Relevant bibliographies by topics / Genetic architecture

Academic literature on the topic 'Genetic architecture'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Genetic architecture"

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Bhandare, Ashray, and Devinder Kaur. "Designing Convolutional Neural Network Architecture Using Genetic Algorithms." International Journal of Advanced Network, Monitoring and Controls 6, no. 3 (January 1, 2021): 26–35. http://dx.doi.org/10.21307/ijanmc-2021-024.

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Abstract In this paper, genetic algorithm (GA) is used to optimally determine the architecture of a convolutional neural network (CNN) that is used to classify handwritten numbers. The CNN is a class of deep feed-forward network, which have seen major success in the field of visual image analysis. During training, a good CNN architecture is capable of extracting complex features from the given training data; however, at present, there is no standard way to determine the architecture of a CNN. Domain knowledge and human expertise are required in order to design a CNN architecture. Typically architectures, The GA determine the exact architecture of a CNN by evolving the various hyper parameters of the architecture for a given application. The proposed method was tested on the MNIST dataset. The results show that the genetic algorithm is capable of generating successful CNN architectures. The proposed method performs the entire process of architecture generation without any human intervention.
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Nivethitha, V., and P. M Abhinaya. "Combinatorics based problem specific software architecture formulation using multi-objective genetic algorithm." International Journal of Engineering & Technology 7, no. 1.7 (February 5, 2018): 79. http://dx.doi.org/10.14419/ijet.v7i1.7.9579.

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In Software Development Process, the design of complex systems is an important phase where software architects have to deal with abstract artefacts, procedures and ideas to discover the most suitable underlying architecture. Due to uncontrolled modifications of the design and frequent change of requirements, many of the working systems do not have a proper architecture. Most of the approaches recover the architectural blocks at the end of the development process which are not appropriate to the system considered. In order to structure these systems software components compositions and interactions should be properly adjusted which is a tedious work. Search-based Software Engineering (SBSE) is an emerging area which can support the decision making process of formulating the software architecture from initial analysis models. Thus component-based architectures is articulated as a multiple optimisation problem using evolutionary algorithms. Totally different metrics is applied looking on the design needs and also the specific domain. Thus during this analysis work, an effort has been created to propose a multi objective evolutionary approach for the invention of the underlying software system architectures beside a versatile encoding structure, correct style metrics for the fitness operate to enhance the standard and accuracy of the software system design.
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LICHTERMANN, DIRK, JESPER EKELUND, LEENA PELTONEN, and MARJO-RIITTA JÄRVELIN. "Genetic Architecture of Temperament." American Journal of Psychiatry 158, no. 8 (August 2001): 1339. http://dx.doi.org/10.1176/appi.ajp.158.8.1339.

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Moreno, G. "Genetic Architecture, Genetic Behavior, and Character Evolution." Annual Review of Ecology and Systematics 25, no. 1 (November 1994): 31–44. http://dx.doi.org/10.1146/annurev.es.25.110194.000335.

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Agibalov, Oleg, and Nikolay Ventsov. "On the issue of fuzzy timing estimations of the algorithms running at GPU and CPU architectures." E3S Web of Conferences 135 (2019): 01082. http://dx.doi.org/10.1051/e3sconf/201913501082.

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We consider the task of comparing fuzzy estimates of the execution parameters of genetic algorithms implemented at GPU (graphics processing unit’ GPU) and CPU (central processing unit) architectures. Fuzzy estimates are calculated based on the averaged dependencies of the genetic algorithms running time at GPU and CPU architectures from the number of individuals in the populations processed by the algorithm. The analysis of the averaged dependences of the genetic algorithms running time at GPU and CPU-architectures showed that it is possible to process 10’000 chromosomes at GPU-architecture or 5’000 chromosomes at CPUarchitecture by genetic algorithm in approximately 2’500 ms. The following is correct for the cases under consideration: “Genetic algorithms (GA) are performed in approximately 2, 500 ms (on average), ” and a sections of fuzzy sets, with a = 0.5, correspond to the intervals [2, 000.2399] for GA performed at the GPU-architecture, and [1, 400.1799] for GA performed at the CPU-architecture. Thereby, it can be said that in this case, the actual execution time of the algorithm at the GPU architecture deviates in a lesser extent from the average value than at the CPU.
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Rajon, Etienne, and Joshua B. Plotkin. "The evolution of genetic architectures underlying quantitative traits." Proceedings of the Royal Society B: Biological Sciences 280, no. 1769 (October 22, 2013): 20131552. http://dx.doi.org/10.1098/rspb.2013.1552.

