Relevant bibliographies by topics / Mendelian genetics

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mendelian genetics'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Mendelian genetics"

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Taylor Hilst. "Mendelian Genetics." American Biology Teacher 67, no. 7 (2005): 435–36. http://dx.doi.org/10.2307/4451879.

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Wright, Karen, and William Diehl-Jones. "An Introduction to Clinical Genetics." Neonatal Network 38, no. 5 (2019): 266–73. http://dx.doi.org/10.1891/0730-0832.38.5.266.

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Understanding the principles of basic genetics is the beginning of understanding more complex and advanced genetic studies, such as epigenetics. This article presents a review of the basic concepts of genetics, Mendelian and non-Mendelian patterns of inheritance, and basic genetic testing.
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de Koning, Dirk-Jan, Henk Bovenhuis, and Johan A. M. van Arendonk. "On the Detection of Imprinted Quantitative Trait Loci in Experimental Crosses of Outbred Species." Genetics 161, no. 2 (2002): 931–38. http://dx.doi.org/10.1093/genetics/161.2.931.

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Abstract In this article, the quantitative genetic aspects of imprinted genes and statistical properties of methods to detect imprinted QTL are studied. Different models to detect imprinted QTL and to distinguish between imprinted and Mendelian QTL were compared in a simulation study. Mendelian and imprinted QTL were simulated in an F2 design and analyzed under Mendelian and imprinting models. Mode of expression was evaluated against the H0 of a Mendelian QTL as well as the H0 of an imprinted QTL. It was shown that imprinted QTL might remain undetected when analyzing the genome with Mendelian models only. Compared to testing against a Mendelian QTL, using the H0 of an imprinted QTL gave a higher proportion of correctly identified imprinted QTL, but also gave a higher proportion of false inference of imprinting for Mendelian QTL. When QTL were segregating in the founder lines, spurious detection of imprinting became more prominent under both tests, especially for designs with a small number of F1 sires.
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Hernandez, Dena G., Xylena Reed, and Andrew B. Singleton. "Genetics in Parkinson disease: Mendelian versus non-Mendelian inheritance." Journal of Neurochemistry 139 (April 18, 2016): 59–74. http://dx.doi.org/10.1111/jnc.13593.

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Lee, Robert W., and Claude Lemieux. "BIPARENTAL INHERITANCE OF NON-MENDELIAN GENE MARKERS IN CHLAMYDOMONAS MOEWUSII." Genetics 113, no. 3 (1986): 589–600. http://dx.doi.org/10.1093/genetics/113.3.589.

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ABSTRACT The first two non-Mendelian gene mutations to be identified in Chlamydomonas moewusii are described. These putative chloroplast gene mutations include one for resistance to streptomycin (sr-nM1) and one for resistance to erythromycin (er-nM1). In one- and two-factor reciprocal crosses, usually over 90% of the germinating zygospores transmitted these mutations and their wild-type alternatives from both parents (biparental zygospores); the remaining zygospores transmitted exclusively the non-Mendelian markers of the mating-type "plus" parent. Among the biparental zygospores, a strong bias in the transmission of non-Mendelian alleles from the mating-type "plus" parent was indicated by an excess of meiotic and postmeiotic mitotic progeny that were homoplasmic for non-Mendelian alleles from this parent compared to those that were homoplasmic for the non-Mendelian alleles from the mating-type "minus" parent. At best, weak linkage was detected between the sr-nM1 and er-nM1 loci. Non-Mendelian, chloroplast gene markers in Chlamydomonas eugametos and Chlamydomonas reinhardtii showed a predominantly uniparental mode of transmission from the mating-type "plus" parent in crosses performed under the same conditions used for the C. moewusii crosses.
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Richards, Martin. "Lay and professional knowledge of genetics and inheritance." Public Understanding of Science 5, no. 3 (1996): 217–30. http://dx.doi.org/10.1088/0963-6625/5/3/003.

