Pleiotropy is the condition in which a gene influences the phenotype of more than one part of the body.
A trivial instance would be that the gene influencing the length of the left leg also influences the length of the right leg.
Pleiotropy exists because there is not a one-to-one relationship between the parts of an organism that a gene influences and the parts of an organism that we recognize as characters.
Pleiotropy describes the genetic effect of a single gene on multiple phenotypictraits.
Antagonistic pleiotropy refers to a situation in which a single gene creates multiple competing effects, such that beneficial effects of a trait created by the gene are offset by 'losses' in other traits.
Pleiotropy, the ability of a single mutant gene to cause multiple mutant phenotypes, is a relatively common but poorly understood phenomenon in biology.
To test the statistical significance of this amount of pleiotropy, we generated a random distribution of phenotypes per gene such that the same properties of the original data set, that is, the same frequency of growth defects in each of the 21 conditions, were maintained (Materials and methods).
Pleiotropy, while frequently observed, is thought to pose evolutionary disadvantages for an organism, including limiting the rate of adaptation and reducing the level of adaptation for some traits in response to selection for others (Otto, 2004).
The twin effects of pleiotropy (where one gene affects many "traits") and polygeny (where one "trait" is the product of many genes) work to create a complex web of genotype-phenotype interactions that renders any simple causative analysis fruitless.
This single evolutionary advantage of increased speed attendant to the minimization of pleiotropy may underlie the totality of the reason for the existence and initial appearance of distinct organs within multicellular biota, a design schema where such distinctive organs operate as a complex, co-ordinated unit whole, yet remain substantially isolated in their behaviors.
Pleiotropy is intrinsic to the nature of all hierarchically layered coding structures, even if code segments (genes, microsubroutines) remain unreused.
Pleiotropy is the phenomenon whereby a single gene has multiple consequences in numerous tissues.
Pleiotropy describes the genetic effect of a single gene on multiple phenotypictraits.
Antagonistic pleiotropy refers to a situation in which a single gene creates multiple competing effects, such that beneficial effects of a trait created by the gene are offset by 'losses' in other traits.
This is roughly equivalent to “relational pleiotropy”, as defined by Hadorn (1961), and describes situations where a simple bio-chemical abnormality has multiple phenotypic consequences, sometimes with little superficial connection to the initiating mutation.
The distinction between Type 6 and Type 4 (Parsimonious pleiotropy) is that in the combinatorial situation, the biochemistry of the protein changes from context to context, sometimes radically (for example, from transcriptional activator to transcriptional repressor).
Cases of unifying pleiotropy are usually easy to recognize, because the biology is interpretable, but there may be situations where it is not immediately apparent.
Pleiotropy is measured by the number of adverse conditions (of 21 tested conditions) under which the homozygous gene-deletion strain shows significantly slower growth than under the control condition.
The numbers of genes in the five bins are 1890, 193, 164, 68, and 71, respectively, in A; 755, 64, 60, 18, and 20, respectively, in B; and 1213, 105, 89, 32, and 33, respectively, in C. Error bar shows one standard error of mean.
Pleiotropy is measured by the number of conditions under which the homozygous gene-deletion strain shows significantly slower growth than under the control condition.
Statin pleiotropy: fact or fiction? American Journal of Critical Care - Find Articles(Site not responding. Last check: 2007-08-12)
The distinction between the clinical benefits of lowering levels of LDL cholesterol and the pleiotropic effects of statin therapy may actually not be dissociated (as reported in current literature) because the effects of hyperlipidemia and of statin therapy on small arteries and arterioles have not been reported.
Studies of arterioles in hyperlipidemic states before and after statin therapy could help determine if "pleiotropy" is appropriate terminology when it can be shown that atheromatous changes also occur in the very small arteries and arterioles and will improve with statin therapy.
The importance of knowing the pathology of the arterioles in hyperlipidemic states are patently evident because the pleiotropic effects of statins are attributed to diseases that result from small vessel pathology.
Pleiotropy is a relatively common, but poorly understood phenomenon in biology defined as the ability of a mutation in a single gene to produce multiple effects in vivo.
The prevalence of pleiotropy is perhaps most striking in the growing number of human diseases for which a mutation in a single gene produces a broad and seemingly unrelated set of symptoms (Brunner and van Driel, 2004).
The results (Figure 8) show that approximately 70% of the mutants have a relatively low degree of pleiotropy, with phenotypes in only one or two conditions, and the remaining 30% are highly pleiotropic, with growth defects in as many as 14 conditions.
ARS | Publication request: Agricultural Fitness of Smooth Bromegrass Populations Selected for Divergent Fiber ...(Site not responding. Last check: 2007-08-12)
These "correlated" changes may occur because a gene controls more than one trait (pleiotropy), because genes controlling the two traits are in close physical proximity on a chromosome (linkage), or because of random segregation (drift).
For forage yield, pleiotropy was the most important factor, indicating that dietary fiber and forage yield share many of the same genes.
Pleiotropy was estimated as the main effect linear response, linkage was estimated as the heterogeneity in linear responses across germplasms, and drift was estimated as asymmetry of linear responses.
A few years later, George Williams extrapolated on this idea by formulating the theory of “antagonistic pleiotropy.” Antagonistic pleiotropy means that some genes that increase the odds of successful reproduction early in life may have deleterious effects later in life.
