Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “preadaptation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

313 records · Page 18Linked to original sources
PubMedDate not supplied

[One more biological characteristic of coccidia in the genus Cryptosporidium (Sporozoa: Apicocomplexa)].

Suckling rats were used as a model host for our previous EM studies of the endogenous development of Cryptosporidium parvum isolated from spontaneously infected calves (Beĭer e. a., 1990; Beĭer, Sidorenko, 1990). In the course of repeated infections it was noticed that the oocysts discharged by the recipient host (rat) were obviously larger than those in the donor's (calf's) isolates. Keeping in mind the presumable taxonomic significance of coccidian oocysts as a constant and rather reliable tool for species discrimination we made a comparative quantitative and statistical analysis of the mean values of oocysts of C. parvum, originating from several sources (table 2): a random human isolate (N 1), several random isolates from spontaneously infected calves (N 2-5), isolates from calves (N 6-8) used as the infecting material for suckling rats, and fecal samples from the experimentally infected rats (N 9-15). The results obtained have shown that the oocysts discharged by rats (N 9-15) were larger that those of calf origin (N 6-8), with the differences being statistically significant with 95% confidence. Besides, within the same host (rat) at least two oocyst groups were distinguished (N 9-11 and 12-15, resp.) whose differences in mean values also appeared statistically significant. The larger oocysts displayed differences in morphology bearing distinct walls which were never observed either in the donor isolates or in the smaller population of the recipient oocysts. The established differences in oocyst dimensions lay presumably within the frames of the normal reaction of C. parvum and other Cryptosporidium species, due to biological peculiarities of unusual life cycles of these unique coccidia: their homoxenous (i.e. confined to one host body only) development is combined with polyxeny (i.e. a wide host specificity that involves the number of host species representing different environmental conditions). The parasite's ability to change its functional morphology and size may appear some kind of preadaption to the number of varying conditions met by these polyxenous coccidia. This and other relevant assumptions are discussed in the paper.

Animals↗
PubMed1997

Developmentally regulated changes in the cell surface architecture of Leishmania parasites.

The cell surface of Leishmania parasites is coated by a highly unusual glycocalyx which varies markedly during the parasite life cycle. The predominant molecule on the extracellular promastigote (sandfly) stage is a complex lipophosphoglycan (LPG), which together with a number of GPI-anchored proteins and a family of low molecular weight glycoinositolphospholipids (GIPLs), forms a morphologically distinct protective coat over the plasma membrane. The structure of the LPG has been shown to vary in different species and during promastigote development in the sandfly. This polymorphism is thought to be important in allowing Leishmania parasites to colonize a range of insect hosts, and in facilitating the regulated migration of promastigotes along the sandfly alimentary canal. Stage-specific changes in LPG are also involved in preadapting promastigotes to life in the mammalian host. This complex glycocalyx coat is absent from the amastigote stage that proliferates in the phagolysosomes of mammalian macrophages, as the expression of both the LPG and GPI-anchored proteins is massively down-regulated. Instead, the plasma membrane of amastigotes is coated by a densely packed layer of parasite-derived GIPLs and host-derived glycosphingolipids. We propose that the down-regulation of the promastigote macromolecules and the acquisition of host glycolipids by amastigotes represents an important strategy to avoid detection by specific and non-specific components of the immune system.

Animals↗
PubMed1997

Pharmacogenetics in biological perspective.

What have we learned? Pharmacogenetics, heritable variation in response to xenobiotics, is present in all forms of life. Initially, human data perhaps have created the most excitement, and they provide much biochemical detail. However, if we look at pharmacogenetic variation of insects and bacteria, we see it as a characteristic of populations; individuals with inborn resistance to various toxicants can cause the survival of a population by the process of Darwinian selection. Diversity of a population and Darwinian selection are different milestones serving population survival. Variation of drug response may represent variation of drug targets, drug metabolism, and probably drug transport. Metabolic variation appears to be the most prominent; at present, it is not clear whether this prominence has historical or biological causes. It is an interesting exercise to compare pharmacogenetic resistance with intoxication and resistance to infection by invasion of disease-carrying bacteria or other pathogens. The big difference is that pathogens tend to show variabilities that drugs do not have. The immune system is made to deal with the genetic variabilities linked to the short life span of most pathogens. However, there are, besides the immune system, several cases of genetic host resistance associated with the long life span of mammalian hosts. Such genetic host resistances are factors equivalent to pharmacogenetic variation. Current data pertain to resistance against malaria, tuberculosis, cholera, and AIDS. Most pharmacogenetic variants within a population are preadaptive, that is, they are established before xenobiotic exposure. Hence, one must postulate a multiplicity of variants in a population capable of resisting a multiplicity of drugs. The persistence of this multiplicity suggests that most variants are either present in heterozygous form and are thereby advantageous for their carriers, or they are selectively neutral mutants. It means that the biological cost of pharmacogenetic diversity, measured in terms of reduced fertility, should be low in a population. The frequencies of variant genes are usually not the same in different populations. Also the nucleotide substitutions in a variable gene often differ between populations. In other words, pharmacogenetic differences between populations are typical events. Pharmacogenetics is usually thought of as the study of a situation in which a single gene product exerts control over a given drug response so that a failure to respond, or an excessive response, may result. However, one should not forget that random variation is always present, probably reflecting the randomness of mutations plus variation of any environmental factors that might contribute. This underlying randomness of variation will always affect the picture of any all-or-none variation. Future pharmacogenetics must deal with both random and monogenic variation.