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Despite almost a century of educational effort, studies of both schoolchildren and adults show that the public understanding of Mendelian genetics is very limited. A similar conclusion is drawn from studies of those who have been offered explanations of inheritance in genetic counselling clinics. The aim of this paper is to provide an explanation of these observations. It is argued that Mendelian explanations of inheritance conflict in a number of ways with a lay knowledge of inheritance that is general in society. Furthermore, it is suggested that lay knowledge is grounded in concepts of kinship which are themselves sustained by everyday social practice and relationships, which may make the lay knowledge of inheritance particularly resistant to change. It is suggested that Mendelian explanations may not be easily assimilated because of the conflicts with pre-existing lay knowledge that an individual holds. Preliminary results are described from an empirical study which tests the hypothesis that ideas of genetic connectedness are derived from concepts of kin relationships. The evidence appears to confirm the hypothesis. Parallels are drawn between the history of the acceptance of Mendel's ideas in the scientific community and the assimilation (or the lack of it) of Mendelian explanations by the public. The paper concludes with a brief discussion of public education in Mendelian genetics in schools and genetic counselling clinics, and the ways in which it could be more effective.
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Coetzee, Gerhard A. "Understanding Non-Mendelian Genetic Risk." Current Genomics 20, no. 5 (2019): 322–24. http://dx.doi.org/10.2174/1389202920666191018085511.

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This opinion paper highlights strategies for a better understanding of non-Mendelian genetic risk that was revealed by genome-wide association studies (GWAS) of complex diseases. The genetic risk resides predominantly in non-coding regulatory DNA, such as in enhancers. The identification of mechanisms, the causal variants (mainly SNPs), and their target genes are, however, not always apparent but are likely involved in a network of risk determinants; the identification presents a bottle-neck in the full understanding of the genetics of complex phenotypes. Here, we propose strategies to identify functional SNPs and link risk enhancers with their target genes. The strategies are 1) identifying finemapped SNPs that break/form response elements within chromatin bio-features in relevant cell types 2) considering the nearest gene on linear DNA, 3) analyzing eQTLs, 4) mapping differential DNA methylation regions and relating them to gene expression, 5) employing genomic editing with CRISPR/cas9 and 6) identifying topological associated chromatin domains using chromatin conformation capture.
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Tommerup, N. "Mendelian cytogenetics. Chromosome rearrangements associated with mendelian disorders." Journal of Medical Genetics 30, no. 9 (1993): 713–27. http://dx.doi.org/10.1136/jmg.30.9.713.

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Hodes, M. E., and Stephen R. Dlouhy. "A Reintroduction to Mendelian Genetics." Cancer Investigation 15, no. 5 (1997): 429–34. http://dx.doi.org/10.3109/07357909709047582.

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Richards, Martin P. M. "Lay understanding of mendelian genetics." Endeavour 22, no. 3 (1998): 93–94. http://dx.doi.org/10.1016/s0160-9327(98)01125-9.

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Dissertations / Theses on the topic "Mendelian genetics"

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Hu, Xianghong. "Statistical methods for Mendelian randomization using GWAS summary data." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/639.

