Journal articles: '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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8

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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9

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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Hwang, Kathleen, Alexander N. Yatsenko, Carolina J. Jorgez, et al. "Mendelian genetics of male infertility." Annals of the New York Academy of Sciences 1214, no. 1 (2010): E1—E17. http://dx.doi.org/10.1111/j.1749-6632.2010.05917.x.

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Scriver, C. R., S. Kaufman, and S. L. C. Woo. "Mendelian Hyperphenylalaninemia." Annual Review of Genetics 22, no. 1 (1988): 301–21. http://dx.doi.org/10.1146/annurev.ge.22.120188.001505.

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Aiello, Lisa B., and Beth Desaretz Chiatti. "Primer in Genetics and Genomics, Article 4—Inheritance Patterns." Biological Research For Nursing 19, no. 4 (2017): 465–72. http://dx.doi.org/10.1177/1099800417708616.

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Since the completion of the Human Genome Project, much has been uncovered about inheritance of various illnesses and disorders. There are two main types of inheritance: Mendelian and non-Mendelian. Mendelian inheritance includes autosomal dominant, autosomal recessive, X-linked, and Y-linked inheritance. Non-Mendelian inheritance includes mitochondrial and multifactorial inheritance. Nurses must understand the types of inheritance in order to identify red flags that may indicate the possibility of a hereditary disorder in a patient or family.

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Zou, Guohua, Deyun Pan, and Hongyu Zhao. "Genotyping Error Detection Through Tightly Linked Markers." Genetics 164, no. 3 (2003): 1161–73. http://dx.doi.org/10.1093/genetics/164.3.1161.

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Abstract The identification of genotyping errors is an important issue in mapping complex disease genes. Although it is common practice to genotype multiple markers in a candidate region in genetic studies, the potential benefit of jointly analyzing multiple markers to detect genotyping errors has not been investigated. In this article, we discuss genotyping error detections for a set of tightly linked markers in nuclear families, and the objective is to identify families likely to have genotyping errors at one or more markers. We make use of the fact that recombination is a very unlikely event among these markers. We first show that, with family trios, no extra information can be gained by jointly analyzing markers if no phase information is available, and error detection rates are usually low if Mendelian consistency is used as the only standard for checking errors. However, for nuclear families with more than one child, error detection rates can be greatly increased with the consideration of more markers. Error detection rates also increase with the number of children in each family. Because families displaying Mendelian consistency may still have genotyping errors, we calculate the probability that a family displaying Mendelian consistency has correct genotypes. These probabilities can help identify families that, although showing Mendelian consistency, may have genotyping errors. In addition, we examine the benefit of available haplotype frequencies in the general population on genotyping error detections. We show that both error detection rates and the probability that an observed family displaying Mendelian consistency has correct genotypes can be greatly increased when such additional information is available.

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15

Fang, Fang, Zhe Xu, Yue Suo, et al. "Gene panel for Mendelian strokes." Stroke and Vascular Neurology 5, no. 4 (2020): 416–21. http://dx.doi.org/10.1136/svn-2020-000352.

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BackgroundMendelian stroke causes nearly 7% of ischaemic strokes and is also an important aetiology of cryptogenic stroke. Identifying the genetic abnormalities in Mendelian strokes is important as it would facilitate therapeutic management and genetic counselling. Next-generation sequencing makes large-scale sequencing and genetic testing possible.MethodsA systematic literature search was conducted to identify causal genes of Mendelian strokes, which were used to construct a hybridization-based gene capture panel. Genetic variants for target genes were detected using Illumina HiSeq X10 and the Novaseq platform. The sensitivity and specificity were evaluated by comparing the results with Sanger sequencing.Results53 suspected patients of Mendelian strokes were analysed using the panel of 181 causal genes. According to the American College of Medical Genetics and Genomics standard, 16 likely pathogenic/variants of uncertain significance genetic variants were identified. Diagnostic testing was conducted by comparing the consistency between the results of panel and Sanger sequencing. Both the sensitivity and specificity were 100% for the panel.ConclusionThis panel provides an economical, time-saving and labour-saving method to detect causal mutations of Mendelian strokes.

