bioRxiv Science⌕ Search

Biology subjects

Szucs, M.

Publications and source records attributed to Szucs, M..

3 recordsLinked to original sources

Geographic variation in resistance of the invasive Drosophila suzukii to parasitism by the biological control agent, Ganaspis brasiliensis

Host-parasitoid interactions are often tied in coevolutionary arms races where parasitoids continuously have to evolve increased virulence as hosts evolve increased resistance. Invasion theories predict that when a host is introduced to a novel region without its coevolved natural enemies, they will evolve lower defenses. Resistance may also differ geographically and temporally due to abiotic and biotic factors. We investigated spatial, temporal and host plant related differences in resistance of the invasive D. suzukii in seven geographically distinct populations in Michigan and of one population from Oregon against a coevolved parasitoid, Ganaspis brasiliensis. Encapsulation rates (resistance) of G. brasiliensis eggs by D. suzukii reached 39% in August and 48% in September regionally. These relatively high levels of resistance in North America contrast with expectations and may be due to the low levels of competition D. suzukii experiences in the invaded range. Encapsulation rates of D. suzukii differed regionally and temporally but not between fruit types. The northernmost site with the lowest encapsulation rate had the highest rate of parasitism suggesting that parasitoids may be able to detect the defensive capacities of their hosts and adjust attack rates accordingly. The lowest encapsulation rates at the northernmost and thus overall coldest site indicate a negative effect of temperature on resistance. However, temporal differences in resistance from August to September were not consistent among sites. These results indicate that there can be regional and temporal variation in the outcome of host-parasitoid interactions between D. suzukii and G. brasiliensis. This may influence the efficacy and biocontrol potential of G. brasiliensis that has been recently approved for field releases against D. suzukii in North America.

evolutionary biology↗

The influence of the way of regression on the results obtained by the receptorial responsiveness method (RRM), a procedure to estimate a change in the concentration of a pharmacological agonist near the receptor

The receptorial responsiveness method (RRM) enables the estimation of a change in the concentration of a degradable agonist, near its receptor, by fitting its model to (at least) two concentration-effect (E/c) curves of a stable agonist of this receptor. One curve should be generated before this change in concentration, while the other one after this change, in the same (or in identical) biological system(s). It follows that RRM yields a surrogate parameter ("cx"), the concentration of the stable agonist that is equieffective with the change in the concentration of the degradable agonist. However, the curve fitting can be implemented several ways, which can affect accuracy, precision and convenience of use. This study utilized data of previous ex vivo investigations. Known concentrations of stable agonists were estimated with RRM by performing individual (local) or global fitting (with one or two model(s)), combined with the use of a logarithmic (logcx) or non-logarithmic parameter (cx), and with ordinary least-squares or robust regression. We found that the individual regression, the most complicated option, was the most accurate, followed closely by the moderately complicated two-model global regression and then by the easy-to-perform one-model global regression. The two-model global fitting was the most precise, followed by the individual fitting (closely) and by the one-model global fitting (from afar). The use of cx and robust regression did not, whereas pairwise fitting (i.e. fitting only two E/c curves at once) did improve the quality of estimation. Thus, the two-model global fitting, performed pairwise, is recommended for RRM, but the individual fitting is a good alternative.

pharmacology and toxicology↗

Zika virus dumbbell-1 structure is critical for sfRNA presence and cytopathic effect during infection

Zika virus (ZIKV) contains multiple conserved RNA structures in the viral 3 untranslated region (UTR), including the structure known as dumbbell-1 (DB-1). Previous research has shown that the DB-1 structure is important for flavivirus genome replication and cytopathic effect (CPE). However, the role of the DB structure and the mechanism by which it contributes to viral pathogenesis is not known. Using recently solved flavivirus DB RNA structural data, we designed two DB-1 mutant ZIKV infectious clones termed ZIKV-TL.PK, which disrupts DB-1 tertiary folding and ZIKV-p.2.5, which alters DB-1 secondary structure formation. In cell culture, we found that viral genome replication of both mutant clones is not significantly affected compared to ZIKV-WT, but viral CPE is considerably decreased. We investigated sub-genomic flaviviral RNA (sfRNA) formation by both DB-1 mutants following A549 infection and found both mutant clones have decreased levels of all sfRNA species compared to ZIKV-WT during infection. To investigate the mechanism of decreased CPE in our DB-1 mutant clones, we assayed ZIKV DB mutant-infected A549 cells for cell viability and caspase activation. We found that cell viability is significantly increased in DB-1 mutant-infected cells compared to ZIKV-WT due to reduced caspase 3 activation. We also show that replication of the ZIKV-P.2.5 mutant was significantly restricted by type I interferon treatment without altering interferon stimulated gene expression. Using a murine model of ZIKV infection, we show that both ZIKV-DB-1 mutants exhibit reduced morbidity and mortality compared to ZIKV-WT virus due to tissue specific attenuation in ZIKV-DB viral replication in the brain tissue. Overall, our data show that the flavivirus DB-1 RNA structure is important for maintaining sfRNA levels during infection which supports caspase-3 dependent, viral cytopathic effect, type 1 interferon resistance, and viral pathogenesis in a mouse model.

microbiology↗