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In the classic view introduced by R. A. Fisher, a quantitative trait is encoded by many loci with small, additive effects. Recent advances in quantitative trait loci mapping have begun to elucidate the genetic architectures underlying vast numbers of phenotypes across diverse taxa, producing observations that sometimes contrast with Fisher's blueprint. Despite these considerable empirical efforts to map the genetic determinants of traits, it remains poorly understood how the genetic architecture of a trait should evolve, or how it depends on the selection pressures on the trait. Here, we develop a simple, population-genetic model for the evolution of genetic architectures. Our model predicts that traits under moderate selection should be encoded by many loci with highly variable effects, whereas traits under either weak or strong selection should be encoded by relatively few loci. We compare these theoretical predictions with qualitative trends in the genetics of human traits, and with systematic data on the genetics of gene expression levels in yeast. Our analysis provides an evolutionary explanation for broad empirical patterns in the genetic basis for traits, and it introduces a single framework that unifies the diversity of observed genetic architectures, ranging from Mendelian to Fisherian.
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Lam, Max, Chia-Yen Chen, Tian Ge, Hailiang Huang, Heiko Runz, and Todd Lencz. "Dissecting the Genetic Architecture of Psychopathology With Cognitive Genetics." Biological Psychiatry 89, no. 9 (May 2021): S44—S45. http://dx.doi.org/10.1016/j.biopsych.2021.02.128.

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ZENG, ZHAO-BANG, CHEN-HUNG KAO, and CHRISTOPHER J. BASTEN. "Estimating the genetic architecture of quantitative traits." Genetical Research 74, no. 3 (December 1999): 279–89. http://dx.doi.org/10.1017/s0016672399004255.

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Understanding and estimating the structure and parameters associated with the genetic architecture of quantitative traits is a major research focus in quantitative genetics. With the availability of a well-saturated genetic map of molecular markers, it is possible to identify a major part of the structure of the genetic architecture of quantitative traits and to estimate the associated parameters. Multiple interval mapping, which was recently proposed for simultaneously mapping multiple quantitative trait loci (QTL), is well suited to the identification and estimation of the genetic architecture parameters, including the number, genomic positions, effects and interactions of significant QTL and their contribution to the genetic variance. With multiple traits and multiple environments involved in a QTL mapping experiment, pleiotropic effects and QTL by environment interactions can also be estimated. We review the method and discuss issues associated with multiple interval mapping, such as likelihood analysis, model selection, stopping rules and parameter estimation. The potential power and advantages of the method for mapping multiple QTL and estimating the genetic architecture are discussed. We also point out potential problems and difficulties in resolving the details of the genetic architecture as well as other areas that require further investigation. One application of the analysis is to improve genome-wide marker-assisted selection, particularly when the information about epistasis is used for selection with mating.
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Latifi, Mohammad, Mohammad Javad Mahdavinezhad, and Darab Diba. "UNDERSTANDING GENETIC ALGORITHMS IN ARCHITECTURE." TURKISH ONLINE JOURNAL OF DESIGN, ART AND COMMUNICATION 6, AGSE (August 10, 2016): 1385–400. http://dx.doi.org/10.7456/1060agse/023.

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Pierce, Khadija Robin. "Comparative Architecture of Genetic Privacy." Indiana International & Comparative Law Review 19, no. 1 (January 1, 2009): 89–128. http://dx.doi.org/10.18060/17600.

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Dissertations / Theses on the topic "Genetic architecture"

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Griffin, Robert. "The genetic architecture of sexual dimorphism." Doctoral thesis, Uppsala universitet, Evolutionsbiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-258986.

