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Introduction to Mendelian Genetics

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• Introduction to Ecology; Major patterns in Earth’s climate
• Behavioral Ecology
• Population Ecology 1
• Population Ecology 2
• Community Ecology 1
• Community Ecology 2
• Ecosystems 1
• Ecosystems 2
• Strong Inference
• What is life?
• What is evolution?
• Evolution by Natural Selection
• Other Mechanisms of Evolution
• Population Genetics: the Hardy-Weinberg Principle
• Phylogenetic Trees
• Earth History and History of Life on Earth
• Origin of Life on Earth
• Gene expression: DNA to protein
• Gene regulation
• Cell division: mitosis and meiosis

Mendelian Genetics

• Chromosome theory of inheritance
• Patterns of inheritance
• Chemical context for biology: origin of life and chemical evolution
• Biological molecules
• Membranes and Transport
• Energy and enzymes
• Respiration, chemiosmosis and oxidative phosphorylation
• Oxidative pathways: electrons from food to electron carriers
• Fermentation, mitochondria and regulation
• Why are plants green, and how did chlorophyll take over the world? (Converting light energy into chemical energy)
• Carbon fixation
• Recombinant DNA
• Cloning and Stem Cells
• Adaptive Immunity
• Human evolution and adaptation

Learning Objectives

• Know and use the vocabulary needed to discuss genetic inheritance including gene, allele, dominant, recessive, gamete, genotype, phenotype, homozygote, heterozygote, carrier
• Explain how chromosomal separation at meiosis leads to segregation of alleles in gametes
• Explain how alignment at metaphase results in independent assortment of (unlinked) genes
• Construct and use a Punnett square for a single trait and for two traits using appropriate terminology
• Determine possible offspring types and phenotypic ratios using probability rules

The terminology of Mendelian inheritance

Gregor Mendel is famous for discovering “particulate inheritance” or the idea that hereditary elements are passed on in discrete units rather than “blended” together at each new generation.  Today we call those discrete units genes .

• A gene is a hereditary factor that determines (or influences) a particular trait.  A gene is comprised of a specific DNA sequence and is located on a specific region of a specific chromosome.  Because of its specific location, a gene can also be called a genetic locus.
• An allele is a particular variant of a gene, in the same way that chocolate and vanilla are particular variants of ice cream.
• An organism’s genotype is the particular collection of alleles found in its DNA.  An organism with two of the same alleles for a particular gene is homozygous at that locus; an organism with two different alleles for a particular gene is heterozygous at that locus.
• An organism’s phenotype is its observable traits.  An organism can have a heterozygous at a particular locus but have a phenotype that looks like only one of the two alleles.  This is because some alleles mask the appearance of others in a dominant/recessive pattern.
• A dominant allele produces its phenotype whether the organism is homozygous or heterozygous at that locus.  For example, in humans the allele for brown eyes is dominant to the allele for blue eyes, so a person who is heterozygous at the eye color locus will have brown eyes.
• A recessive allele produces its phenotype only when homozygous at the locus; its phenotype is masked if the locus is heterozygous.  For example, a person must have two copies of the blue eye color allele to have blue eyes.
• Sometimes specific recessive alleles are associated with diseases or conditions .  A person who is heterozygous for the gene will be phenotypically normal but carry a copy of the recessive, disease-associated allele.  This person is said to be a carrier and can pass on the disease allele to his or her offspring.

Crosses with a single trait & the principle of segregation

All of the concepts above are illustrated in the types of experiments that Mendel carried out with pea plants. Pea plants aren’t a particularly exciting organism to study, but they were very useful in figuring out basic patterns of inheritance!  The reason they were so useful is that they have a lot of traits that are caused by a single gene with a simple dominant/recessive inheritance pattern (this is actually pretty rare in general – but more on that later ).  So what does that statement in bold mean?  A classic example is pea shape. Peas can be either round or wrinkly, but not anything in between. Whether they are round or wrinkly is controlled by a single gene with two alleles, and the round allele is dominant to the wrinkly allele.  The inheritance pattern if you cross homozygous round and homozygous wrinkly pea plants is illustrated here:

In the P generation, pea plants that are true-breeding for the dominant yellow phenotype are crossed with plants with the recessive green phenotype. This cross produces F1 heterozygotes with a yellow phenotype. Punnett square analysis can be used to predict the genotypes of the F2 generation. Source: OpenStax Biology (https://cnx.org/resources/83af4d98c6e7004c52f95071a357b686d11dc819/Figure_12_02_02.png)

You can see in the first generation (F1) that all offspring produce round seeds, even though they both the round and wrinkly alleles.  If the F1 generation self-fertilizes (pea plants – like most plants – produce both male and female gametes), then you now see some offspring that produce rounds seeds and some that produce wrinkly seeds.  The round:wrinkly seed producers exist in approximately a 3:1 ratio, illustrated by constructing a Punnett square.