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Úbeda, Francisco, and David Haig. "On the Evolutionary Stability of Mendelian Segregation." Genetics 170, no. 3 (2005): 1345–57. http://dx.doi.org/10.1534/genetics.104.036889.

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17

Moll, Michael B., and Robert D. Allen. "Student Difficulties with Mendelian Genetics Problems." American Biology Teacher 49, no. 4 (1987): 229–33. http://dx.doi.org/10.2307/4448497.

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18

Collins, Angelo, and James H. Stewart. "The Knowledge Structure of Mendelian Genetics." American Biology Teacher 51, no. 3 (1989): 143–49. http://dx.doi.org/10.2307/4448880.

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19

McLysaght, Aoife. "The deceptive simplicity of mendelian genetics." PLOS Biology 20, no. 7 (2022): e3001691. http://dx.doi.org/10.1371/journal.pbio.3001691.

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SANDLER, IRIS, and LAURENCE SANDLER. "On the Origin of Mendelian Genetics." American Zoologist 26, no. 3 (1986): 753–68. http://dx.doi.org/10.1093/icb/26.3.753.

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21

Ozias-Akins, Peggy, and Peter J. van Dijk. "Mendelian Genetics of Apomixis in Plants." Annual Review of Genetics 41, no. 1 (2007): 509–37. http://dx.doi.org/10.1146/annurev.genet.40.110405.090511.

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22

Kingston, H. M. "ABC of clinical genetics. Mendelian inheritance." BMJ 298, no. 6670 (1989): 375–78. http://dx.doi.org/10.1136/bmj.298.6670.375.

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23

DiMauro, Salvatore. "Mitochondrial encephalomyopathies: Back to mendelian genetics." Annals of Neurology 45, no. 6 (1999): 693–94. http://dx.doi.org/10.1002/1531-8249(199906)45:6<693::aid-ana2>3.0.co;2-#.

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Hinkle, Gregory, and Lynn Margulis. "Non-Mendelian genetic systems." Genome 31, no. 1 (1989): 486–87. http://dx.doi.org/10.1139/g89-094.

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SPENCER, HAMISH G., and DIANE B. PAUL. "The failure of a scientific critique: David Heron, Karl Pearson and Mendelian eugenics." British Journal for the History of Science 31, no. 4 (1998): 441–52. http://dx.doi.org/10.1017/s0007087498003392.

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The bitterness and protracted character of the biometrician–Mendelian debate has long aroused the interest of historians of biology. In this paper, we focus on another and much less discussed facet of the controversy: competing interpretations of the inheritance of mental defect. Today, the views of the early Mendelians, such as Charles B. Davenport and Henry H. Goddard, are universally seen to be mistaken. Some historians assume that the Mendelians' errors were exposed by advances in the science of genetics. Others believe that their mistakes could have been identified by contemporaries. Neither interpretation takes account of the fact that the lapses for which the Mendelian eugenicists are now notorious were, in fact, mostly identified at the time by the biometricians David Heron and Karl Pearson. In this paper we ask why their objections had so little impact. We think the answer illustrates an important general point about the social prerequisites for effective scientific critique.

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Price, Courtney G., Emma M. Knee, Julie A. Miller, et al. "Following Phenotypes: An Exploration of Mendelian Genetics Using Arabidopsis Plants." American Biology Teacher 80, no. 4 (2018): 291–300. http://dx.doi.org/10.1525/abt.2018.80.4.291.

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Arabidopsis thaliana, a model system for plant research, serves as the ideal organism for teaching a variety of basic genetic concepts including inheritance, genetic variation, segregation, and dominant and recessive traits. Rapid advances in the field of genetics make understanding foundational concepts, such as Mendel's laws, ever more important to today's biology student. Coupling these concepts with hands-on learning experiences better engages students and deepens their understanding of the topic. In our article, we present a teaching module from the Arabidopsis Biological Resource Center as a tool to engage students in lab inquiry exploring Mendelian genetics. This includes a series of protocols and assignments that guide students through growing two generations of Arabidopsis, making detailed observations of mutant phenotypes, and determining the inheritance of specific traits, thus providing a hands-on component to help teach genetics at the middle and high school level.

