Response of body size and developmental time of Tribolium castaneum to constant versus fluctuating thermal conditions.

Temperature has profound effects on biological functions at all levels of organization. In ectotherms, body size is usually negatively correlated with ambient temperature during development, a phenomenon known as The Temperature-Size Rule (TSR). However, a growing number of studies have indicated that temperature fluctuations have a large influence on life history traits and the implications of such fluctuations for the TSR are unknown. Our study investigated the effect of different constant and fluctuating temperatures on the body mass and development time of red flour beetles (Tribolium castaneum Herbst, 1797); we also examined whether the sexes differed in their responses to thermal conditions. We exposed the progeny of half-sib families of a T. castaneum laboratory strain to one of four temperature regimes: constant 30°C, constant 25°C, fluctuating with a daily mean of 30°C, or fluctuating with a daily mean of 25°C. Sex-specific development time and body mass at emergence were determined. Beetles developed the fastest and had the greatest body mass upon emergence when they were exposed to a constant temperature of 30°C. This pattern was reversed when beetles experienced a constant temperature of 25°C: slowest development and lowest body mass upon emergence were observed. Fluctuations changed those effects significantly - impact of temperature on development time was smaller, while differences in body mass disappeared completely. Our results do not fit TSR predictions. Furthermore, regardless of the temperature regime, females acquired more mass, while there were no differences between sexes in development time to eclosion. This finding fails to support one of the explanations for smaller male size: that selection favors the early emergence of males. We found no evidence of genotype × environment interactions for selected set of traits.

Contribution of E. coli AlkA, TagA glycosylases and UvrABC-excinuclease in MMS mutagenesis.

MMS, an S(N)2 alkylating agent, is a moderate inducer of SOS mutagenesis and adaptive response. Our previous studies have shown that transient starvation of Escherichia coli AB1157argE3 strain causes a decrease of MMS-induced argE3-->Arg(+) reversions and this decrease is accompanied by the disappearance of the Fpg protein sensitive sites on plasmids isolated from MMS-treated and subsequently starved bacteria. This suggests that in such cells the mutation frequency decline (MFD) repair takes place. Here, we study the relation between MMS-induced mutagenesis as well as mutation frequency decline during starvation, and the repair of alkylated bases and AP-sites by base and nucleotide excision repair systems. In the AB1157alkA(-) strain, MMS-induced mutagenesis was over five-fold higher than in the wild type strain and no MFD repair occurred during starvation. Surprisingly, the lack of TagA glycosylase diminished MMS mutagenesis and accelerated the MFD effect. However, in double tagA(-)alkA(-) mutant, the frequency of Arg(+) reversions increased over 10-fold during 60 min of aminoacid starvation after MMS-treatment. Lack of the uvrA gene function did not affect the MMS-induced mutation rate and MFD in AB1157alkA(+)tagA(+). Starvation of MMS treated AB1157tagAalkAuvrA triple mutant caused a decrease of mutation frequency almost to the level of spontaneous mutation rate. Examination of the repair of 3-MeAde, 7-MeGua and AP sites during starvation using repair glycosylases and plasmids isolated from MMS-treated and starved bacteria revealed that in E. coli uvr(+) but tagAalkA strain, neither 3-MeAde nor 7-MeGua were repaired during 60 min starvation and these persistent lesions could be responsible for the induction of the SOS system and an increase in mutation rate during starvation. In the triple tagAalkAuvrA mutant the repair of 3-MeAde, 7-MeGua and AP sites was carried out effectively and this could explain the observed decrease in the mutation rate during starvation. These results suggest that only in the absence of the "first choice" repair enzymes TagA, AlkA glycosylases and UvrABC excinuclease, a third error-free repair system of alkylated bases is activated. In the absence of only TagA and AlkA glycosylases, UvrABC excinuclease mediates activation of the SOS response, and this results in an increase of mutagenesis induced by the presence of alkylated bases in DNA.

[Enteropathic acrodermatitis in light of personal observations]. / Acrodermatitis enteropathica w swietle wlasnych obserwacji.

Observations are reported carried out on the course and treatment of enteropathic acrodermatitis in 14 children. In the children the characteristic clinical picture before treatment was associated with low serum zinc level. Determination of serum zinc level during the treatment with zinc sulphate is without decisive importance for the selection of maintenance doses and the drug must be taken often during many years. In the choice of the therapeutic dose the clinical effects should be taken into account, and the dose may not be so high that it would normalized serum zinc level.