Punnett squares illustrate the fact that each pea plant gamete contains only one allele for each trait.  Even though adult pea plants have two copies of each allele, these two alleles become into different gametes.  Thus when two gametes come together to create a new plant, each gamete carries one allele resulting in two alleles in the new plant.  The idea that each gamete carries only one allele for each trait is the principle of segregation ; that is, the two alleles for a particular trait are segregated into different gametes.

Crosses with two traits and the principle of independent assortment

Pea plants have a lot of other traits beyond seed shape, and Mendel studied seven other traits.  Things become more complex when you follow more than one trait at at time .  Here is a cross looking at both pea shape (round or wrinkly) and pea color (yellow or green).  Follow the logic of the cross below to see why offspring demonstrate a 9:3:3:1 ratio of different phenotypes.

This dihybrid cross of pea plants involves the genes for seed color and texture. Source: OpenStax Biology (https://cnx.org/resources/ceb880bf9a58402dc053bb94ff94ec158ffc2a3a/Figure_12_03_02.png)

Punnett squares that show two or more traits illustrate the idea that alleles for different traits (different genes) are segregated independently of each other.   Yellow seeds are not always round, and green seeds are not always wrinkly; there can be yellow wrinkly seeds, yellow round seeds, green wrinkly seeds, and green round seeds. The idea that alleles for different traits are segregated independently is the  principle of independent assortment .

Mendel’s laws and meiosis

Mendel’s laws (principles) of segregation and independent assortment are both explained by the physical behavior of chromosomes during meiosis.

Segregation occurs because each gamete inherits only one copy of each chromosome.  Each chromosome has only one copy of each gene; therefore each gamete only gets one allele.  Segregation occurs when the homologous chromosomes separate during meiotic anaphase I .  This principle is illustrated here:

Source: Adapted from Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Independent_assortment_%26_segregation-it.svg)

Independent assortment occurs because homologous chromosomes are randomly segregated into different gametes; ie, one gamete does not only get all maternal chromosomes while the other gets all paternal chromosomes. Independent assortment occurs when homologous chromosomes align randomly at the metaphase plate during meiotic metaphase I . This principle is illustrated here:

chromosomes. Source: Adapted from Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Independent_assortment_%26_segregation-it.svg) and OpenStax Biology (http://cnx.org/resources/c6a4bad683d231988b861985dfa445fff58e0bd4/Figure_11_01_03.jpg)

  Random, independent assortment during metaphase I can be demonstrated by considering a cell with a set of two chromosomes ( n = 2). In this case, there are two possible arrangements at the equatorial plane in metaphase I. The total possible number of different gametes is 2^ n , where n equals the number of chromosomes in a set. In this example, there are four possible genetic combinations for the gametes. With n = 23 in human cells, there are over 8 million possible combinations of paternal and maternal genotypes in a potential offspring.

In class, we will use the information discussed above to determine possible offspring types and phenotypic ratios using simple probability rules. For crosses that involve 2 or more independently assorting traits, using probability rules can be much faster and easier than using 4 x 4 Punnett squares (for 2-factor crosses) or 8 x 8 Punnett squares (for 3-factor crosses. The number of possible gametes is 2^N, where N is the number of factors (genes), and the size of the Punnett square needed is 2^N x 2^N! So instead, we can calculate the outcomes for each factor or gene, then multiply the results.

Example: a cross of AaBbCcDd x AaBbCcDd, where A, B, C and D are 4 different genes, with the dominant alleles given as A, B, C, and D, and the recessive alleles are a, b, c, and d, respectively. What proportion of the progeny will have the dominant phenotype for A and B, and recessive for c and d?

If we look at just Aa x Aa, we know that 3/4 of the progeny will have the dominant A phenotype.