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Grieshammer, Uta, and Johnny C. Wynne. "Mendelian and Non-Mendelian Inheritance of Three Isozymes in Peanut (Arachis hypogaea L.)1." Peanut Science 17, no. 2 (1990): 101–5. http://dx.doi.org/10.3146/i0095-3679-17-2-13.

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Abstract Because of the importance of peanut (Arachis hypogaea L.) as an oil, food, and feed source worldwide and the contributions of breeding and genetics to yield and quality improvement, it is desirable to understand the genetic structure of the plant. Isozymes have been used to gain an understanding of the genetic structure of several plant species. However, we found no literature on the inheritance of isozymes in peanut. The F1 and F2 seed of several crosses between cultivars and plant introduction lines of three botantical types of peanut were used to investigate the inheritance of three isozymes by horizontal starch gel electrophoresis: phosphohexose isomerase (PHI), isocitrate dehydrogenase (IDH), and glutamate oxaloacetate transaminase (GOT). Each of the three enzymes displayed two different banding patterns, the difference being the presence vs. the absence of either one (IDH) or two (PHI, GOT) bands. Chi-square analysis for goodness of fit of the observed F2 segregation ratios to ratios expected from genetic models indicated that the polymorphisms for both PHI and IDH are controlled by single genes. Two loci, Phi-1 and Idh-1, respectively, are proposed. Sixty-five of 71 F1 progeny monitored for GOT showed the banding pattern of the male parent. The F2 progeny segregated into the two parental types, but the ratios did not fit a simple genetic model. Possible explanations for the observed paternal inheritance of GOT include biparental transmission of plastids, prezygotic RNA synthesis and genomic imprinting.

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Veitia, R. A., S. Caburet, and J. A. Birchler. "Mechanisms of Mendelian dominance." Clinical Genetics 93, no. 3 (2017): 419–28. http://dx.doi.org/10.1111/cge.13107.

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Harper, P. S. "Mendelian Inheritance in Man." Journal of Medical Genetics 30, no. 4 (1993): 352. http://dx.doi.org/10.1136/jmg.30.4.352-a.

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Harper, P. S. "Mendelian Inheritance in Man." Journal of Medical Genetics 24, no. 11 (1987): 719. http://dx.doi.org/10.1136/jmg.24.11.719.

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Harper, P. S. "Mendelian Inheritance in Man." Journal of Medical Genetics 28, no. 4 (1991): 287. http://dx.doi.org/10.1136/jmg.28.4.287.

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Giménez, Estela, Elena Benavente, Laura Pascual, et al. "An F2 Barley Population as a Tool for Teaching Mendelian Genetics." Plants 10, no. 4 (2021): 694. http://dx.doi.org/10.3390/plants10040694.

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In the context of a general genetics course, mathematical descriptions of Mendelian inheritance and population genetics are sometimes discouraging and students often have serious misconceptions. Innovative strategies in expositive classes can clearly encourage student’s motivation and participation, but laboratories and practical classes are generally the students’ favourite academic activities. The design of lab practices focused on learning abstract concepts such as genetic interaction, genetic linkage, genetic recombination, gene mapping, or molecular markers is a complex task that requires suitable segregant materials. The optimal population for pedagogical purposes is an F2 population, which is extremely useful not only in explaining different key concepts of genetics (as dominance, epistasis, and linkage) but also in introducing additional curricular tools, particularly concerning statistical analysis. Among various model organisms available, barley possesses several unique features for demonstrating genetic principles. Therefore, we generated a barley F2 population from the parental lines of the Oregon Wolfe Barley collection. The objective of this work is to present this F2 population as a model to teach Mendelian genetics in a medium–high-level genetics course. We provide an exhaustive phenotypic and genotypic description of this plant material that, together with a description of the specific methodologies and practical exercises, can be helpful for transferring our fruitful experience to anyone interested in implementing this educational resource in his/her teaching.