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Phenotypic differences between the sexes evolve largely because selection favours a different complement of traits in either sex. Theory suggests that, despite its frequency, sexual dimorphism should be generally constrained from evolving because the sexes share much of their genome. While selection can lead to adaptation in one sex, correlated responses to selection can be maladaptive in the other. In this thesis I use Drosophila to examine the extent to which the shared genome constrains the evolution of sexual dimorphism and whether the sex chromosomes might play a special role in resolving intralocus sexual conflict. Gene expression data shows that intersexual genetic correlations are generally high, suggesting that genes often affect both sexes. The intersexual genetic correlation is negatively associated with sex-bias in expression in D. melanogaster, and the rate of change in sex-bias between D. melanogaster and six closely related species, showing that a sex-specific genetic architecture is a prerequisite for the evolution of sex difference. In further studies I find that genetic variance affecting lifespan is found in the male-limited Y chromosome within a population, which could offer a route to the evolution of further sexual dimorphism in lifespan, though the amount of variance was small suggesting adaptive potential from standing genetic variance is limited. Genetic variance on the X chromosome is also expected to be depleted once the sex chromosomes evolve, but here I find no evidence of depletion in either sex. Dosage compensation does not appear to double the male X-linked genetic variance, but this effect may be complex to detect. Finally, the X chromosome appears to be enriched for sex-specific genetic variance, and the consequences of this are explored using a variety of analytical methods to test biologically meaningful aspects of G-matrix structure. In summary, this thesis suggests that the evolution of sexual dimorphism is generally constrained by the shared genome, but intralocus sexual conflict could be resolved by novel mutations on the Y chromosomes, and by standing sex-specific genetic variance on the X chromosome. It highlights a special role for the X chromosome in the evolution of sexual dimorphism.
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Futema, M. "The genetic architecture of familial hypercholesterolaemia." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1417767/.

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Familial Hypercholesterolaemia (FH) is a common autosomal dominant disorder of the defective plasma clearance of LDL-cholesterol. Mutations in three genes, LDLR/APOB/PCSK9, can be detected in 60-90% of definite FH patients. DNA-based testing for FH mutations has important clinical utility and is recommended by the UK and European guidelines to identify affected relatives. This thesis aimed to determine the frequency and spectrum of FH mutations in two independent cohorts of FH patients (from one Oxford lipid clinic, and of Indian background). The FH mutation spectrum was shown to be highly heterogeneous and the mutation detection rate was significantly dependent on the pre-treatment total cholesterol and triglyceride levels. This project also validated the findings that a proportion of clinically diagnosed FH patients have a polygenic cause of hypercholesterolaemia due to an accumulation of common mild LDL-C-raising alleles by analysing LDL-C gene score in 88 mutation negative and 21 mutation positive FH patients, and by replicating the results in further 231 FH patients. A high-throughput DNA sequencing method was assessed as a novel diagnostic tool for detection of FH mutations, and compared it with the currently used methods. This highlighted the need for updating the current FH mutation screening methods as well as the need for more efficient bioinformatics for the next generation sequencing data analysis. Lastly, whole exome sequencing of 125 definite FH patients with no mutations detected in known genes was performed to identify novel monogenic causes of FH. Variants in two genes, CH25H and INSIG2, were identified as potential novel FH mutations. Overall, the results of this thesis demonstrate the heterogeneous FH aetiology and help to understand the genetic architecture of the disease.
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Agarwala, Vineeta. "Integrating empirical data and population genetic simulations to study the genetic architecture of type 2 diabetes." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11120.

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Most common diseases have substantial heritable components but are characterized by complex inheritance patterns implicating numerous genetic and environmental factors. A longstanding goal of human genetics research is to delineate the genetic architecture of these traits - the number, frequencies, and effect sizes of disease-causing alleles - to inform mapping studies, elucidate mechanisms of disease, and guide development of targeted clinical therapies and diagnostics. Although vast empirical genetic data has now been collected for common diseases, different and contradictory hypotheses have been advocated about features of genetic architecture (e.g., the contribution of rare vs. common variants). Here, we present a framework which combines multiple empirical datasets and simulation studies to enable systematic testing of hypotheses about both global and locus-specific complex trait architecture. We apply this to type 2 diabetes (T2D).
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Jain, Mahim. "Unraveling the genetic architecture of human traits." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509963.

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Reid, Robert Alan. "Genetic engineering of plant architecture in wheat." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29843.

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Particle bombardment of immature scutella was used to generate multiple lines of transgenic wheat with either PHY A, PHYB or PHYC from Arabidopsis or PHY A from oat.;Responses of segregating transgenic seedlings to cFR light were used as a screen for biologically active lines. The 'short coleoptile' phenotype under cFR was shown to segregate with the oat PHYA transgene and rtPCR detection of transcript. All of the transgenic lines containing the Arabidopsis PHYA and several oat PHYA lines demonstrated phenotypes indistinct to wild-type, possibly demonstrating transcriptional silencing.;Biologically active lines with Mendelian segregation ratios of 3:1 were selected for further analysis and homozygous individuals for each identified by PCR. Southern analysis of selected lines demonstrated that all originated from a distinct transformation event and harboured at least a single intact copy of the transgene. The complexity of gene integration was related to observed gene dosage and silencing effects.;Adult transgenic plants under white light with high R:FR ratio, demonstrated an increased chlorophyll content, a reduced production of superfluous tillers, a reduction in sensitivity to shortened day-length and an increased developmental rate leading to a reduction in days to heading.;The transgenic lines demonstrated an altered response to shade. In addition to the phenotypes observed under white light, plant height was significantly reduced and harvest index increased compared to the nulls, these responses were distinct to the those observed under white light and suggest an altered response to reduced R:FR.;The results suggest that oat PHYA is biologically active in transgenic wheat and that over-expressing PHYA alters the responses of etiolated seedlings to cFR, the light grown morphology and development of adult plants, and the responses of the plants to shade.
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Merrill, Richard. "Genetic architecture and ecological speciation in Heliconius butterflies." Thesis, University of Cambridge, 2013. https://www.repository.cam.ac.uk/handle/1810/244602.