Similarly, for just Bb x Bb, 3/4 of the progeny will have the dominant B phenotype. For Cc x Cc, 1/4 of the progeny will have the recessive c phenotype (cc genotype). For Dd x Dd, 1/4 of the progeny will have the recessive d phenotype (dd genotype). The rules of probability say that, if these genes are sorting independently, we can just multiply these proportions:

The proportion of ABcd phenotype among the progeny = 3/4 x 3/4 x 1/4 x 1/4 = 9/256

Here’s a quick summary of many of these ideas from Ted Ed:

and here is Khan Academy’s take:

UN Sustainable Development Goal (SDG) 3: Good Health and Wellbeing- Understanding genetic inheritance is important for identifying, diagnosing, and treating genetic disorders.

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• Published: 02 September 2019

Mendel for the modern era

Nature Genetics volume  51 ,  page 1297 ( 2019 ) Cite this article

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• Plant genetics

The genome of the model genetic organism Pisum sativum , or pea plant, links nineteenth-century genetics to twenty-first-century genomics, serving as a symbol of how far the genetics field has developed and how greatly technologies have advanced. Almost every student’s introduction to genetics currently involves learning Mendel’s laws; we envision that genomics and genome sequencing will become just as foundational in the education of future geneticists.

Genetics surrounds us. It is everywhere in the popular media. Increasingly, members of the public are being made aware of issues relating to genomic technologies, whether through having their DNA sequenced through companies such as 23andMe or Ancestry.com, hearing about reports of genome-edited babies or debating how genetically modified crops should be labeled. An interested and engaged public is a positive thing, and we support educational endeavors to promote genetic literacy.

The basic principles of inheritance and independent segregation were worked out through Gregor Johann Mendel’s meticulous study of the pea plant in the gardens of Brno in the 1850s and 1860s. Generations of students have learned about dominant and recessive traits through the examples of pea plant height, and pea pod or seed color and shape. The simple laws elucidated by Mendel are experimentally analyzed in classrooms worldwide. Although genetic analysis has become orders of magnitude more sophisticated, Mendel and his humble pea plants are a great guide and entry point into the study of inheritance.

Although most genetics students become familiar with the traits of the pea—including green versus yellow and wrinkled versus smooth, often placed within the ordered Punnett square—as their first foray into genetic study, we believe that a simultaneous, complementary introduction to genomics would also be appropriate. A basic understanding of what a genome is and how it operates, along with a sense of the complexity and sheer amount of information that genomes hold, is important to teach as early as possible. When public policy is being shaped around the privacy of individuals’ genetic data, regulation of gene-edited or genetically modified agricultural products, and guidelines for gene-based therapies to treat diseases, it is crucial for the public to have a basic working knowledge of genetics and genomics. In addition, with the increasing interest in the direct-to-consumer genetic testing used by individuals to find out more about their ancestry, people should understand what those tests are reporting and, more importantly, what their limitations are. This understanding would often require a deeper knowledge of population genetics, but basic principles, from Mendel to genome sequencing, would aid in interpretation.

For example, knowing about the laws of segregation and independent assortment would help people put the understanding of family disease risk variants (how your DNA relates to that of your parents or siblings) into context. Being familiar with concepts of recombination and inheritance would enrich understanding and interpretation of ancestry information. This understanding would also help reduce hype and avoid over-interpretation of genetics findings. Having a fundamental understanding of genetics principles, stemming from Mendel and extending into the genomics era, would empower patients or people getting their DNA sequenced by commercial companies to be better informed and less likely to misinterpret the results.

Although education in genetics is important, we believe that the genomics era has ushered in the need for having a working knowledge of central concepts related to genome biology. Ideally, fundamentals such as the size of the genome, and its linear composition of DNA organized compactly into higher-order chromosomes, would be widespread knowledge. Where genes reside and how they operate from the genome are, of course, still being worked out on the research front. However, the broader concepts, and the links between single genes the whole genome, should be appreciated by a general audience.

Consequently, we are excited to publish the genome sequence of Mendel’s pea plant . Although the individual genes and sequences of Mendel’s seven original traits have been known for a while, we believe that the genome sequencing of the pea plant represents a symbolic milestone for genetics, bringing the foundational experimental studies in basic models into the modern sequencing era. We hope that Gregor Mendel would approve.