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Рудник, А. Ю., М. А. Федяков, and О. С. Глотов. "Genetics in Ophthalmology." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 8(217) (August 31, 2020): 44–45. http://dx.doi.org/10.25557/2073-7998.2020.08.44-45.

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На сегодняшний день в базе данных Online Mendelian Inheritance in Man (OMIM) описано более 6613 заболеваний и фенотипов, 4241 имеют доказанную генетическую основу, не менее 45% вкючают офтальмологические проявления. В статье приведен ряд клинический примеров пациентов с офтальмологическими симптомами различных генетических заболеваний (алкаптонурия, болезнь Штаргардта, синдром микроцефалии с или без хориоретинопатии; астроцитарная гамартома) с целью демонстрации эффективного клинико-диагностического скрининга генетической патологии у пациентов. So far, the Online Mendelian Inheritance in Man (OMIM) database describes more than 6613 diseases and phenotypes, 4241 have a proven genetic basis, 45% of which are combined with ophthalmological manifestations. The article provides a number of clinical examples of patients with ophthalmological manifestations of various genetic diseases (alcaptonuria, Stadgart ‘s disease, microcephaly syndrome with or without choriretinopathy; Astrocytic gamartoma) to demonstrate effective clinical-diagnostic screening of genetic pathology in patients.

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Müller-Wille, Staffan, and Giuditta Parolini. "Punnett squares and hybrid crosses: how Mendelians learned their trade by the book." BJHS Themes 5 (2020): 149–65. http://dx.doi.org/10.1017/bjt.2020.12.

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AbstractThe rapid reception of Gregor Mendel's paper ‘Experiments on plant hybrids’ (1866) in the early decades of the twentieth century remains poorly understood. We will suggest that this reception should not exclusively be investigated as the spread of a theory, but also as the spread of an experimental and computational protocol. Early geneticists used Mendel's paper, as well as reviews of Mendelian experiments in a variety of other publications, to acquire a unique combination of experimental and mathematical skills. We will analyse annotations in copies of Mendel's paper itself, in early editions and translations of this paper, and in early textbooks, such as Reginald Punnett's Mendelism (1905) or Wilhelm Johannsen's Elemente der exakten Erblichkeitslehre (1909). We will examine how readers used copies of such works to reproduce the logic behind Mendelian experiments, either by recalculating results, or by retracing the underlying combinatorial reasoning. We will place particular emphasis on the emergent role of diagrams in teaching and learning the practice of Mendelian genetics.

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Úbeda, F. "Why Mendelian segregation?" Biochemical Society Transactions 34, no. 4 (2006): 566–68. http://dx.doi.org/10.1042/bst0340566.

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The discovery of alleles that are able to distort segregation during meiosis in their favour raises the question of why Mendelian segregation is the rule and segregation distortion the exception. Previous research on this topic was limited by an unrealistic assumption: equal segregation in the two sexes. Úbeda and Haig [(2005) Genetics 170, 1345–1357] provide a new model allowing sex-specific segregation distortion. This model shows that natural selection favours departure from Mendelian expectations. The evolutionary instability of Mendelian segregation under more realistic assumptions requires a new paradigm that explains its ubiquity.

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Danner, M. A., J. Z. Ribeiro, F. Zanette, J. V. M. Bittencourt, and A. M. Sebbenn. "Mendelian segregation in eight microsatellite loci from hand- and open-pollinated progenies of Araucaria angustifolia (Bert.) O. Kuntze (Araucariaceae)." Silvae Genetica 62, no. 1-6 (2013): 18–24. http://dx.doi.org/10.1515/sg-2013-0003.