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Mendelian Randomization (MR) is a powerful tool for accessing causality of exposure on an outcome using genetic variants as the instrumental variables. Much of the recent developments is propelled by the increasing availability of GWAS summary data. However, the accuracy of the MR causal effect estimates could be challenged in case of the MR assumptions are violated. The source of biases could attribute to the weak effects arising because of polygenicity, the presentence of horizontal pleiotropy and other biases, e.g., selection bias. In this thesis, we proposed two works, expecting to deal with these issues.In the first part, we proposed a method named 'Bayesian Weighted Mendelian Randomization (BMWR)' for causal inference using summary statistics from GWAS. In BWMR, we not only take into account the uncertainty of weak effects owning to polygenicity of human genomics but also models the weak horizontal pleiotropic effects. Moreover, BWMR adopts a Bayesian reweighting strategy for detection of large pleiotropic outliers. An efficient algorithm based on variational inference was developed to make BWMR computationally efficient and stable. Considering the underestimated variance provided by variational inference, we further derived a closed form variance estimator inspired by a linear response method. We conducted several simulations to evaluate the performance of BWMR, demonstrating the advantage of BWMR over other methods. Then, we applied BWMR to access causality between 126 metabolites and 90 complex traits, revealing novel causal relationships. In the second part, we further developed BWMR-C: Statistical correction of selection bias for Mendelian Randomization based on a Bayesian weighted method. Based on the framework of BWMR, the probability model in BWMR-C is built conditional on the IV selection criteria. In such way, BWMR-C delicated to reduce the influence of the selection process on the causal effect estimates and also preserve the good properties of BWMR. To make the causal inference computationally stable and efficient, we developed a variational EM algorithm. We conducted several comprehensive simulations to evaluate the performance of BWMR-C for correction of selection bias. Then, we applied BWMR-C on seven body fat distribution related traits and 140 UK Biobank traits. Our results show that BWMR-C achieves satisfactory performance for correcting selection bias. Keywords: Mendelian Randomization, polygenicity, horizontal pleiotropy, selection bias, variation inference.
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Lalonde, Emilie. "The application of next-generation sequencing technologies: from Mendelian diseases to cancer." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104572.