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It is now widely accepted that adaptation to different ecological niches can result in the evolution of new species. However, when gene flow persists speciation must overcome the antagonism between selection and recombination: Specifically, if gene flow persists, recombination will break down the genetic associations between alleles that characterise emerging species and cause reproductive isolation. Accordingly, genetic architectures that impede recombination can slow the breakdown of linkage disequilibrium and facilitate speciation. Mimicry in tropical butterflies has long been championed as an example of adaptation driving speciation. In the Neotropical genus Heliconius, distantly related pairs of unpalatable species often converge on the same bright warning-pattern to more efficiently advertise their distastefulness to predators. In contrast, closely related taxa often belong to different mimicry rings. The sister species, Heliconius melpomene and H. cydno are sympatric across much of Central and northern South America. Using artificial butterflies I reveal selection against non-mimetic hybrid colour patterns between these two species. These colour patterns are also used as mating cues and mimetic shifts may cause both pre-mating and post-mating isolation. However, shifts in colour pattern cannot drive reproductive isolation alone; rather, they must be accompanied by corresponding mate preferences. Associations between trait and preference loci may be broken down by mating and subsequent recombination. I demonstrate a genetic linkage between loci for both male and female mate preference and wing colour pattern in Heliconius cydno and H. melpomene. In addition, I present evidence for further associations between alleles affecting hybrid sterility and host-plant use and colour pattern loci. All this implies that linkage between traits that contribute to reproductive and ecological isolation is a general phenomenon in Heliconius with an underlying adaptive basis. Overall these results expose a genetic mechanism that, by impeding recombination, can facilitate speciation in the face of gene flow.
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Dolgin, Elie. "The effects of breeding systems on genetic architecture." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/2487.

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Differences in reproductive strategies are a major factor influencing the patterns of genetic variability. Inbreeding and other non-recombining breeding systems can have profound effects on the efficacy of natural selection, which should be manifested in the patterns of genetic diversity within and between species. The impact of an organism’s breeding system can be investigated through a number of approaches. In this thesis, I use mathematical modelling, computer simulations, breeding schemes, quantitative life history measures, and molecular biological techniques to explore many of the consequences of breeding system evolution. Following a general introduction in Chapter 1, I explore the dynamics of transposable elements (TEs)—selfish mobile sequences of DNA that have deleterious effects upon their hosts. Sexual reproduction and recombination are important for constraining TE abundance, and in the absence of sex, an unchecked proliferation of TEs may cause a population to go extinct. In Chapter 2, I use a theoretical framework to analyze TE dynamics under asexual reproduction. Here, I show that while small populations are driven to extinction by element accumulation, large asexual populations can prevent this fate and be cured of vertically transmitted TEs. These results may help explain an "evolutionary scandal": the persistence of ancient asexual lineages, such as the bdelloid rotifers. In Chapter 3, I extend the computer simulations used in the previous chapter to explore the effects of reduced recombination on the distribution and abundance of TEs in sexual populations. I show that TEs become fixed as a result of Hill-Robertson effects in the form of Muller’s ratchet, but only in regions of extremely low recombination when excision is effectively absent and synergism between elements is weak. These results should help explain genomic patterns of TE distributions. In the remainder of the thesis, I turn to testing the genetic effects of androdioecy—the breeding system in which populations are comprised of separate male and hermaphrodite individuals—using the nematode Caenorhabditis elegans and related species. This unusual breeding system promotes high levels of inbreeding, yet males are maintained at appreciable frequencies. In Chapter 4, I measure lifehistory traits in the progeny of inbred versus outcrossed C. elegans and the related outcrossing species, C. remanei, to compare levels of inbreeding depression. I show that highly inbred C. remanei show dramatic reductions in brood size and relative fitness compared to outcrossed individuals, whereas pure strains of C. elegans performed better than crosses between strains, indicating outbreeding depression. The results are discussed in relation to the evolution of androdioecy and the effect of mating system on the level of inbreeding depression. Like C. elegans, C. briggsae reproduces by self-fertile hermaphrodites, and both species have similarly low levels of molecular diversity. But the global sampling of natural populations has been limited and geographically biased. In Chapter 5, I describe the first cultured isolates of C. elegans and C. briggsae from sub-Saharan Africa, characterize these samples for patterns of nucleotide polymorphism and vulva precursor cell lineage variation, and conduct a series of hybrid crosses in C. briggsae to test for genetic incompatibilities. With the new African isolates, I show distinct differences in levels of genetic and phenotypic diversity between the two species. Despite many similarities between C. elegans and C. briggsae, the results indicate that there may be more subtle, and previously unknown, differences in their natural histories. Finally, I return to the question of the impact of reduced recombination on TE dynamics in Chapter 6, by comparing population frequencies of TEs in natural populations of selfing and outcrossing Caenorhabditis species. I show that in the selfing species, C. elegans, transposons are less polymorphic and segregate at higher frequencies compared with the outcrossing species, C. remanei. Estimates of the intensity of selection based on the population frequencies of polymorphic elements suggest that transposons are selectively neutral in C. elegans, but subject to weak purifying selection in C. remanei. These results are consistent with a reduced efficacy of natural selection against transposable elements in selfing populations.
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So, Hon-cheong, and 蘇漢昌. "Genetic architecture and risk prediction of complex diseases." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4452805X.

