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My teaching is through the Ecology & Evolutionary Biology department, and I also teach through IBG.

I teach EBIO 3800 Evolutionary Biology and EBIO 4700/5700 Quantitative Genetics most spring semesters, and I have taught as part of the IBG ProSeminar. I have also taught or been involved with other courses, including the EBIO DEI Seminar and EBIO 4270/5270 Population Genetics.

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Genetics Learning Goals and Teaching Principles

I teach multiple genetics courses, including Evolutionary Biology, Quantitative Genetics, Population Genetics, and a professional seminar at IBG. Every time I teach a course or a topic, I tend to revisit the materials, updating or revising as I see fit. Since 2020, I have been revising materials and thinking through the big ideas of genetics with an eye to inclusive pedagogy and the recognition that the way genetics is classically taught can reinforce misperceptions (see below). As I have been doing this, it has helped to formalize my thinking into a set of updated learning goals & big ideas of genetics, as well as principles of teaching genetics and developing/revising genetics curricula. The lists of goals and principles below represent the way I think about and approach teaching genetics materials, and specifically think about teaching these topics in ways that can reduce misperceptions and misuses of genetics concepts. These come from a mix of published sources (e.g., Duncan 2009 , Donovan 2024��, Donovan 2019��) as well as from helpful discussion with colleagues and my own work and experience.

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Learning goals & big ideas of genetics.

These span molecular ��genetics as well as population & quantitative genetics, and the application of these big ideas to human genetics.��

Notably, not every big idea is applicable to every course – some are more appropriate for introductory courses, some for molecular genetics courses, some for population or quantitative genetics courses.

1. All organisms contain genetic information (mostly in the form of DNA).
2. Genetic information is stored in a universal code that is passed to the next generation.
3. A gene is a sequence of DNA that performs some function. Often this is through coding of proteins, but in many cases it is through non-protein-coding RNA or through other regulatory effects such as influencing the 3D structure of the genome.
4. Genes often have more than one function (pleiotropy).
5. In many organisms (including humans) most of the genome is non-coding and non-genic.
6. In multicellular organisms, genes’ functions are often expressed in specific cells or tissues, rather than universally expressed. This is controlled by gene regulation. Most functional genetic variation within populations influences gene regulation and these effects are small.
7. Mutation is random, and most mutations have no effect on observable phenotypes.
8. Recombination generates new combinations of alleles at different genes, and acts as a source of variation.
9. Most traits of interest, including most human health and behavioral traits, are complex and multifactorial. This means that variation is a result of a complex interplay among many, many genes (often >1,000s) throughout the genome each with very small individual effects, many different environmental influences, and interactions among all these factors.
10. Phenotypic similarity among individuals is related to the degree of sharing of alleles. It is also influenced by shared environments. Disentangling these two influences can be challenging.
11. The size of a population is fundamental to determining how much genetic variation exists within that population.
12. Selection alters allele frequencies within and among populations; adaptation occurs via such shifts, but for complex traits, adaptation can occur through very subtle allele frequency shifts at thousands of loci.
13. Movement of alleles among populations connects them into a shared history.
14. Sharing of alleles within and among populations can be quantified in multiple ways and that sharing reflects the history of those individuals and populations. In humans, nearly all common alleles are shared among all human populations, because of our shared human history.
15. In humans, claims of genetic differences among groups driving disparities among those groups are not supported. Within-group variation can be genetically influenced even while among-group variation is not. Environmental variation at the among-group level can lead to differences when there are no underlying genetic differences among those groups.

Principles of teaching genetics and developing/revising genetics curricula:

My approach to developing curricula rests on three key tenets:

• Both molecular and population & quantitative genetics concepts are important for students to understand (see big ideas above).
• Teaching genetics has the potential to counter misunderstandings about genetic variation in humans, in ways that can reduce racially prejudicial views.
• A central finding of the last 15 years of genetics research is that most human health and behavioral traits are multifactorial.
  • This means these traits are highly complex, with many, many genes throughout the genome contributing individually very small effects, nuanced environmental influences, and interactions among all of these things.
  • A deterministic view of genetics, where students think of genetics is destiny, is largely incorrect when applied to these traits, yet a deterministic view is what is classically taught with Mendelian examples, Punnett’s squares, and trait examples of simple, monogenic architecture.

Beyond these three tenets, an additional three interrelated findings, rooted in evidence and experiments, illustrate the power and potential of teaching genetics, specifically with regard to how students understand human genetic variation:

• Teaching about the overwhelming genetic similarity of human populations helps decrease racial prejudice.
• Teaching about the multifactorial genetic basis of human complex traits helps decrease racial prejudice.
• Evidence suggests that a progression or sequence of teaching molecular genetics first, then introducing population and multifactorial genetics leads to retaining both the molecular genetics big ideas as well as a more nuanced understanding of human genetics.