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Abstract In order to use molecular markers in population genetics studies, it is important to confirm that the molecular markers used present a Mendelian segregation. The aim of this paper was to investigate the genetic segregation of eight microsatellite loci of Araucaria angustifolia (Bert.) O. Kuntze (Araucariaceae). The study was carried out comparing genetic segregation in hand- and open-pollinated progenies of maternal dioecious and monoecious trees. The Mendelian segregation was confirmed for all eight loci studied (Ag20, Ag23, Ag45, Aang01, Aang14, Aang28, As90 and CRCAc1), as no deviation from the expected segregation hypothesis was detected in the studied progenies. Therefore, these eight loci can be used for further population genetics studies of A. angustifolia.

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37

Lawson, Anton E. "Introducing Mendelian Genetics through a Learning Cycle." American Biology Teacher 58, no. 1 (1996): 38–42. http://dx.doi.org/10.2307/4450070.

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Allen, Robert D., and Michael B. Moll. "A Realistic Approach to Teaching Mendelian Genetics." American Biology Teacher 48, no. 4 (1986): 227–30. http://dx.doi.org/10.2307/4448270.

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Mertens, Thomas R. "Using Human Pedigrees to Teach Mendelian Genetics." American Biology Teacher 52, no. 5 (1990): 288–90. http://dx.doi.org/10.2307/4449111.

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40

Burian, Richard M. "On the internal dynamics of mendelian genetics." Comptes Rendus de l'Académie des Sciences - Series III - Sciences de la Vie 323, no. 12 (2000): 1127–37. http://dx.doi.org/10.1016/s0764-4469(00)01248-8.

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Vicedo, Marga. "What Is that Thing Called Mendelian Genetics?" Social Studies of Science 25, no. 2 (1995): 370–82. http://dx.doi.org/10.1177/030631295025002018.

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Rahit, K. M. Tahsin Hassan, and Maja Tarailo-Graovac. "Genetic Modifiers and Rare Mendelian Disease." Genes 11, no. 3 (2020): 239. http://dx.doi.org/10.3390/genes11030239.

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Despite advances in high-throughput sequencing that have revolutionized the discovery of gene defects in rare Mendelian diseases, there are still gaps in translating individual genome variation to observed phenotypic outcomes. While we continue to improve genomics approaches to identify primary disease-causing variants, it is evident that no genetic variant acts alone. In other words, some other variants in the genome (genetic modifiers) may alleviate (suppress) or exacerbate (enhance) the severity of the disease, resulting in the variability of phenotypic outcomes. Thus, to truly understand the disease, we need to consider how the disease-causing variants interact with the rest of the genome in an individual. Here, we review the current state-of-the-field in the identification of genetic modifiers in rare Mendelian diseases and discuss the potential for future approaches that could bridge the existing gap.

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All-Robyn, J. A., D. Kelley-Geraghty, E. Griffin, N. Brown, and S. W. Liebman. "Isolation of omnipotent suppressors in an [eta+] yeast strain." Genetics 124, no. 3 (1990): 505–14. http://dx.doi.org/10.1093/genetics/124.3.505.

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Abstract Omnipotent suppressors decrease translational fidelity and cause misreading of nonsense codons. In the presence of the non-Mendelian factor [eta+], some alleles of previously isolated omnipotent suppressors are lethal. Thus the current search was conducted in an [eta+] strain in an effort to identify new suppressor loci. A new omnipotent suppressor, SUP39, and alleles of sup35, sup45, SUP44 and SUP46 were identified. Efficiencies of the dominant suppressors were dramatically reduced in strains that were cured of non-Mendelian factors by growth on guanidine hydrochloride. Wild-type alleles of SUP44 and SUP46 were cloned and these clones were used to facilitate the genetic analyses. SUP44 was shown to be on chromosome VII linked to cyh2, and SUP46 was clearly identified as distinct from the linked sup45.

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Chen, Nancy, Cristopher V. Van Hout, Srikanth Gottipati, and Andrew G. Clark. "Using Mendelian Inheritance To Improve High-Throughput SNP Discovery." Genetics 198, no. 3 (2014): 847–57. http://dx.doi.org/10.1534/genetics.114.169052.