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Wells, Rachel. "Genetic control of canopy architecture in Brassica napus." Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439928.

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Liu, Jimmy Zhenli. "The genetic architecture of immune-mediated complex diseases." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708737.

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Books on the topic "Genetic architecture"

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Bulayeva, Kazima, Oleg Bulayev, and Stephen Glatt. Genomic Architecture of Schizophrenia Across Diverse Genetic Isolates. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31964-3.

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Berkeley, Yvonne Patricia. The genetic architecture of sexual behaviour, including the Coolidge effect, in the laboratory rat. Birmingham: University of Birmingham, 1986.

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Renwick, Pamela Jean. Inter-individual variation in the molecular genetic architecture of the hypoxanthine phosphoribosyltransferase encoding region of man. Birmingham: University of Birmingham, 1996.

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Lynch, Michael. The origins of genome architecture. Sunderland, MA: Sinauer Associates, 2007.

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Frame and generic space. Rotterdam: 010 Publishers, 2006.

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The origins of genome architecture. Sunderland, Mass: Sinauer Associates, 2007.

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N, Turnbull Colin G., ed. Plant architecture and its manipulation. Oxford: Blackwell Publishing, 2005.

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Powell, David, ed. Delta-4: A Generic Architecture for Dependable Distributed Computing. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84696-0.

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Powell, David. Delta-4: A Generic Architecture for Dependable Distributed Computing. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991.

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1951-, Powell David, ed. A Generic fault-tolerant architecture for real-time dependable systems. Boston: Kluwer Academic Publishers, 2001.

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Book chapters on the topic "Genetic architecture"

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Gondro, Cedric. "Populations and Genetic Architecture." In Use R!, 105–61. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14475-7_4.

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Arking, Robert. "The Genetic Architecture of Longevity." In Life-Span Extension, 59–73. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-507-1_4.

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Nedjah, Nadia, and Luiza de Macedo Mourelle. "Hardware Architecture for Genetic Algorithms." In Innovations in Applied Artificial Intelligence, 554–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11504894_76.

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Bachmanov, Alexander A. "Genetic Architecture of Sweet Taste." In Sweetness and Sweeteners, 18–47. Washington, DC: American Chemical Society, 2008. http://dx.doi.org/10.1021/bk-2008-0979.ch002.

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Räihä, Outi, Kai Koskimies, and Erkki Mäkinen. "Genetic Synthesis of Software Architecture." In Lecture Notes in Computer Science, 565–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-89694-4_57.

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Martins, Tiago, and Rui Neves. "Architecture." In Stock Exchange Trading Using Grid Pattern Optimized by A Genetic Algorithm with Speciation, 25–42. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-76680-1_3.

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Sing, Charles F., Martha B. Haviland, and Sharon L. Reilly. "Genetic Architecture of Common Multifactorial Diseases." In Ciba Foundation Symposium 197 - Variation in the Human Genome, 211–32. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514887.ch12.