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The field of medical informatics has been primarily driven by advances in technology. In recent years, “next-generation sequencing” (NGS) has emerged as an affordable and quick means for accurate, large-scale sequencing at a single-base resolution, generating many gigabases of data per sequencing run. As with all new technological innovations, considerable development and improvements of analysis software is required, specifically to accurately extract relevant information from these large datasets. In this thesis, we explore two applications of next-generation sequencing to human health: sequencing of all protein coding exons (i.e. exome sequencing) of patients with Fowler Syndrome, a rare, prenatally lethal Mendelian disease, and sequencing of mRNA (i.e. RNA-Seq) of breast cancer cell lines and tumors from BRCA1 germline mutation carriers. We focus on both the bioinformatics developments and the application to human health in a “simple” Mendelian disease and in a genetically complex cancer. Indeed, in both these studies, we aim to find genetic events which may improve patient care. The discovery of the gene causing Fowler Syndrome will lead to improved genetic counseling for affected families and may influence choices such as family planning or preventive measures (e.g. prenatal or preimplantation genetic diagnosis). Delineation of transcripts which unambiguously characterize or contribute to BRCA1-related breast cancers could lead to new biomarkers or therapeutic options. In the first study, we develop a bioinformatics pipeline capable of identifying Mendelian disease genes from exome sequencing data. These diseases are typically caused by a single mutation which affects the protein coding sequence; thus, exome sequencing can be used to detect all coding variants in an individual which are then filtered to identify the most likely causative mutation. The successful application of this pipeline is demonstrated in Fowler Syndrome. We found that mutations in the gene FLVCR2 are responsible for this recessive disease using only two affected individuals. Next, we use mRNA sequencing to identify alternative splice isoforms which may contribute to tumorigenesis in breast cancers caused by BRCA1 germline mutations. This subtype of breast cancer accounts for a large proportion of familial breast cancers and is associated with a poorer than expected prognosis. These breast cancers are characterized by several dysregulated cellular processes but the role of alternative splicing in tumorigenesis has not been investigated in BRCA1-related breast cancers. We find several highly recurrent splice junctions that are more abundant in BRCA1-related breast cancers than in controls but none which clearly contribute to breast cancer tumorigenesis. This study illustrates the heterogeneity of BRCA1-related breast cancers at the level of RNA splicing. In summary, in this thesis we show that NGS is an effective tool for global identification and analysis of genetic events in an individual and will thus enable the transition to personalized-medicine.<br>Le domaine d'informatique médicale avance primordialement grâce aux développements technologiques. Durant les années récentes, le « séquençage de nouvelle-génération » (SNG) a émergé comme un moyen abordable et rapide pour le séquençage à grande échelle. Cette technologie possède une grande précision, avec une résolution au niveau d'une seule base d'ADN, générant plusieurs gigabases d'information. Comme toutes innovations technologiques, des développements et améliorations des logiciels analytiques sont essentiels, en particulier pour extraire avec précision les informations pertinentes à partir de ces grands ensembles de données. Dans cette thèse, nous explorons deux applications de SNG à la santé humaine: le séquençage de tous les exons codant les protéines (i.e. séquençage d'exome) des patients avec le Syndrome Fowler, une maladie Mendélienne rare et létale, et le séquençage des ARNm (i.e. ARN-Seq) des lignées cellulaires et tumeurs des patients du cancer de sein portant une mutation germinale de BRCA1. Nous nous concentrons sur les développements bioinformatiques et les applications pour la santé humaine dans une maladie Mendélienne « simple » et dans un cancer génétiquement complexe. En effet, dans les deux études, nous essayons de trouver des événements génétiques qui pourraient améliorer le soin des patients. La découverte du gène qui cause le Syndrome Fowler rendra les conseils génétiques plus complets pour les familles atteintes par cette maladie et pourrait influencer les choix de planification familiale ou de mesure préventive (par exemple, le diagnostic génétique prénatal ou préimplantatoire). La découverte des isoformes qui caractérisent ou contribuent sans ambigüité au cancer de sein relié à BRCA1 pourrait mener à des nouveaux biomarqueurs et traitements. Dans la première étude, nous développons une approche bioinformatique capable d'identifier les gènes causant les maladies Mendéliennes à partir des données du séquençage d'exome. Ces maladies sont généralement causées par une seule mutation qui change la séquence des protéines; ainsi, le séquençage d'exome peut être utilisé pour identifier toutes les variations dans l'exome d'un individu qui sont ensuite filtrées pour trouver la mutation causative la plus probable. Nous démontrons notre succès avec l'application de cette approche dans le Syndrome Fowler. Nous avons trouvé que des mutations dans le gène FLVCR2 causent cette maladie récessive, en utilisant seulement deux individus. Ensuite, nous utilisons le séquençage des ARNm pour identifier des isoformes alternatifs qui pourraient contribuer à la tumorigenèse dans les cancers de sein causé par des mutations de BRCA1. Ce type de cancer de sein représente une grande proportion des cancers de sein familiale et est associé avec une prognose moins favorable. Ces cancers de sein sont caractérisés par des processus cellulaires dérégulés; pourtant, le rôle de l'épissage alternatif dans la tumorigène n'a jamais été exploré dans les cancers de sein relié à BRCA1. Nous trouvons plusieurs jonctions d'épissages très récurrents qui sont plus abondantes dans les cancers de sein relié à BRCA1, par rapport aux autres cancers de sein, mais aucune contribuant clairement à la tumorigène du cancer de sein. Cette étude démontre le hétérogénéité des cancers de relié à BRCA1au niveau de l'épissage alternatif. En bref, dans cette thèse nous montrons que le SNG est un outil effectif pour l'identification et l'analyse globale des événements génétiques dans un individu, permettant ainsi la transition vers la médicine personnalisée.
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Deans, Natalie Christine. "Molecular mechanisms that underlie non-Mendelian inheritance patterns in Zea mays." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu159541311114259.

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Assimes, Themistocles L., and Robert Roberts. "Genetics: Implications for Prevention and Management of Coronary Artery Disease." ELSEVIER SCIENCE INC, 2016. http://hdl.handle.net/10150/623131.

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An exciting new era has dawned for the prevention and management of CAD utilizing genetic risk variants. The recent identification of over 60 susceptibility loci for coronary artery disease (CAD) confirm not only the importance of established risk factors, but also the existence of many novel causal pathways that are expected to improve our understanding of the genetic basis of CAD and facilitate the development of new therapeutic agents over time. Concurrently, Mendelian randomization studies have provided intriguing insights on the causal relationship between CAD-related traits, and highlight the potential benefits of long-term modifications of risk factors. Lastly, genetic risk scores of CAD may serve not only as prognostic, but also as predictive markers and carry the potential to considerably improve the delivery of established prevention strategies. This review will summarize the evolution and discovery of genetic risk variants for CAD and their current and future clinical applications.
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Chen, Anlu. "Applying Forward Genetic Approaches to Rare Mendelian Disorders and Complex Traits." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1532522241487661.