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Mendelian Genetics

The Mendelian Concept of a Gene

In the 1860’s, an Austrian monk named Gregor Mendel introduced a new theory of inheritance based on his experimental work with pea plants.  Prior to Mendel, most people believed inheritance was due to a blending of parental ‘essences’, much like how mixing blue and yellow paint will produce a green color.  Mendel instead believed that heredity is the result of discrete units of inheritance, and every single unit (or gene ) was independent in its actions in an individual’s genome.  According to this Mendelian concept, inheritance of a trait depends on the passing-on of these units.  For any given trait, an individual inherits one gene from each parent so that the individual has a pairing of two genes. We now understand the alternate forms of these units as ‘ alleles ’.  If the two alleles that form the pair for a trait are identical, then the individual is said to be homozygous and if the two genes are different, then the individual is heterozygous for the trait.

Based on his pea plant studies, Mendel proposed that traits are always controlled by single genes. However, modern studies have revealed that most traits in humans are controlled by multiple genes as well as environmental influences and do not necessarily exhibit a simple Mendelian pattern of inheritance(see “Mendel’s Experimental Resultsâ€).

Mendel’s Experimental Results

Mendel then theorized that genes can be made up of three possible pairings of heredity units, which he called ‘factors’: AA, Aa, and aa.  The big ‘A’ represents the dominant factor and the little ‘a’ represents the recessive factor.  In Mendel’s crosses, the starting plants were homozygous AA or aa, the F1 generation were Aa, and the F2 generation were AA, Aa, or aa.  The interaction between these two determines the physical trait that is visible to us.

Mendel’s Law of Dominance predicts this interaction; it states that when mating occurs between two organisms of different traits, each offspring exhibits the trait of one parent only.  If the dominant factor is present in an individual, the dominant trait will result.  The recessive trait will only result if both factors are recessive.

Mendel’s Laws of Inheritance

Mendel’s observations and conclusions are summarized in the following two principles, or laws.

Law of Segregation The Law of Segregation states that for any trait, each parent’s pairing of genes (alleles) split and one gene passes from each parent to an offspring.  Which particular gene in a pair gets passed on is completely up to chance.

Law of Independent Assortment The Law of Independent Assortment states that different pairs of alleles are passed onto the offspring independently of each other.  Therefore, inheritance of genes at one location in a genome does not influence the inheritance of genes at another location.

CLICK HERE   to learn more about patterns of inheritance based on Mendel’s discoveries

Bowler, PJ. The Mendelian revolution: The emergence of hereditarian concepts in modern science and society. Journal of the History of the Behavioral Sciences. 1990 October; 26:379-382.

Castle, WE. Mendel’s Law of Heredity. Proceedings of the American Academy of Arts and Sciences. 1903 January; 38:535-548.

El-Hani, CN. Between the cross and the sword: The crisis of the gene concept. Genetics and molecular Biology. 2007; 30:297-307.

Mendel, G. Experiments in plant hybridization. 1865 February.

O’Neil, Dennis. “Basic Principles of Genetics: Mendel’s Genetics.”  Basic Principles of Genetics: Mendel’s Genetics . N.p., n.d. Web. 03 Nov. 2012 <http://anthro.palomar.edu/mendel/mendel_1.htm>.

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Corcos, A., & Monaghan, F. (1990). Mendel’s work and its rediscovery: A new perspective. Critical Reviews in Plant Sciences, 9 , 197–212.

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The deceptive simplicity of mendelian genetics

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Affiliation Smurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland

• Aoife McLysaght

Published: July 19, 2022

• https://doi.org/10.1371/journal.pbio.3001691
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Mendel, a genius experimentalist, meticulously uncovered the genetic basis of heredity in work that transformed the science of biology. But does the alluring simplicity of Mendel’s laws sometimes obscure the true complexity of genetics?

Citation: McLysaght A (2022) The deceptive simplicity of mendelian genetics. PLoS Biol 20(7): e3001691. https://doi.org/10.1371/journal.pbio.3001691

Copyright: © 2022 Aoife McLysaght. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The author received no specific funding for this work.

Competing interests: The authors have declared that no competing interests exist.

Gregor Johann Mendel was born 200 years ago this July. He is commonly referred to as the “father of genetics” because he was the first to understand that heredity works through the inheritance of discrete factors that come in pairs—what we now know as genes. This was a pressing question of the time, and had confounded no less a visionary than Charles Darwin, for whom it was the missing piece in understanding the mechanism of natural selection. Mendel’s expertly designed experiments, combined with his brilliant capacity for deduction, revealed the basis of heredity and thus the common language of all biology. To this day, his work is taught to every biology student; his name is invoked to describe certain kinds of inheritance; and, one might argue, the perceived simplicity of his results has sustained an unhelpfully simplistic view of genetics.