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Wise, Carol A. "The Genetic Architecture of Idiopathic Scoliosis." In Molecular Genetics of Pediatric Orthopaedic Disorders, 71–89. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2169-0_5.

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Mitchell, Kevin J. "The Genetic Architecture of Neurodevelopmental Disorders." In The Genetics of Neurodevelopmental Disorders, 1–28. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118524947.ch1.

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Prasad, Rashmi B., and Leif Groop. "Genetic Architecture of Type 2 Diabetes." In Textbook of Diabetes, 187–204. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924853.ch14.

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Conference papers on the topic "Genetic architecture"

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Lu, Zhichao, Ian Whalen, Yashesh Dhebar, Kalyanmoy Deb, Erik Goodman, Wolfgang Banzhaf, and Vishnu Naresh Boddeti. "NSGA-Net: Neural Architecture Search using Multi-Objective Genetic Algorithm (Extended Abstract)." In Twenty-Ninth International Joint Conference on Artificial Intelligence and Seventeenth Pacific Rim International Conference on Artificial Intelligence {IJCAI-PRICAI-20}. California: International Joint Conferences on Artificial Intelligence Organization, 2020. http://dx.doi.org/10.24963/ijcai.2020/659.

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Convolutional neural networks (CNNs) are the backbones of deep learning paradigms for numerous vision tasks. Early advancements in CNN architectures are primarily driven by human expertise and elaborate design. Recently, neural architecture search (NAS) was proposed with the aim of automating the network design process and generating task-dependent architectures. This paper introduces NSGA-Net -- an evolutionary search algorithm that explores a space of potential neural network architectures in three steps, namely, a population initialization step that is based on prior-knowledge from hand-crafted architectures, an exploration step comprising crossover and mutation of architectures, and finally an exploitation step that utilizes the hidden useful knowledge stored in the entire history of evaluated neural architectures in the form of a Bayesian Network. The integration of these components allows an efficient design of architectures that are competitive and in many cases outperform both manually and automatically designed architectures on CIFAR-10 classification task. The flexibility provided from simultaneously obtaining multiple architecture choices for different compute requirements further differentiates our approach from other methods in the literature.
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Frénoy, Antonine, François Taddei, and Dusan Misevic. "Constrained Genetic Architecture Promotes Cooperation." In Artificial Life 14: International Conference on the Synthesis and Simulation of Living Systems. The MIT Press, 2014. http://dx.doi.org/10.7551/978-0-262-32621-6-ch004.

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Lomurno, Eugenio, Stefano Samele, Matteo Matteucci, and Danilo Ardagna. "Pareto-optimal progressive neural architecture search." In GECCO '21: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3449726.3463146.

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Sinha, Nilotpal, and Kuan-Wen Chen. "Neural architecture search using progressive evolution." In GECCO '22: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3512290.3528707.

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Sinha, Nilotpal, and Kuan-Wen Chen. "Novelty driven evolutionary neural architecture search." In GECCO '22: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3520304.3528889.

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Nebro, Antonio J., Cristóbal Barba-González, José García Nieto, José A. Cordero, and José F. Aldana Montes. "Design and architecture of the jMetaISP framework." In GECCO '17: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3067695.3082466.

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Liang, Jason, Elliot Meyerson, and Risto Miikkulainen. "Evolutionary architecture search for deep multitask networks." In GECCO '18: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3205455.3205489.

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Sinha, Nilotpal, and Kuan-Wen Chen. "Evolving neural architecture using one shot model." In GECCO '21: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3449639.3459275.

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Feng, Ben, Dayiheng Liu, and Yanan Sun. "Evolving transformer architecture for neural machine translation." In GECCO '21: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3449726.3459441.

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Lopes, Vasco, Miguel Santos, Bruno Degardin, and Luís A. Alexandre. "Efficient guided evolution for neural architecture search." In GECCO '22: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3520304.3528936.

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Reports on the topic "Genetic architecture"

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Eshel, Amram, Jonathan P. Lynch, and Kathleen M. Brown. Physiological Regulation of Root System Architecture: The Role of Ethylene and Phosphorus. United States Department of Agriculture, December 2001. http://dx.doi.org/10.32747/2001.7585195.bard.

