact was parasite density dependent and explored mechanisms underlying the response of rice photosynthesis to parasitism. Photosynthesis and related parameters were measured at a range of light use intensities. Host photosynthesis was negatively affected while light use efficiency was negatively affected only later on in the growth process. Except for dark respiration rates, which were never affected by parasite infection, suppression of host photosynthesis at light saturation, the initial light-use efficiency, chlorophyll content, specific leaf area and shoot weight were parasite density dependent with a stronger effect for higher parasite densities. Only at 56 days after sowing, the slope of the linear relationship between light adapted quantum efficiency of PSII electron transport (ΦPSII) and the quantum yield of CO2 assimilation (ΦCO2) of infected plants was less than those of un-infected plants. There was a considerable time lag between the parasite’s acquisition of benefits from the association, in terms of growth (previously observed around 42 DAS), and the reduction of host photosynthesis (around 56 DAS). Expression of relative reductions in host growth rates started at the same time as the relative suppression of host photosynthesis. This indicated that R. fistulosa affects host growth by first extracting assimilates and making considerable gains in growth, before impacting host photosynthesis and growth.