Though the vocabulary had not yet been invented, Mendel’s experiments comprising statistical analysis of meticulous crosses of pea plants laid the foundation for our understanding of the gene and the relationship and difference between inherited genes (genotype) and the physical form of an organism (phenotype) [ 1 ]. The idea was ahead of its time—35 years ahead of its time to be precise—but when his work was “rediscovered” in 1900, it finally found a receptive audience. This moment marked the beginning of an extraordinary period of discovery. William Bateson, who became a fervent champion of Mendel and coined the word “genetics,” correctly predicted that the science of heredity would be soon transformed [ 2 , 3 ].

Reading Mendel’s Versuche (“Experiments”) [ 1 ] today, it is striking to recognize our modern understanding of heredity in his results and interpretations, and it is easy to forget how far outside the contemporary mainstream ideas his conclusions were. Indeed, the conventional view that persisted into the early 20th century was that heredity occurred by blending of parental characteristics, a bit like mixing paint colors—a view shared by Darwin and his biometrician cousin Galton, who called it “Ancestral Heredity” [ 3 , 4 ]. The blending idea appeared, at least superficially, to fit quantitative traits such as human height, that we now understand to be complex genetic traits controlled by many individual genes, each with various forms (alleles or genetic variants) all inherited in a mendelian fashion.

In Versuche , Mendel devotes some time to explaining his experimental design [ 1 ]: He was careful to choose pea varieties that allowed a “sharp and certain separation,” and not ones where there was a gradient of forms. As distinct from complex genetic traits, the variation in these “mendelian” traits was largely controlled by a single gene. In fact, it is hard to imagine how anyone might have arrived at an accurate understanding of the mechanism of heredity from first principles by examining complex genetic traits—the multitude of different factors would seem to make it impenetrably complicated without an existing understanding of the nature of the gene. While we can readily understand complex genetic traits using a mendelian framework [ 5 , 6 ], a focus on complex traits may have been what prevented others, including Darwin, from understanding heredity [ 3 , 4 ]. The essence of experimental design is to simplify the problem just the right amount. Mendel was a genius experimentalist, with his work surely being the most advanced experimental biology of his time. He reduced the problem of heredity to one of beguiling simplicity.

I could not imagine trying to teach genetics without starting with Mendel. Genetics is incredibly (beautifully, fascinatingly, bewilderingly) complex. We now know that most traits—physical, biochemical, behavioral—are influenced by many different genetic variants, individually of small effect, acting in combination with the environment and stochastic processes during development. Even identical twins, who share all their genes, are not actually identical. And in terms of evolutionary genetics, we know that natural selection is most often acting on infinitesimal differences that only over long periods of time create eventual dramatic changes. But to explain any of this, it helps to first understand Mendel’s work and the simple experimental crosses where two versions of a gene generate forms that are sharply and certainly different, so we start there.

The important thing though is not to stop there. All too often, the popular conception of genetics is expressed with a phrase that begins “the gene for…” It is easy to see how the simplified scenario that Mendel necessarily constructed for his experiments could be misunderstood as the whole picture. It would appear to be irresistible to describe “the gene for eye color” or “the gene for tongue-rolling,” even though these classic, textbook examples of “mendelian” traits have been known to be multifactorial for decades. This temptation then spills over into discussion of “the gene for” any particular human trait or disease, when the reality is more often better described as a tendency or a propensity, which may or may not be realized. The effect of a genetic variant depends, to a greater or lesser extent, on the genetic and environmental context it happens to be in. Contrary to popular belief, the genes do not determine the trait, rather they shape the landscape of probabilities.

This deterministic view of genetics is the most insidious misconception of genetics—it is easy to learn and very difficult to abandon. It is culturally encoded in how we talk about inheritance, and becomes a hurdle to understanding and appreciating the powerful science of genetics [ 7 ]. In thinking genes determine everything, we risk losing sight of the true complexity of genetics and the intimate role of context. Someone carrying a genetic risk factor for, say, type 2 diabetes or heart disease, may never develop those conditions, and can even shift the balance of probabilities with healthy diet and exercise. And while a small minority of human diseases, including Huntington’s chorea and cystic fibrosis, are determined by variation at a single locus, even “simple” traits are often modified by more than one gene [ 6 ].