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Specific Objectives and Related Results: 1) Determine the effect of phosphorus availability on ethylene production by roots. Test the hypothesis that phosphorus availability regulates ethylene production Clear differences were found between the two plants that were studied. In beans ethylene production is affected by P nutrition, tissue type, and stage of development. There are genotypic differences in the rate of ethylene production by various root types and in the differential in ethylene production when P treatments are compared. The acceleration in ethylene production with P deficiency increases with time. These findings support the hypothesis that ethylene production may be enhanced by phosphorus deficiency, and that the degree of enhancement varies with genotype. In tomatoes the low-P level did not enhance significantly ethylene production by the roots. Wildtype cultivars and ethylene insensitive mutants behaved similarly in that respect. 2) Characterize the effects of phosphorus availability and ethylene on the architecture of whole root systems. Test the hypothesis that both ethylene and low phosphorus availability modify root architecture. In common bean, the basal roots give rise to a major fraction of the whole root system. Unlike other laterals these roots respond to gravitropic stimulation. Their growth angle determines the proportion of the root length in the shallow layers of the soil. A correlation between ethylene production and basal root angle was found in shallow rooted but not deep-rooted genotypes, indicating that acceleration of ethylene synthesis may account for the change in basal root angle in genotypes demonstrating a plastic response to P availability. Short-time gravitropic response of the tap roots of young bean seedlings was not affected by P level in the nutrient solution. Low phosphorus specifically increases root hair length and root hair density in Arabidopsis. We tested 7 different mutants in ethylene perception and response and in each case, the response to low P was lower than that of the wild-type. The extent of reduction in P response varied among the mutants, but every mutant retained some responsiveness to changes in P concentration. The increase in root hair density was due to the increase in the number of trichoblast cell files under low P and was not mediated by ethylene. Low P did not increase the number of root hairs forming from atrichoblasts. This is in contrast to ethylene treatment, which increased the number of root hairs partly by causing root hairs to form on atrichoblasts. 3) Assess the adaptive value of root architectural plasticity in response to phosphorus availability. A simulation study indicated that genetic variation for root architecture in common bean may be related to adaptation to diverse competitive environments. The fractal dimension of tomato root system was directly correlated with P level.
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de, C., G. Gross, L. Gommans, J. Vollbrecht, and D. Spence. Generic AAA Architecture. RFC Editor, August 2000. http://dx.doi.org/10.17487/rfc2903.

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Quanrud, Richard B. Generic Architecture Study. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada227075.

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Guiltinan, Mark J., and Donald Thompson. Molecular Genetic Analysis of Maize Starch Branching Isoforms: Modulation of Starch Branching Enzyme Isoform Activities in Maize to Produce Starch with Novel Branching Architecture and Properties. Office of Scientific and Technical Information (OSTI), July 2009. http://dx.doi.org/10.2172/961611.

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Eshed-Williams, Leor, and Daniel Zilberman. Genetic and cellular networks regulating cell fate at the shoot apical meristem. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699862.bard.

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The shoot apical meristem establishes plant architecture by continuously producing new lateral organs such as leaves, axillary meristems and flowers throughout the plant life cycle. This unique capacity is achieved by a group of self-renewing pluripotent stem cells that give rise to founder cells, which can differentiate into multiple cell and tissue types in response to environmental and developmental cues. Cell fate specification at the shoot apical meristem is programmed primarily by transcription factors acting in a complex gene regulatory network. In this project we proposed to provide significant understanding of meristem maintenance and cell fate specification by studying four transcription factors acting at the meristem. Our original aim was to identify the direct target genes of WUS, STM, KNAT6 and CNA transcription factor in a genome wide scale and the manner by which they regulate their targets. Our goal was to integrate this data into a regulatory model of cell fate specification in the SAM and to identify key genes within the model for further study. We have generated transgenic plants carrying the four TF with two different tags and preformed chromatin Immunoprecipitation (ChIP) assay to identify the TF direct target genes. Due to unforeseen obstacles we have been delayed in achieving this aim but hope to accomplish it soon. Using the GR inducible system, genetic approach and transcriptome analysis [mRNA-seq] we provided a new look at meristem activity and its regulation of morphogenesis and phyllotaxy and propose a coherent framework for the role of many factors acting in meristem development and maintenance. We provided evidence for 3 different mechanisms for the regulation of WUS expression, DNA methylation, a second receptor pathway - the ERECTA receptor and the CNA TF that negatively regulates WUS expression in its own domain, the Organizing Center. We found that once the WUS expression level surpasses a certain threshold it alters cell identity at the periphery of the inflorescence meristem from floral meristem to carpel fate [FM]. When WUS expression highly elevated in the FM, the meristem turn into indeterminate. We showed that WUS activate cytokinine, inhibit auxin response and represses the genes required for root identity fate and that gradual increase in WUCHEL activity leads to gradual meristem enlargement that affect phyllotaxis. We also propose a model in which the direction of WUS domain expansion laterally or upward affects meristem structure differently. We preformed mRNA-seq on meristems with different size and structure followed by k-means clustering and identified groups of genes that are expressed in specific domains at the meristem. We will integrate this data with the ChIP-seq of the 4 TF to add another layer to the genetic network regulating meristem activity.
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Rothganger, Fredrick, and Arun Rodrigues. Generic Spiking Architecture (GenSA). Office of Scientific and Technical Information (OSTI), September 2020. http://dx.doi.org/10.2172/1673456.