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Kaplan, Norman, Tom Darden, and Charles H. Langley. "EVOLUTION AND EXTINCTION OF TRANSPOSABLE ELEMENTS IN MENDELIAN POPULATIONS." Genetics 109, no. 2 (1985): 459–80. http://dx.doi.org/10.1093/genetics/109.2.459.

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ABSTRACT A model of the evolution of a transposable element family in a Mendelian host population is proposed that incorporates heritable phenotypic mutations in the elements. The temporal behavior of the numbers of mutant and wild-type elements is studied, and the expected extinction time of the transposable element family is examined. Our results indicate that, if the mutant can be transposed equally well in the presence of the wild type, then it can be expected to be found in preponderance, whereas elements, such as retroviruses, where the transposing genome and its phenotypic expression are coupled, may be characterized by a low mutant frequency.

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46

Papp, Zoltan. "Changing Public Demand in the Genetic Counseling during the Past Decades." Donald School Journal of Ultrasound in Obstetrics and Gynecology 5, no. 2 (2011): 175–85. http://dx.doi.org/10.5005/jp-journals-10009-1194.

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ABSTRACT Before discovering genetic rules, genetic counseling was based on empirical observations. In this process, it was important to recognize that certain diagnoses were more frequent in certain couples’ descendants. The 20th century witnessed revolutionary progress in the science of genetics that coincided with increasing societal demands and therefore became an integral part of modern genetic counseling. Genetic screening is changing from Mendelian disease ascertainment to predictive testing. We are also learning that the phenotypes of even simple Mendelian disorders are influenced by complex genetic and environmental factors. Moreover, developing knowledge about genotype/phenotype associations and many other aspects of genetic epidemiology will increasingly require referral to clinical geneticists.

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VanWinkle-Swift, Karen P., and Jang-Hee Hahn. "THE SEARCH FOR MATING-TYPE-LIMITED GENES IN THE HOMOTHALLIC ALGA CHLAMYDOMONAS MONOICA." Genetics 113, no. 3 (1986): 601–19. http://dx.doi.org/10.1093/genetics/113.3.601.

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ABSTRACT The non-Mendelian erythromycin resistance mutation ery-u1 shows bidirectional uniparental inheritance in crosses between homothallic ery-u1 and ery-u1 + strains of Chlamydomonas monoica. This inheritance pattern supports a general model for homothallism invoking intrastrain differentiation into opposite compatible mating types and, further, suggests that non-Mendelian inheritance is under mating-type (mt) control in C. monoica as in heterothallic species. However, the identification of genes expressed or required by one gametic cell type, but not the other, is essential to verify the existence of a regulatory mating-type locus in C. monoica and to understand its role in cell differentiation and sexual development. By screening for a shift from bidirectional to unidirectional transmission of the non-Mendelian ery-u1 marker, a mutant with an apparent mating-type-limited sexual cycle defect was obtained. The responsible mutation, mtl-1, causes a 1000-fold reduction in zygospore germination in populations homozygous for the mutant allele and, approximately, a 50% reduction in germination for heterozygous (mtl-1/mtl-1 +) zygospores. By next screening for strains unable to yield any viable zygospores in a cross to mtl-1, a second putative mating-type-limited mutant, mtl-2, was obtained. The mtl-2 strain, although self-sterile, mates efficiently with mtl-2 + strains and shows a unidirectional uniparental pattern of inheritance for the ery-u1 cytoplasmic marker, similar to that observed for crosses involving mtl-1. Genetic analysis indicates that mtl-1 and mtl-2 define unique unlinked Mendelian loci and that the sexual cycle defects of reduced germination (mtl-1) or self-sterility (mtl-2) cosegregate with the effect on ery-u1 cytoplasmic gene transmission. By analogy to C. reinhardtii, the mtl-1 and mtl-2 phenotypes can be explained if the expression of these gene loci is limited to the mt + gametic cell type, or if the wild-type alleles at these loci are required for the normal formation and/or functioning of mt + gametes only.