We are not mere vessels for our genes. Humans, uniquely, and starting with Mendel, are the only species that has developed an understanding of heredity and how genetic information is transmitted across generations and how genes help shape all biological life on this planet. Though we describe supposed single-gene deterministic traits as “mendelian,” I know of no evidence that suggests Mendel himself conceived of such a fanciful system. We honor Mendel by remembering his work, acknowledging its significance, and not attributing to him our modern-day errors of interpretation and oversimplification.

Acknowledgments

Sincere thanks to Adam Rutherford, Kevin Mitchell, and David McConnell for stimulating conversations during the writing of this piece.

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Mendelian genetics

Aspects of genetic inheritance documented by Gregor Mendel. Mendelian genetics mainly refers to the ideas that (1) traits are influenced by discrete heritable elements (now known as genes) that come in different varieties (now known as alleles), (2) for a particular gene, each individual carries two alleles, one inherited from each parent, (3) during reproduction, one allele from each pair is randomly selected to be passed to the offspring and united with the other parent’s alleles, (4) because of these characteristics, trait ratios among offspring are predictable if the parental genotypes are known. For more details,  see our historical essay on the topic .

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Mendelian genetics.

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            Gregor Mendel's Law of segregation states that an organism must have 2 genetic factors called alleles for each trait. Furthermore, these alleles must separate during gamete formation in meiosis I, and then recombine at fertilization in a new genetic combination in the offspring. There are two types of alleles: dominant and recessive. In gamete formation, there is a possibility of three gene combinations depending of the genotypes (genetic makeup) of the parents. These combinations can consist of DD (homozygous dominant), Dd (heterozygous dominant), and dd (homozygous recessive). Each parent during gamete formation will donate one allele, which will form these examples of unlinked monohybrid genes. However offspring also inherit dihybrid genes, which are genes that contain four alleles that code for more than one trait (ex. TI, ti). Here too there are both dominant and recessive alleles. After Mendel performed dihybrid test crosses, he formulated the Law of Independent Assortment. This law states that factors for one trait are inherited independently of factors for another trait and that all genetic combinations are possible in offspring. However, the Law of Independent Assortment and Segregation only pertain to unlinked genes. This is because while unlinked genes are located on separate chromosomes, linked genes are located on the same chromosome. So for example, the genes that code for red hair and freckles could be located on the same gene, and would therefore not segregate independently as predicted by Mendel's laws. Linked genes can be undone by the process of crossing-over, which produces recombinant gametes. Crossing-over occurs during prophase I of meiosis and is the exchange of alleles between non-sister chromatids of a bivalent. This process has hence unlinked certain genes, therefore reapplying the validity of the Laws of Independent Assortment and Segregation.

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Essays Related to Mendelian Genetics

1. mindsets and intelligence.

Emerging in the 1850's, Mendelian genetics dominated the beliefs of the scientific and the general public regarding the theories of intelligence in relation to success in life (Jensen, 2006; Shenk, 2010). ... The method used by scientists to study the function of nature and nurture in the source of traits is called behavioral genetics, and it permits for the heritability of traits to be estimated. ... Defining the Concept of Mindset - Growth and Fixed Hence, the mistaken knowledge concerning the meaning of heritability and the old acceptance of the G+E model initiated by Mendelian geneti...

• Word Count: 3294
• Approx Pages: 13
• Has Bibliography
• Grade Level: Undergraduate

2. Lab Report - Fruit Fly Experiment

Because of his carefully conducted breeding experiments with pea plants, Gregor Mendel, who is known as the father of genetics, was the first person to discover the basic principles of heredity. ... Together, all five concepts make up the Mendelian model that is soon to be demonstrated. ... In fruit fly genetics, a normal fly is called a "wild type" and has red eyes, a grey body color and normal wings. ...

• Word Count: 1238
• Approx Pages: 5
• Grade Level: High School

3. The Importance of Medicine

Introduction Over the years, humankind has had the urge to achieve optimal health. Consequently, theories and diverse categories of therapies arose with the scientific development of medicine taking an upper hand (Gray, 2000, p.1). Treatment has become more dependent on technology and more subjectiv...

• Word Count: 2337
• Approx Pages: 9

4. Bio-ethics and Genetic Engineering

.)- The danger of genetic engineering lies in the fact that the individuality of life could be lost as natural selection is gives way to forced selection to propagate and incode a few preferred genetics traits in the lab. ... Do we want to replace the Mendelian laws of inheritance with genetically sliced humanoids? ...