An example of antagonistic pleiotropy in humans is p53, a gene that directs damaged cells to stop reproducing or die.
Because of antagonistic pleiotropy, it is likely that tinkering with genes to improve late-life fitness could have a detrimental effect on health at younger ages.
Rather, everything we know about these genes suggests they were present in eukaryotic founder cells shortly after, or even congruent with, the emergence of eukaryotes from their prokaryotic ancestors, and have been stringently conserved ever since.
It is suggested that the evolutionary theory of senescence should be focused on those evolutionary principles that have been validated experimentally, and that the notion of antagonistic pleiotropy be dropped from theories of the evolution of senescence.
This notion suggests that allelic variants of genes involved in promoting senescence would likely have been positively selected on the basis of whether or not they enhance an individual’s ability to survive until the reproductive period, and/or to carry out reproductive activities in a successful fashion.
The one-gene-one-character view was abandoned early in the history of genetics owing to the discovery of numerous pleiotropic effects of mutations with major effects on morphology.
The universal pleiotropy hypothesis of Wright was the reaction to this discovery.
There is for instance no evidence of extensive pleiotropy of genes influencing abdominal and sternopleural bristle number in Drosophila melanogaster (Davies, 1971; Mackay et al., 1992a).
Pleiotropy, Natural Selection, and the Evolution of Senescence -- Williams 2001 (1): 13 -- Science's SAGE KE Jump to: Page Content, Section Navigation, Site Navigation, Site Search, Account Information, or Site Tools.
Abstract: A new individual entering a population may be said to have a reproductive probability distribution.
These include the expectation that rapid morphogenesis should be associated with rapid senescence, that senescence should always be a generalized deterioration of many organs and systems, and that postreproductive periods be short and infrequent in any wild population.
It can also test for gene ×; time interaction, polygenic pleiotropy – defined in the longitudinal context as a trait being determined by the same set of genes at distinct time points – and distinguish between major genepleiotropy and co-incident linkage [6-8].
We describe and apply a test of the null hypothesis of complete pleiotropy versus the alternative of incomplete pleiotropy based on a factor-analytic parameterization of the polygenic variance component.
Havill and Mahaney [14] find evidence for incomplete pleiotropy in the polygenic component of SBP in the fourth and sixth decades of life, although their estimates of the proportion of polygenic variance due to shared genes are lower than ours for comparable age ranges.
The results of the third and fourth series of simulations show that the observed benefits of non-separable coding are not simply due to the noise in the system.
Fitness landscapes that show a high degree of epistasis are usually considered difficult for genetic algorithms; however, there are some known exceptions to this rule (Manela and Campbell, 1992; Reeves and Wright, 1995; Rochet et al., 1998; Kwasnicka 1997, 1998, 1999).
While we realize that realistic problems of interest to evolutionary computation are non-separable, it is hoped that the very simplicity of our model will make it more amenable to a mathematical treatment than the existing models for which effects of pleiotropy and epistasis have been studied.
However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations.
Pervasive biophysical pleiotropy within the ß-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained.
The ‘biophysical pleiotropy’ they’re talking about here, from the paper, appears to mean that the protein products of various missense mutants end up ‘interacting’ with other proteins/chemical compounds that make up the cell in such a way as to minimize the ‘resistance’ that will be 8217;selected’; for.
The purpose of this article is to provide students and researchers entering the field of aging studies with an introduction to the evolutionary theories of aging, as well as to orient them in the abundant modern scientific literature on evolutionary gerontology.
At present the most viable evolutionary theories are the mutation accumulation theory and the antagonistic pleiotropy theory; these theories are not mutually exclusive, and they both may become a part of a future unifying theory of aging.
Antagonistic pleiotropy theory: Late-acting deleterious genes may even be favored by selection and be actively accumulated in populations if they have any beneficial effects early in life.
Aging can be viewed as a progressive decrease in reserve capacity and a progressive approach towards a threshold of frailty, so that there is an increasing probability that any crisis, which could be weathered when young, now results in death.
Antagonistic pleiotropyNatural selection is relatively unconcerned about events that happen late in the life span.
This can be regarded as an application of antagonistic pleiotropy, in which the early benefits of investing in reproduction rather than maintenance/repair result in the adverse effects of declining physiology as we outlive our "natural" life spans.
Well, if the properties of a protein are selected for, then a principle of low pleiotropy would apply, which is that the more features of a protein that exon shuffling affects, the less likely it is that the resulting product is useful.
I'll conclude by mentioning that this kind of selection would be expected to operate on other genetic units besides exons, such as regulatory sequences and whole genes-- any unit of duplication.
The principles of modularity and low pleiotropy should apply here as well, and offer another point of view for approaching questions about the evolution of development and the genetic correlation of characters.
A standard multivariate principal components (PCs) method was utilized to identify clusters of variables that may be controlled by a common gene or genes (pleiotropy).
While it has been shown that the PC approach has greater power to detect major pleiotropic genes [10], the power to detect genes with small effects is likely to be limited.
In addition, our investigation was highly dependent on the extent of pleiotropy modeled in the simulated data set as well as our selection of variables for analysis.