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Booker, C. P. Generic Distributed Simulation Architecture. Office of Scientific and Technical Information (OSTI), May 1999. http://dx.doi.org/10.2172/759129.

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Joel, Daniel M., Steven J. Knapp, and Yaakov Tadmor. Genomic Approaches for Understanding Virulence and Resistance in the Sunflower-Orobanche Host-Parasite Interaction. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7592655.bard.

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Oroginal Objectives: (i) identify DNA markers linked to the avirulence (Avr) locus and locate the Avr locus through genetic mapping with an inter-race Orobanche cumana population; (ii) develop high-throughput fingerprint DNA markers for genotypingO. cumana races; (iii) identify nucleotide binding domain leucine rich repeat (NB-LRR) genes encoding R proteins conferring resistance to O. cumana in sunflower; (iv) increase the resolution of the chromosomal segment harboring Or₅ and related R genes through genetic and physical mapping in previously and newly developed mapping populations of sunflower; and (v) develop high-throughput DNA markers for rapidly and efficiently identifying and transferring sunflower R genes through marker-assisted selection. Revisions made during the course of project: Following changes in O. cumana race distribution in Israel, the newly arrived virulent race H was chosen for further analysis. HA412-HO, which was primarily chosen as a susceptible sunflower cultivar, was more resistant to the new parasite populations than var. Shemesh, thus we shifted sunflower research into analyzing the resistance of HA412-HO. We exceeded the deliverables for Objectives #3-5 by securing funding for complete physical and high-density genetic mapping of the sunflower genome, in addition to producing a complete draft sequence of the sunflower genome. We discovered limited diversity between the parents of the O. cumana population developed for the mapping study. Hence, the developed DNA marker resources were insufficient to support genetic map construction. This objective was beyond the scale and scope of the funding. This objective is challenging enough to be the entire focus of follow up studies. Background to the topic: O. cumana, an obligate parasitic weed, is one of the most economically important and damaging diseases of sunflower, causes significant yield losses in susceptible genotypes, and threatens production in Israel and many other countries. Breeding for resistance has been crucial for protecting sunflower from O. cumana, and problematic because new races of the pathogen continually emerge, necessitating discovery and deployment of new R genes. The process is challenging because of the uncertainty in identifying races in a genetically diverse parasite. Major conclusions, solutions, achievements: We developed a small collection of SSR markers for genetic mapping in O. cumana and completed a diversity study to lay the ground for objective #1. Because DNA sequencing and SNPgenotyping technology dramatically advanced during the course of the study, we recommend shifting future work to SNP discovery and mapping using array-based approaches, instead of SSR markers. We completed a pilot study using a 96-SNP array, but it was not large enough to support genetic mapping in O.cumana. The development of further SNPs was beyond the scope of the grant. However, the collection of SSR markers was ideal for genetic diversity analysis, which indicated that O. cumanapopulations in Israel considerably differ frompopulations in other Mediterranean countries. We supplied physical and genetic mapping resources for identifying R-genes in sunflower responsible for resistance to O. cumana. Several thousand mapped SNP markers and a complete draft of the sunflower genome sequence are powerful tools for identifying additional candidate genes and understanding the genomic architecture of O. cumana-resistanceanddisease-resistance genes. Implications: The OrobancheSSR markers have utility in sunflower breeding and genetics programs, as well as a tool for understanding the heterogeneity of races in the field and for geographically mapping of pathotypes.The segregating populations of both Orobanche and sunflower hybrids are now available for QTL analyses.
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Quanrud, Richard B. A Program Manager's Guide to Generic Architectures. Fort Belvoir, VA: Defense Technical Information Center, May 1989. http://dx.doi.org/10.21236/ada227074.

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Peterson, A. S., Jr Stanley, and Jay L. Mapping a Domain Model and Architecture to a Generic Design. Fort Belvoir, VA: Defense Technical Information Center, May 1994. http://dx.doi.org/10.21236/ada283747.

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