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Schnable, P. S., and P. A. Peterson. "The Mutator-Related Cy Transposable Element of Zea Mays L. Behaves as a near-Mendelian Factor." Genetics 120, no. 2 (1988): 587–96. http://dx.doi.org/10.1093/genetics/120.2.587.

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Abstract The bz-rcy allele arose in a single gamete of the TEL (transposable-element laden) population, when the rcy receptor element inserted into the Bronze1 locus. This newly arisen receptor allele conditions a stable bronze kernel phenotype in the absence of the independently segregating regulatory element, Cy. In the presence of Cy, bz-rcy conditions fully colored spots on a bronze background. The spots represent clonal sectors arising from mutations of bz-rcy to Bz'. Although Cy exhibits genetic interactions with the Mutator system it differs from Mu-homologous elements in its near-Mendelian behavior which is in contrast to the non-Mendelian inheritance of Mutator and Mu-homologous elements. Evidence is presented which suggests that the timing and mode of Cy transposition differ from those of Mu1.

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49

Lisch, D., P. Chomet, and M. Freeling. "Genetic characterization of the Mutator system in maize: behavior and regulation of Mu transposons in a minimal line." Genetics 139, no. 4 (1995): 1777–96. http://dx.doi.org/10.1093/genetics/139.4.1777.

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Abstract Most Mutator lines of maize harbor several different classes of Mu transposons, each of which may be present in high copy number. The regulatory element is also often found in high copy number, and it is this element's behavior that is presumed to cause the non-Mendelian inheritance of Mutator activity. Using a very simple Mutator line, we demonstrate tha MuDR-1, a regulator of the Mutator system, can functionally replace standard non-Mendelian Mutator activity and that MuDR-1 is associated with the loss of methylation of the termini of another Mu transposon. Further, we show that Mu transposons can transpose duplicatively, that reinsertion tends to be into unlinked sites, and that MuDR-1 frequently suffers deletions. Changes in chromosomal position and the mode of sexual transmission are shown to be associated with changes in the frequency of MuDR-1 duplication and with the activity of MuDR-1 as monitored by the excision frequency of a reporter transposon of the Mu family, Mu1. Our data are derived from a Minimal Mutator Line in which there are relatively few Mu transposons, including one MuDR-1 regulator and as few as one Mu1 reporter. The seemingly enigmatic results that have been obtained using more complicated Mu genotypes are reinterpreted using simple Mendelian principles. We have borrowed a gap-repair model from Drosophila biologists to explain both duplications and deletions of MuDR-1.

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Scott, J., C. Leeck, and J. Forney. "Molecular and genetic analyses of the B type surface protein gene from Paramecium tetraurelia." Genetics 134, no. 1 (1993): 189–98. http://dx.doi.org/10.1093/genetics/134.1.189.

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Abstract The gene encoding the B type variable surface protein from Paramecium tetraurelia stock 51 has been cloned and sequenced. The 7,182 nucleotide open reading frame contains no introns and encodes a cysteine-rich protein that has a periodic structure including three nearly perfect tandem repeats in the central region. Interestingly, the B gene is located near a macronuclear telomere as was shown previously for two other paramecium surface protein genes. In this paper, we characterize four independent mutants with complete macronuclear deletions of the B gene. Previous analysis of different macronuclear deletion mutants of the A surface protein gene demonstrated two types of inheritance: typical Mendelian segregation (as illustrated by d12) and cytoplasmic inheritance (shown by d48). F1 analysis of four B- mutants crossed with wild-type cells reveals heterozygous F1 cell lines derived from both parental cytoplasms contain approximately the same copy number of the B gene, as expected for a recessive Mendelian mutation. Analysis of F2 progeny from three of these four B- mutant crosses indicates that one of the three exhibits a Mendelian 1:1 segregation ratio of B+ and B- cell lines. The other two show a preponderance of B+ cells, but this is not correlated with the parental cytoplasmic type. In addition to having a large number of B+ individuals, the d12.144, A-, B- mutant produced some F2 progeny that stably maintain less than normal macronuclear amounts of the A gene and/or the B gene.

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Journal articles on the topic 'Mendelian genetics'

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