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Evensen, C.

Publications and source records attributed to Evensen, C..

3 recordsLinked to original sources

Co-occurrence networks can preserve emergent properties of ecological communities

Interaction networks, in which nodes represent species and edges represent direct interactions between species, have a long and impactful history in community ecology. However, co-occurrence networks, where edges represent statistical relationships among species presences or abundances, are often easier to construct from lab and field data. It is clear that co-occurrence edges often do not represent direct interactions, but frameworks for the interpretation of co-occurrence networks have not kept pace with their generation. It is therefore unclear when and how these networks can be used to gain insight into community dynamics. Here, we use a Generalized Lotka-Volterra-based model to explore the contexts in which emergent properties of species interaction networks are identifiable in their resulting co-occurrence networks. We find that, in spite of many differences in direct edges, key features of the true interaction network, such as unipartite modularity, high-degree nodes (hubs), and bipartite modularity and nestedness, can be preserved in co-occurrence networks. In contrast, node degree distributions are not preserved even in the most idealized scenarios. We propose that networks derived from large co-occurrence datasets could therefore be used in future empirical work to test existing hypotheses of how emergent network structures drive ecological community dynamics.

ecology↗

Multispecies interactions and the community context of the evolution of virulence

In nature, host-parasite/pathogen relationships are embedded in a network of ecological interactions that have the potential to shape the evolutionary trajectories of shared pathogens. Understanding this community context of infectious disease evolution is important for wildlife, agricultural, and human systems alike - illustrated, for example, by the increasing risk of zoonotic disease emergence. We introduce an eco-evolutionary model that examines ecological feedbacks across a range of host-host interactions. Specifically, we analyze a model of the evolution of virulence of a pathogen infecting hosts who themselves exhibit competitive, mutualistic, or exploitative relationships. We find that pathogen specialism is necessary for inter-host interactions to impact parasite evolution. An important general result is that increasing competition between hosts leads to higher shared pathogen virulence, while increasing mutualism leads to lower virulence. Across a range of scenarios, the nature of pathogen specialization is critical to the outcome - for instance, if hosts only differ in initial susceptibility to infection, there is no impact of host-host interactions on virulence evolution. In contrast, specialization in terms of onward transmission, host tolerance, or intra-host pathogen growth rate critically impact the evolution of virulence. For example, stronger specialism in transmission selects for lower virulence, while stronger specialism in tolerance and growth rate selects for higher virulence. Our work provides testable hypotheses for multi-host disease systems, predicts how changing interaction networks may impact the evolution of virulence, and broadly demonstrates the importance of looking beyond pairwise relationships to understand evolution in realistic natural contexts.

evolutionary biology↗

Kinetic-Mechanistic Evidence for Which E. coli RNA Polymerase-{lambda}PR Open Promoter Complex Initiates and for Stepwise Disruption of Contacts in Bubble Collapse

In transcription initiation, specific contacts between RNA polymerase (RNAP) and promoter DNA are disrupted as the RNA-DNA hybrid advances into the cleft, resulting in escape of RNAP. From the pattern of large and small rate constants for steps of initiation at {lambda}PR promoter at 19{degrees}C, we proposed that in-cleft interactions are disrupted in extending 3-mer to 5-mer RNA, -10 interactions are disrupted in extending 6-mer to 9-mer, and -35 interactions are disrupted in extending 10-mer to 11-mer, allowing RNAP to escape. Here we test this mechanism and determine enthalpic and entropic activation barriers of all steps from kinetic measurements at 25{degrees}C and 37{degrees}C. Initiation at 37{degrees}C differs significantly from expectations based on lower-temperature results. At low concentration of the second iNTP (UTP), synthesis of full-length RNA at 37{degrees}C is slower than at 25{degrees}C and no transient short RNA intermediates are observed, indicating a UTP-dependent bottleneck step early in the 37{degrees}C mechanism. Analysis reveals that the 37{degrees}C {lambda}PR OC (RPO) cannot initiate and must change conformation to a less-stable initiation complex (IC) capable of binding the iNTP. We find that IC is the primary {lambda}PR OC species below 25{degrees}C, and therefore conclude that IC must be the I3 intermediate in RPO formation. Surprisingly, Arrhenius activation energy barriers to five steps where RNAP-promoter in-cleft and -10 contacts are disrupted are much smaller than for other steps, including a negative barrier for the last of these steps. We interpret these striking effects as enthalpically-favorable, entropically-unfavorable, stepwise bubble collapse accompanying disruption of RNAP contacts. SignificanceTranscription initiation is highly regulated. To understand regulation, mechanisms of initiation and escape of RNA polymerase (RNAP) from the promoter must be understood. RNAP forms a highly-stable open complex (RPO) with {lambda}PR promoter at 37{degrees}C. From experiments determining effects of temperature on rate constants for each step of RNA synthesis, we find that RPO cannot bind the initiating nucleotides, that the I3 intermediate and not RPO is the initiation complex, and that contacts of RNAP with single-stranded DNA of the discriminator and -10 region and with -35 duplex DNA are disrupted stepwise as the RNA-DNA hybrid moves into the cleft. Evidence is obtained for stepwise bubble collapse and base stacking accompanying disruption of interactions of the single-stranded discriminator and -10 regions with RNAP.

biochemistry↗