• Word Count: 2814
• Approx Pages: 11

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Genetic Alliance. A Guide to Genetics and Health. Washington (DC): Genetic Alliance; 2006.

A Guide to Genetics and Health.

Why is genetics important to my family and me.

Genetics helps to explain:

• What makes you unique, or one of a kind
• Why family members look alike
• Why some diseases like diabetes or cancer run in families
• How learning your family health history can help you stay healthy
• Why you should bring your family health history to your healthcare provider

Taking time to learn about health and diseases that run in your family is worth it! It will help you understand your own health and make healthy choices.

• What makes me unique?

Every person is unique. Part of what makes you unique is your genes. Genes are the instructions inside each of your cells. They control how you look and how your body works. Since everyone has slightly different genes, everyone has a different set of instructions. Genes are one reason why you are unique!

• Tell me more about my genes
• A person has two copies of each gene, one from the mother and one from the father.
• Genes carry instructions that tell your cells how to work and grow.
• Cells are the building blocks of the body. Every part of your body is made up of billions of cells working together.
• Genes are arranged in structures called chromosomes. Humans have 23 pairs of chromosomes. Copies of the chromosomes are found in each cell.
• Chromosomes are made up of DNA. DNA is the special code in which the instructions in your genes are written.
• Why do family members have things in common?

Children inherit pairs of genes from their parents. A child gets one set of genes from the father and one set from the mother. These genes can match up in many ways to make different combinations. This is why many family members look a lot alike and others don’t look like each other at all. Genes can also increase the risk in a family for getting certain health conditions.

Families also share habits, diet, and environment. These influence how healthy we are later in life.

You share a lot with your family—including what can make you sick.

• Why do some diseases run in families?

Some diseases are caused when there is a change in the instructions in a gene. This is called a mutation. Every person has many mutations. Sometimes these changes have no effect or are even slightly helpful. But sometimes they can cause disease.

Most common diseases are caused by a combination of mutations, lifestyle choices, and your environment. Even people with similar genes may or may not get an illness if they make different choices or live in a different environment.

Thousands of diseases are caused by a specific change in the DNA of a single gene. Many of these diseases are rare. These conditions usually develop when an individual is born with a mutated gene.

If a rare disease runs in your family, be sure to write it down. Do not forget to learn about common conditions that affect your family’s health.

Visit page 10 to learn about some diseases that run in families.

Common Disease: Diabetes

Changes in your genes passed on by your parents may make you more likely to develop type 2 diabetes. If you are active and eat a healthy diet, you may be able to lower your risk.

Single Gene Disorder: Sickle Cell Anemia

Sickle cell anemia is caused by a mutation in a single gene passed from each parent.

• How can family health history help me stay healthy?

Your family health history tells you which diseases run in your family. Health problems that develop at a younger age than usual can be a clue that your family has a higher risk. Though you cannot change your genes, you can change your behavior.

Knowing your family health history will help you:

• Identify risks due to shared genes.
• Understand better what lifestyle and environmental factors you share with your family.
• Understand how healthy lifestyle choices can reduce your risk of developing a disease.
• Talk to your family about your health.
• Tell your healthcare provider about the diseases that run in your family.

Share your family health history with your healthcare provider.

Ask if you can be screened for a disease that runs in your family.

• Why should I bring my family health history to my healthcare provider?

Your healthcare provider (doctor, nurse, or physician’s assistant) may use your family health history and current health to figure out your risk for developing a disease. Your provider can then help decide which screenings you get and which medicines you might take.

Based on your family health history, a healthcare provider may order a genetic test or refer you to a genetic counselor or geneticist. Genetic tests can show if you have a gene change that increases your risk for disease. They can also tell if you have a gene change that you might pass on to your children. Your healthcare provider can help you:

• Understand the results of your tests.
• Learn of any treatments for a disease found by the test.

All newborn babies born in the U.S. and many other countries are tested for certain genetic diseases that may make them sick. This is called newborn screening. If the screening test finds a problem, a healthcare provider will help you understand what can be done to help the baby.

All Genetic Alliance content, except where otherwise noted, is licensed under a Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

• Cite this Page Genetic Alliance. A Guide to Genetics and Health. Washington (DC): Genetic Alliance; 2006. Why is genetics important to my family and me?
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