arXiv subjects

Madeleine Opitz

Publications and source records attributed to Madeleine Opitz.

3 recordsLinked to original sources

arXiv2018

Boosting Functional Response Models for Location, Scale and Shape with an Application to Bacterial Competition

We extend Generalized Additive Models for Location, Scale, and Shape (GAMLSS) to regression with functional response. This allows us to simultaneously model point-wise mean curves, variances and other distributional parameters of the response in dependence of various scalar and functional covariate effects. In addition, the scope of distributions is extended beyond exponential families. The model is fitted via gradient boosting, which offers inherent model selection and is shown to be suitable for both complex model structures and highly auto-correlated response curves. This enables us to analyze bacterial growth in \textit{Escherichia coli} in a complex interaction scenario, fruitfully extending usual growth models.

stat.ME↗

arXiv2018

CsrA and its regulators control the time-point of ColicinE2 release in Escherichia coli

The bacterial SOS response is a cellular reaction to DNA damage, that, among other actions, triggers the expression of colicin - toxic bacteriocins in Escherichia coli that are released to kill close relatives competing for resources. However, it is largely unknown, how the complex network regulating toxin expression controls the time-point of toxin release to prevent premature release of inefficient protein concentrations. Here, we study how different regulatory mechanisms affect production and release of the bacteriocin ColicinE2 in Escherichia coli. Combining experimental and theoretical approaches, we demonstrate that the global carbon storage regulator CsrA controls the duration of the delay between toxin production and release and emphasize the importance of CsrA sequestering elements for the timing of ColicinE2 release. In particular, we show that ssDNA originating from rolling-circle replication of the toxin-producing plasmid represents a yet unknown additional CsrA sequestering element, which is essential in the ColicinE2-producing strain to enable toxin release by reducing the amount of free CsrA molecules in the bacterial cell. Taken together, our findings show that CsrA times ColicinE2 release and reveal a dual function for CsrA as an ssDNA and mRNA-binding protein, introducing ssDNA as an important post-transcriptional gene regulatory element.

q-bio.MN↗

arXiv2014

Chemical warfare and survival strategies in bacterial range expansions

Dispersal of species is a fundamental ecological process in the evolution and maintenance of biodiversity. Limited control over ecological parameters has hindered progress in understanding of what enables species to colonise new area, as well as the importance of inter-species interactions. Such control is necessary to construct reliable mathematical models of ecosystems. In our work, we studied dispersal in the context of bacterial range expansions and identified the major determinants of species coexistence for a bacterial model system of three Escherichia coli strains (toxin producing, sensitive, and resistant). Genetic engineering allowed us to tune strain growth rates and to design different ecological scenarios (cyclic and hierarchical). We found that coexistence of all strains depended on three strongly interdependent factors: composition of inoculum, relative strain growth rates, and effective toxin range. Robust agreement between our experiments and a thoroughly calibrated computational model enabled us to extrapolate these intricate interdependencies in terms of phenomenological biodiversity laws. Our mathematical analysis also suggested that cyclic dominance between strains is not a prerequisite for coexistence in competitive range expansions. Instead, robust three-strain coexistence required a balance between growth rates and either a reduced initial ratio of the toxin-producing strain, or a sufficiently short toxin range.

q-bio.PE↗