The above points lead to five primary guiding principles:

• Use a teaching progression of molecular genetic concepts followed by multifactorial and population genetics that highlight complex traits. This full progression may not be possible in every class, but over the course of a degree, this should be the objective, to build toward complex models of understanding how genetics works and how the models and analyses are applied.
• Choose examples that reduce the tendency to view genetics in essentialist and deterministic ways.
• Choose examples that highlight genetic complexity, the probabilistic nature of multifactorial genetics, and the intricacy of the roles of many, many genes, environments, and interactions among them all.
• Exposing students to historical examples of how genetics has been misused and misrepresented is important to teach the consequences of misunderstanding and manipulation of science.
• Exposing students to examples of how genetics has been used appropriately and can help impact our understanding of life, including evolution and human health, is also important.

Choosing examples:

It is worth noting that when teaching any given learning goal, context matters and the appropriate examples will vary. This means that when developing materials or curricula, honing in on the specific learning goal is the first step, but choosing appropriate examples within the larger framework of inclusive pedagogy should always be kept in mind:

• Certain big ideas are better understood in simple Mendelian models of inheritance than others, primarily examples to demonstrate the molecular genetics concepts, such as developmental and transmission genetics.
  • An example would be that all genes are present in all (genome-containing) cells, but are expressed only in certain tissues and at developmental times.
  • Examples from drosophila manipulating hox gene expression in different body segments show this to be the case, and it is intuitive as a demonstration because of the easily visualized phenotypic effects, i.e., these are often Mendelian traits.
• Other big ideas do not need simple Mendelian models of inheritance to demonstrate, where single-locus, dominant allele examples are counterproductive and reinforce incorrect views.
  • Monogenic trait examples emphasize a model of gene action that is not common and not the most relevant for students to understand the traits that we care most about, particularly in humans.
  • When teaching genotype-phenotype relationships and how they are estimated, using complex traits as examples is critical to demonstrate the multifactoral nature of these and avoid the misperceptions noted above.
  • Mutation examples often use Mendelian traits, but do not have to. Other examples could be utilized, like mutations affecting gene expression and eQTLs.

Human examples:

I study the genetic architecture of human phenotypes, and am interested in how genetic variation influences human health and behavior as well as how environments influence these traits and how genes and environments interact. This wonderful complexity of human genetics is both a strength and a challenge to teach. Using human examples is a good thing in certain situations, but not all. The following tenets are how I have approached bringing examples from human genetics into the classroom:

• When examples emphasize Mendelian disorders or highly penetrant alleles, they emphasize a model of trait genetic architecture that does not apply to most traits students think about (e.g., behavioral traits or many complex diseases and disorders); therefore, those monogenic examples should be avoided.
• Mendelian examples using very rare developmental or musculoskeletal disorders should be avoided – these are real, medically important examples, but in a broad genetics course, they (1) emphasize deterministic genetic views and (2) may make individuals carrying such alleles feel as though they are less valued or ‘othered’. While appropriate for medical genetics or developmental genetics courses, they are unnecessary and potentially problematic for introductory or general genetics courses, and should be avoided.
• Examples of monogenic traits that happen to have large prevalence differences among human populations should also be avoided. Classic examples routinely taught in introductory genetics and evolutionary biology courses include cystic fibrosis and sickle cell disease. These are real, medically important examples, and they can be useful, but in the context of introductory or general genetics courses, they emphasize two aspects that are very rare – (1) genetically deterministic traits & (2) traits where the allele frequencies are very different among human populations. These issues combine to lead to racialized views and misperceptions of genetics.
• Alternatively, some human examples can emphasize the multifactorial nature of most complex traits, and thereby reduce genetic deterministic views. These can be wonderful examples.
  • Height is a good example, where we intuitively understand that genetics influences height, but we often overemphasize the variance explained by genetics. The current best understanding of the genetics of height is ultra-polygenic, with thousands of independent loci spread throughout the genome, each with miniscule effects. Simultaneously, patterns of increases in average height over very recent history demonstrate that even for this classic “genetic” trait, environmental influences matter and can have strong impacts, thus helping to reinforce a multifactorial view of genetics even for this height.
  • Expression and eQTLs are likely another broad example, which can be a structuring example throughout a course. Most associations identified to-date are regulatory, not protein-altering. Many eQTLs also have additive gene action, and most genes have more than one regulatory element and eQTLs affecting their expression. Thus, building an example from molecular genetics that emphasizes the mechanisms of transcription and regulation as well as highlighting the polygenic nature of gene expression and building up this model to how many genes (and their many underlying eQTLs) affect trait variation could be a useful structure. The role of environmental variation in gene expression is also often extensive, so building up models of genetics with expression regulation can also be a good stepping-stone to multifactorial genetic understanding.
• The history of genetics as a field and its uses and misuses should be transparently presented. This includes acknowledging the misuse and misrepresentation of human genetics and its role in historical and ongoing discrimination, prejudice, and atrocities.
• The promise and potential of human genetics is great, as is the responsibility to teach it in ways that counter misperceptions and misuses. Human genetics is fundamentally about our shared human experience, and the potential to leverage genetics research to understand that shared experience, identify new ways to treat disease, and uncover what it is to be human is a breathtaking subject to explore and be a part of.

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Updated 2024/11/18

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