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O'Neill, Eric Michael. "Evolutionary Consequences of the Introduction of Eleutherodactylus Coqui to Hawaii." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/305.

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The introduction of a species to areas outside its native range can result in ecological and genetic changes of evolutionary significance. The frog Eleutherodactylus coqui was introduced to Hawaii, from Puerto Rico, in the late 1980s and has lost genetic variation in mitochondrial DNA. The extent to which founder effects have influenced phenotypic variation in the introduced range is unknown. In this study I compared phenotypic variation in life-history traits, advertisement calls, and stripe patterns among introduced and native populations of the frog Eleutherodactylus coqui. I also conducted laboratory experiments to determine the influence of genetics and temperature on trait variation. Body size in wild populations was positively correlated with elevation in both ranges, but the slope of elevation on body size was greater in Puerto Rico than in Hawaii. Advertisement call frequencies and rates were negatively correlated with elevation but duration was positively correlated with elevation. Frequencies were correlated with body size, but rate, duration, and intensity were not. Color patterns are more variable in Puerto Rico than Hawaii and appear to be maintained by balancing selection in Puerto Rico. Lab results indicate that body size is negatively correlated with temperature, which may explain Bergmann's rule in the field, but patterns of intrinsic growth rate may explain differences in the effect of elevation between Hawaii and Puerto Rico. Body size appears to explain most of the variation in call frequencies, whereas temperature explained most of the variation in rate and duration. Color patterns appear to be determined by a single locus with five alleles. Founder effects appear to explain the difference between Hawaii and Puerto Rico in color pattern variation and in clinal variation in body size and call frequencies. The loss of genetic variation in these traits is likely to have evolutionary consequences for this species in Hawaii.
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Moore, John M. "Using human examples to teach Mendelian genetic concepts : assessing acquisition and retention." Virtual Press, 1989. http://liblink.bsu.edu/uhtbin/catkey/558371.

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This study was designed to investigate whether or not Mendelian genetics instruction using human examples, in contrast to traditional genetic examples, would facilitate the acquisition and retention of four genetic concepts: (1) complete dominance, (2) incomplete dominance, (3) law of segregation, and (4) law of independent assortment. A pre/post/delayed-posttest was designed to assess the acquisition and retention of the concepts and the formation of misconceptions of genetic concepts. A written Piagetian Task Instrument (PTI) was employed to detect cognitive growth toward the formal operational level of thought.Eighty ninth-grade biology students from Marion High School, Marion, Indiana were used in the study. The students were assigned randomly to two control and two treatment groups. Students in the control groups. were instructed in Mendelian genetics using traditional genetic examples to explain the concepts. Students in the treatment groups were instructed in Mendelian genetics using only human examples to explain the concepts.Students who were instructed in Mendelian genetics using human examples acquired and retained those concepts better and acquired fewer misconceptions than students who were instructed using traditional examples.Students who were instructed in Mendelian genetics using human examples did not differ from those instructed via traditional examples with respect to their movement from concrete operational toward formal operational thought.<br>Department of Biology
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Schilling, Taylor. "Non-Mendelian Inheritance in C. elegans: A Violation of The Law of Independent Assortment." Cleveland State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=csu1611776149127827.

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Lin, Michelle [Verfasser], and Jobst [Akademischer Betreuer] Meyer. "Genetics of common psychiatric disorders: A Mendelian perspective based on genetic analyses of large pedigrees / Michelle Lin ; Betreuer: Jobst Meyer." Trier : Universität Trier, 2012. http://d-nb.info/1197698183/34.

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Raykova, Doroteya. "Genetics of Two Mendelian Traits and Validation of Induced Pluripotent Stem Cell (iPSC) Technology for Disease Modeling." Doctoral thesis, Uppsala universitet, Medicinsk genetik och genomik, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-246228.