Animals↗
PubMed1997

[Analysis of the dependence of the frequency of emergence of His+-reversions in Salmonella typhimurium on the density of the cell population].

The dependence of the appearance of mutants on the number of viable cells plated on a selective medium was analyzed with the spontaneous His+ reversion system in the histidine auxotroph of Salmonella typhimurium strain BA13. The frequency of spontaneous His+ revertants was shown to be inversely proportional to the number of plated cells. Evaluation of residual culture growth on a histidine-deficient medium suggests that this factor cannot be the reason behind the inverse dependence. The results of experiments involving previously added His+ revertants showed that the inverse relationship between mutant frequency and population density is not connected with the inhibition of preadaptive revertant growth by nonmutant cells. Moreover, an inhibitory effect of the culture medium on the frequency of spontaneous His+ revertants upon histidine starvation was detected. On the basis of these results, it was assumed that the His+ reversion generated by histidine starvation is suppressed by metabolites of starved cells.

Adaptation, Physiological↗
PubMed1998

CD1.1 expression by mouse antigen-presenting cells and marginal zone B cells.

Mouse CD1.1 is an MHC class I-like, non-MHC-encoded, surface glycoprotein that can be recognized by T cells, in particular NK1.1+ T cells, a subset of alphabeta T cells with semiinvariant TCRs that promptly releases potent cytokines such as IL-4 and IFN-gamma upon stimulation. To gain insight into the function of CD1.1, a panel of nine mAbs was generated and used to biochemically characterize and monitor the surface expression of CD1.1 on different cell types. CD1.1 is a heavily glycosylated, beta2-microglobulin-associated surface protein. Its recognition by a panel of 12 V alpha14-positive and -negative CD1-specific alphabeta T cell hybridomas was blocked by two groups of mAbs that bound to adjacent clusters of epitopes, indicating that different alphabeta TCRs bind to the same region of CD1.1, presumably above the groove. Remarkably, CD1.1 was mainly expressed by dendritic cells, B cells, and macrophages, suggesting a function in Ag presentation to Th cells. Furthermore, the cell type that expressed the highest levels of CD1.1 was the splenic marginal zone B cell, a distinct subset of B cells that also expresses CD21 (the C3d receptor) and may be involved in natural responses to bacterial Ags. Altogether, the results support the idea that CD1.1 may function in recruiting a form of innate help from specialized cytokine producer alphabeta T cells to APCs, a role that might be important at the preadaptive phase of immune responses to some microbial pathogens.

Animals↗
PubMedDate not supplied

[Prevention of nitric oxide hyperproduction by adaptation to stressor effects].

As was shown earlier, acute hypotensive shock induced by nitrogen oxide (NO) hyperproduction can be prevented by dosed adaptation to environmental factors. In this work we tested the hypothesis that the mechanism of this adaptive effect is based on limiting NO hyperproduction. It was shown that rat adaptation to stress completely prevented arterial depression and sharply increased revival rate of the animals after heat shock. Hypotension induced by heat shock was accompanied by almost 2.5-fold increase in NO production (EPR analysis) as compared to the control. At the background of preadaptation, heat shock did not increase NO production relative to the animals not subjected to heat shock. The data obtained agree with the proposal that the adaptation initiates NO-dependent mechanisms of limiting NO hyperproduction. Such limiting seems to be negatively regulated by NO.

Adaptation, Physiological↗
PubMed2026

Historical metabolic adaptation potentiates the rapid evolution of flonicamid resistance in Myzus persicae.

Rapid adaptation to novel environments is often shaped not only by newly acquired mutations but also by historical genetic backgrounds established through prior evolutionary events. However, the extent to which such historical contingency contributes to the rapid evolution of insecticide resistance remains poorly understood. Here, we investigated the emergence of resistance to flonicamid, a recently deployed insecticide, in the green peach aphid, Myzus persicae. We show that constitutive overexpression of the P450 enzymes CYP6CY3 and CYP6CY4, already widespread in populations of M. persicae before flonicamid deployment, confers a previously cryptic tolerance phenotype to flonicamid. However, biochemical and transgenic analyses demonstrated that these metabolic adaptations provide only weak protection against flonicamid. Following flonicamid deployment, however, a novel target-site mutation, NaamV251I, in the recently identified molecular target of 4-trifluoromethylnicotinamide (TFNA-AM), emerged in M. persicae on a genetic background of CYP6CY3 or CYP6CY4 overexpression. Structural modeling, enzymatic assays, and CRISPR-Cas9 genome editing demonstrated that this mutation reduces target sensitivity and independently confers moderate resistance. Strikingly, combining the nicotinamidase (Naam) mutation with pre-existing CYP6CY3 or CYP6CY4 overexpression produced substantially elevated resistance phenotypes that far exceeded the effects of either mechanism alone. Our results demonstrate that the pre-existing metabolic background did not itself evolve further following flonicamid deployment but fundamentally altered the phenotypic consequences of a subsequently acquired target-site mutation. These findings provide direct evidence that historical adaptive variation can potentiate rapid resistance evolution to newly introduced insecticides and reveal how interactions between past and contemporary adaptations shape evolutionary responses to novel environmental challenges.

Animals↗