We studied the effect of density on feeding success of 2 fleas, Xenopsylla conformis and Xenopsylla ramesis, when exploiting rodents Meriones crassus and Gerbillus dasyurus. We tested 2 alternative hypotheses: (i) that intraspecific interference competition occurs and, thus, feeding success of a flea decreases with an increase in density and (ii) that facilitation via suppression of a host defence system occurs and thus, feeding success of a flea increases with an increase in density. The mean size of a bloodmeal and the proportion of highly engorged individuals in X. conformis feeding on both hosts were affected by density. When on G. dasyurus, both the size of a bloodmeal and the proportion of highly engorged individuals were lower at low (5-15 fleas per host) than at high (25-50 fleas per host) densities. The opposite was true when this flea fed on M. crassus. The mean bloodmeal size and proportions of highly engorged X. ramesis parasitizing either host were not affected by flea density. This study showed that the density dependence of feeding success of a flea (a) varied both between fleas and within-fleas between hosts and (b) indicated either intraspecific competition or facilitation via the host in a particular flea-host association.
We tested the hypothesis that a negative fitness-density relationship exists in haematophagous ectoparasites. We studied the effect of flea density on the number of blood meals necessary for starting oviposition and egg production in Xenopsylla conformis and Xenopsylla ramesis when exploiting two rodent hosts, Meriones crassus and Gerbillus dasyurus. The number of blood meals taken by a flea prior to first oviposition was similar in both flea species but was dependent on flea density and differed significantly between hosts. When parasitizing G. dasyurus, females of both flea species required a similar number of blood meals to start oviposition, independent of density. By contrast, fleas on M. crassus at higher densities needed less blood meals than at lower densities. Egg production of female fleas differed significantly between flea and host species and was affected by flea density. X. ramesis produced more eggs than X. conformis. When parasitizing G. dasyurus, density did not affect the number of eggs produced by X. conformis, however, when on M. crassus, this flea produced significantly less eggs at the highest density. The number of eggs produced by X. ramesis at high densities was significantly lower than at low densities when it parasitized either host species. Results of this study demonstrated that reproductive success of fleas was density dependent and, in general, decreased with an increase in density. However, the effect of density on reproductive performance was manifested differently on different host species.
Endogenous molecular circadian clocks drive daily rhythmic changes at the cellular, physiological, and behavioral level for adaptation to and anticipation of environmental signals. The core molecular system consists of autoregulatory feedback loops, where clock proteins inhibit their own transcription. A complex and not fully understood interplay of regulatory proteins influences activity, localization and stability of clock proteins to set the pace of the clock. This study focuses on the molecular function of Ribosomal S6 Kinase (RSK) in the Drosophila melanogaster circadian clock. Mutations in the human rsk2 gene cause Coffin–Lowry syndrome, which is associated with severe mental disabilities. Knock-out studies with Drosophila ortholog rsk uncovered functions in synaptic processes, axonal transport and adult behavior including associative learning and circadian activity. However, the molecular targets of RSK remain elusive. Our experiments provide evidence that RSK acts in the key pace maker neurons as a negative regulator of Shaggy (SGG) kinase activity, which in turn determines timely nuclear entry of the clock proteins Period and Timeless to close the negative feedback loop. Phosphorylation of serine 9 in SGG is mediated by the C-terminal kinase domain of RSK, which is in agreement with previous genetic studies of RSK in the circadian clock but argues against the prevailing view that only the N-terminal kinase domain of RSK proteins carries the effector function. Our data provide a mechanistic explanation how RSK influences the molecular clock and imply SGG S9 phosphorylation by RSK and other kinases as a convergence point for diverse cellular and external stimuli.
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