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Novel technologies for genome analysis have provided almost unlimited opportunities to uncover structural gene variants behind human disorders. Whole exome sequencing (WES) is especially useful for understanding rare Mendelian conditions, because it reduces the requirements for a priori clinical data, and can be applied on a small number of patients. However, supporting functional data on the effect of specific gene variants are often required to power these findings. A variety of methods and biological model systems exists for this purpose. Among those, induced pluripotent stem cells (iPSCs), which are capable of self-renewal and differentiation, stand out as an alternative to animal models. In papers I and II we took advantage of WES to identify gene variants underlying autosomal recessive pure hair and nail ectodermal dysplasia (AR PHNED) as well as autosomal dominant familial visceral myopathy (FVM). We identified a homozygous variant c.821T&gt;C (p.Phe274Ser) in the KRT74 gene as the causative mutation in AR PHNED, supported by the fact that Keratin-74 was undetectable in hair follicles of an affected family member. In a family segregating FVM we found a heterozygous tandem base substitution c.806_807delinsAA (p.(Gly269Glu)) in the ACTG2 gene in the affected members. This novel variant is associated with a broad range of visceral symptoms and a variable age of onset. In Paper III we explored the similarity between clonally derived iPSC lines originating from a single parental fibroblast line and we highlighted the necessity to use lines originating from various donors in disease modeling because of biological variation. Paper IV focused on how the genomic integrity of iPSCs is affected by the choice of reprogramming methods. We described several novel cytogenetic rearrangements in iPSCs and we identified a chromosome 5q duplication as a candidate aberration for growth advantage. In summary, this doctoral thesis brings novel findings on unreported disease-causing variants, as supported by extensive genetic analysis and functional data. A novel molecular mechanism behind AR PHNED is presented and the phenotypic spectrum associated with FVM is expanded. In addition, the thesis brings novel understanding of benefits and limitations of the iPSC technology to be considered for disease modeling.
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Books on the topic "Mendelian genetics"

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Clarke, G. M. Mendelian genetics. Centre for Statistical Education, 1986.

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Russell, Peter J. iGenetics: A Mendelian approach. Pearson/Benjamin Cummings, 2005.

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Ostrer, Harry. Non-mendelian genetics in humans. Oxford University Press, 1998.

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1933-, Millar P., Lauvergne J. J, and Dolling, C. H. S. 1925-, eds. Mendelian inheritance in cattle 2000. Wageningen Pers, 2000.

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Darden, Lindley. Theory change in science: Strategies from Mendelian genetics. Oxford University Press, 1991.

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Kim, Kyung-Man. Explaining scientific consensus: The case of Mendelian genetics. Guilford Press, 1994.

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Lane, Patrick. Tutoring Mendelian genetics: The simulation of genetic inheritance in an intelligent tutoring system. TheAuthor], 1996.

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Mendelian inheritance in man: A catalog of human genes and genetic disorders. Johns Hopkins University Press, 1994.

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McKusick, Victor A. Mendelian inheritance in man: A catalog of human genes and genetic disorders. Johns Hopkins University Press, 1998.

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A, Francomano Clair, and Antonarakis Stylianos E, eds. Mendelian inheritance in man: Catalogs of autosomal dominant, autosomal recessive, and X-linked phenotypes. Johns Hopkins University Press, 1992.

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Book chapters on the topic "Mendelian genetics"

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Patanella, Daniel. "Mendelian Genetics." In Encyclopedia of Child Behavior and Development. Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_1758.

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Francke, U. "Microdeletions and Mendelian Phenotypes." In Human Genetics. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_24.

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Xu, Shizhong. "Review of Mendelian Genetics." In Quantitative Genetics. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-83940-6_2.

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Stauffer, Sarah, Aaron Gardner, Wilko Duprez, Dewi Ayu Kencana Ungu, and Philip Wismer. "Mendelian Inheritance." In Labster Virtual Lab Experiments: Basic Genetics. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-57999-2_1.

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Kowles, Richard. "Non-Mendelian Inheritance." In Solving Problems in Genetics. Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4613-0205-6_10.

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Patwardhan, Dhruti. "Mendelian Principle of Inheritance." In Genetics Fundamentals Notes. Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-7041-1_2.

