The typical life cycle of aphids includes several parthenogenetic generations and a single sexual generation (cyclical parthenogenesis), but some species or populations are totally asexual (obligate parthenogenesis). Genetic variability is generally low in these asexually reproducing populations, that is, few genotypes are spread over large geographic areas. Both genetic drift and natural selection are often invoked to account for this low genetic variability. The peachpotato aphid, Myzus persicae, which encompasses both cyclical and obligate parthenogens, has developed several insecticide resistance mechanisms as a consequence of intense insecticide use since the 1950s. We collected asexually reproducing M. persicae from oilseed rape and examined genetic variability at eight microsatellite loci and three insecticide resistance genes to determine whether their genetic structure was driven by drift and/or selection. We identified only 16 multilocus microsatellite genotypes among 255 individuals. One clone, which combined two insecticide resistance mechanisms, was frequently detected in all populations whatever their location over a large geographical area (the northern half of France). These unexpected findings suggest that drift is not the unique cause of this low variability. Instead, the intensification of both insecticide treatments and oilseed rape cultivation may have favored a few genotypes. Thus, we propose that selective pressures resulting from human activities have considerably modified the genetic structure of M. persicae populations in northern France in a relatively short period of time. Heredity (2005) 94, 630-639.
Activation of PPARgamma by synthetic ligands, thiazolidinediones, inhibits the proliferation of cancer cells. In this report, focusing our attention on ciglitazone, we show that ciglitazone inhibits melanoma growth by inducing apoptosis and cell-cycle arrest, whereas normal melanocytes are resistant to ciglitazone. In melanoma cells, ciglitazone-induced apoptosis is associated with caspase activations and a loss of mitochondrial membrane potential. Induction of cell-cycle arrest by ciglitazone is associated with changes in expression of key cell-cycle regulators such as p21, cyclin D1, and pRB hypophosphorylation. Cell-cycle arrest occurs at low ciglitazone concentrations and through a PPARgamma-dependent pathway, whereas the induction of apoptosis is caused by higher ciglitazone concentrations and independently of PPARgamma. These results allow an effective molecular dissociation between proapoptotic effects and growth inhibition evoked by ciglitazone in melanoma cells. Finally, we show that in vivo treatment of nude mice by ciglitazone dramatically inhibits human melanoma xenograft development. The data presented suggest that ciglitazone might be a better candidate for clinical trials in melanoma treatment than the thiazolidinediones currently used in the treatment of type 2 diabetes, such as rosiglitazone, which is devoid of a proapoptotic PPARgamma-independent function.
SUMMARYIncrease in seawater temperature is one of the major effects of global climate change that affects marine organisms, including Cnidaria. Among them, gorgonians from the NW Mediterranean Sea, such as the species Eunicella singularis, have suffered spectacular and extensive damage. We thus investigated in a controlled laboratory experiment the response of E. singularis to a long-term increase in temperature and we took a special interest in its photosynthetic and calcification response to the stress. Two populations collected at 15 and 35 m depths were studied in order to determine whether there was a difference in sensitivity to thermal stress between living depths. Our results show: (a) that calcification and photosynthesis were impacted only when gorgonians were maintained for more than two weeks at 26°C, and (b) that colonies of E. singularis living in shallow waters were less tolerant than those living in deep waters. Because E. singularis is a symbiotic species, we have also discussed the potential role of symbiosis in the thermotolerance response.
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