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Bradshaw, John E. "Mendelian Genetics and Linkage Maps." In Plant Breeding: Past, Present and Future. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23285-0_4.

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Lesage, Suzanne. "Genetics of Mendelian Forms of Parkinson’s Disease." In Movement Disorder Genetics. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17223-1_1.

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Lee, Keekok. "Biotic Artefacts: Mendelian Genetics and Hybridisation." In Philosophy and Revolutions in Genetics. Palgrave Macmillan UK, 2005. http://dx.doi.org/10.1057/9780230599024_4.

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Smith-Keary, Peter. "The transmission of genes I: Mendelian ratios in eucaryotes." In Molecular Genetics. Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-11732-1_4.

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Conference papers on the topic "Mendelian genetics"

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Rossi, Elena, and Gianfranco Santovito. "INTRODUCTION TO MENDELIAN GENETICS IN PRIMARY SCHOOL." In International Conference on Education and New Learning Technologies. IATED, 2016. http://dx.doi.org/10.21125/edulearn.2016.1274.

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Musa, A. A., and N. Reinsch. "220. Hedging genetic diversity using a similarity matrix based on Mendelian sampling." In World Congress on Genetics Applied to Livestock Production. Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_220.

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Bernstein, R., M. Du, A. Hoppe, and K. Bienefeld. "622. New approach to identify Mendelian inconsistencies between SNP and pedigree information in the honey bee." In World Congress on Genetics Applied to Livestock Production. Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_622.

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Tammen, I., M. Mather, Z. Li, J. Nothman, D. P. Vanichkina, and F. W. Nicholas. "176. Online Mendelian Inheritance in Animals (OMIA) – future proofing of a globally used animal genetics knowledgebase." In World Congress on Genetics Applied to Livestock Production. Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_176.

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Deep, Anurag, Sahana Murthy, and Paike Jayadeva Bhat. "Geneticus Investigation: An Agent-Based Modeling System for Teaching-Learning Hypothetico-Deductive Reasoning in Mendelian genetics." In 2016 IEEE Eighth International Conference on Technology for Education (T4E). IEEE, 2016. http://dx.doi.org/10.1109/t4e.2016.042.

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Giraldo, Patricia, Estela Giménez, Elena Benavente, et al. "An F2 Barley Population as a Tool for Teaching Mendelian Genetics." In The 1st International Electronic Conference on Plant Science. MDPI, 2020. http://dx.doi.org/10.3390/iecps2020-08590.

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"VIRTUAL BIOLOGY EXERCISE FOR THE ACTIVE LEARNING OF MENDELIAN GENETICS AND DEVELOPMENT OF KEY COMPETENCES." In 3rd International Conference on Computer Supported Education. SciTePress - Science and and Technology Publications, 2011. http://dx.doi.org/10.5220/0003336103900393.

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Lakhan, Shaheen. "The Emergence of Modern Biotechnology in China." In InSITE 2006: Informing Science + IT Education Conference. Informing Science Institute, 2006. http://dx.doi.org/10.28945/3038.

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Science and technology of Republican China (1912-1949) often replicated the West in all hierarchies. However, in 1949 when the Chinese Communist Party (CCP) declared the nation the People's Republic of China, it had assumed Soviet pseudo-science, namely neo-Lamarckian and anti-Mendelian Lysenkoism, which led to intense propaganda campaigns that victimized intellectuals and natural scientists. Not until the 1956 Double Hundred Campaign had China engaging in meaningful exploration into modern genetics with advancements of Morgan. The CCP encouraged discussions on the impact of Lysenkoism which cultivated guidelines to move science forward. However, Mao ended the campaign by asserting the Anti-Rightist Movement (1957) that reinstated the persecution of intellectuals, for he believed they did not contribute to his socialist ethos of the working people. The Great Leap Forward (1958-1959), an idealist and unrealistic attempt to rapidly industrialize the nation, and the Cultural Revolution (1966-1976), a grand attempt to rid China of the "technological elite," extended China's lost years to a staggering two decades. Post-Mao China rapidly revived its science and technology frontier with specialized sciences: agricultural biotechnology, major genomic ventures, modernizing Traditional Chinese Medicine, and stem-cell research. Major revisions to the country’s patent laws increased international interest in China’s resources. However, bioethical and technical standards still need to be implemented and locally and nationally monitored if China’s scientific advances are to be globally accepted and commercialized.
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Gondro, C., and J. C. M. Magalhaes. "Chapter 7 A Simple Genetic Algorithm for Studies of Mendelian Populations." In Recent Advances in Artificial Life. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812701497_0007.

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Chen, Jing, Pengfei Zhu, Jinghui Pan, and Tao Wang. "Exploring genetic mechanisms underlying EEG endophenotypes via summary-data-based Mendelian randomization." In 2022 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2022. http://dx.doi.org/10.1109/bibm55620.2022.9995493.

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Reports on the topic "Mendelian genetics"

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Dubcovsky, Jorge, Tzion Fahima, and Ann Blechl. Positional cloning of a gene responsible for high grain protein content in tetraploid wheat. United States Department of Agriculture, 2003. http://dx.doi.org/10.32747/2003.7695875.bard.

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High Grain Protein Content (GPC) is a desirable trait in breadmaking and pasta wheat varieties because of its positive effects on quality and nutritional value. However, selection for GPC is limited by our poor understanding of the genes involved in the accumulation of protein in the grain. The long-term goal of this project is to provide a better understanding of the genes controlling GPC in wheat. The specific objectives of this project were: a) to develop a high-density genetic map of the GPC gene in tetraploid wheat, b) to construct a T. turgidum Bacterial Artificial Chromosome (BAC) library, c) to construct a physical map of the GPC gene and identify a candidate for the GPC gene. A gene with a large effect on GPC was detected in Triticum turgidum var. dicoccoides and was previously mapped in the short arm of chromosome 6B. To define better the position of the Gpc-B1 locus we developed homozygous recombinant lines with recombination events within the QTL region. Except for the 30-cM region of the QTL these RSLs were isogenic for the rest of the genome minimizing the genetic variability. To minimize the environmental variability the RSLs were characterized using 10 replications in field experiments organized in a Randomized Complete Block Design, which were repeated three times. Using this strategy, we were able to map this QTL as a single Mendelian locus (Gpc-B1) on a 2.6-cM region flanked by RFLP markers Xcdo365 and Xucw67. All three experiments showed that the lines carrying the DIC allele had an average absolute increase in GPC of 14 g/kg. Using the RFLP flanking markers, we established the microcolinearity between a 2.l-cM region including the Gpc-B1 gene in wheat chromosome 6BS and a 350-kb region on rice chromosome 2. Rice genes from this region were used to screen the Triticeae EST collection, and these ESTs were used to saturate the Gpc-B1 region with molecular markers. With these new markers we were able to map the Gpc-B1 locus within a 0.3-cM region flanked by PCR markers Xucw83 and Xucw71. These flanking markers defined a 36-kb colinear region with rice, including one gene that is a potential candidate for the Gpc-B1 gene. To develop a physical map of the Gpc-B1 region in wheat we first constructed a BAC library of tetraploid wheat, from RSL#65 including the high Gpc-B1 allele. We generated half- million clones with an average size of l3l-kb (5.1 X genome equivalents for each of the two genomes). This coverage provides a 99.4% probability of recovering any gene from durum wheat. We used the Gpc-BI flanking markers to screen this BAC library and then completed the physical map by chromosome walking. The physical map included two overlapping BACs covering a region of approximately 250-kb, including two flanking markers and the Gpc-B1 gene. Efforts are underway to sequence these two BACs to determine if additional wheat genes are present in this region. Weare also developing new RSLs to further dissect this region. We developed PCR markers for flanking loci Xucw79andXucw71 to facilitate the introgression of this gene in commercial varieties by marker assisted selection (httQ://maswheat.ucdavis.edu/ orotocols/HGPC/index.hlm). Using these markers we introgressed the Gpc-B1 gene in numerous pasta and common wheat breeding lines.
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