Genetics in the Classroom

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00:00:07.21 Hello.
00:00:09.03 I’m Rick Amasino from the University of Wisconsin,
00:00:11.20 and I’d like to talk about our development of materials
00:00:15.10 to get genetics into the classroom,
00:00:17.16 in particular the K-12 classroom.
00:00:21.02 There are lots of organisms
00:00:23.05 that are suitable for classrooms.
00:00:24.12 Shown here are a few, such as the nematode C elegans
00:00:27.06 or yeast or Drosophila.
00:00:29.10 But also, plants are a good classroom model.
00:00:32.16 I’d like to talk a little bit about the advantages of plants.
00:00:36.12 Unlike Drosophila, they don’t fly away.
00:00:38.14 But more importantly,
00:00:40.23 plants are easy and inexpensive to grow,
00:00:43.18 the seeds are very easy to store from year to year,
00:00:47.03 and many of the phenotypes
00:00:49.08 — the genetic variation or mutants that plants exhibit —
00:00:52.11 are easy to visualize without any equipment like a microscope,
00:00:55.24 and I’ll show you some of those phenotypes
00:00:57.29 of various mutants in a moment.
00:01:00.14 But first, I wanted to talk about the particular type of plant
00:01:03.08 that we’ve been developing for classroom models,
00:01:06.16 and that particular plant is Brassica rapa.
00:01:11.20 Brassica rapa as a model for classrooms
00:01:14.20 was first introduced by Paul Williams,
00:01:16.19 who bred very rapid cycling versions
00:01:19.01 of Brassica rapa.
00:01:20.24 These are plants that go from seed to seed
00:01:23.12 in about eight weeks or so.
00:01:25.16 And you can see, by…
00:01:28.23 as a scale, here, the fingers of someone
00:01:31.08 pollinating these plants with a toothpick,
00:01:33.09 how small they are.
00:01:35.10 They’re flowering within a week or so of planting.
00:01:38.16 And so, the lines that Paul Williams developed
00:01:43.08 have self-incompatibility.
00:01:45.09 That means they need to find a different plant
00:01:47.22 in order to have a pollination event and produce seeds.
00:01:51.18 But for a genetic model for the classroom
00:01:53.16 — and these are a wonderful model for many things —
00:01:56.02 we wanted to extend it as a genetic model
00:01:58.23 by making self-compatible fast plants.
00:02:01.26 And by me, I’m referring to me and my colleague Scott Woody,
00:02:05.14 who’s been my partner in this effort
00:02:08.00 at the University of Wisconsin.
00:02:09.24 And we’ve worked along with teams of undergraduates and high school students
00:02:14.08 to develop a self-compatible version of Brassica rapa
00:02:18.20 that has this rapid life cycle, as a genetic model.
00:02:23.27 Some of the advantages of Brassica rapa
00:02:26.05 compared to another well-known plant genetic model,
00:02:30.08 Arabidopsis thaliana,
00:02:32.19 are that the Brassica rapa flowers are larger.
00:02:35.03 What that means is that they’re much easier
00:02:37.21 to do pollinations with — to cross one plant with another.
00:02:40.03 Also, their seeds are much larger,
00:02:43.03 so they’re easier to handle and plant in an orderly manner.
00:02:46.20 And finally, shown here is Scott Woody
00:02:49.12 holding our Brassica rapa plants
00:02:51.12 versus Arabidopsis.
00:02:53.07 Brassica rapa tends to grow in an upright manner;
00:02:56.15 it doesn’t flop over and get entangled
00:02:58.23 as Arabidopsis does.
00:03:01.24 So, it’s much more of a friendlier model for classroom use.
00:03:06.07 What I want to show you now are some of the mutants
00:03:08.18 that we’ve found with our teams of undergraduates
00:03:12.17 and high school students
00:03:14.08 working along with Scott.
00:03:16.08 Here’s an example of a mutant, an albino mutant,
00:03:19.07 that is illustrated here as these light-yellow plants.
00:03:23.19 This is a mutant that doesn’t produce as much chlorophyll
00:03:26.07 as the normal plant,
00:03:27.25 and the normal plant we call the wild type.
00:03:29.24 This is caused by a single gene mutation
00:03:32.00 that’s recessive, so thus you see this nice pattern
00:03:35.10 of Mendelian segregation
00:03:38.27 in this population of plants
00:03:41.08 in which the albino mutant is segregating.
00:03:43.19 In other words, it forms a nice Mendelian segregation pattern
00:03:47.00 where 1/4 of the plants are homozygous mutant,
00:03:51.09 or shown here in this illustration
00:03:53.19 as “little a little a”.
00:03:56.01 And one of the things that you can do with this in the classroom,
00:03:58.02 for example,
00:04:00.02 is save seed from the plants that are green
00:04:01.29 — the so-called plants that have a wild type phenotype —
00:04:05.03 and the students could find, for example,
00:04:07.21 that some of these will breed true
00:04:09.23 — those that are homozygous big A and don’t carry the defective gene
00:04:13.12 for the albino trait --
00:04:15.16 but others that are heterozygous,
00:04:17.18 in other words they have one copy of the mutant
00:04:19.18 and one copy of the wild or normal…
00:04:21.28 wild type or normal gene,
00:04:24.15 will in the next generation,
00:04:26.10 when self-pollinated,
00:04:28.10 produce mutants again from a plant that had been green.
00:04:32.01 Another example of a mutant are mutants that cannot see light.
00:04:34.29 These are in a particular light sensor
00:04:37.06 called phytochrome.
00:04:40.04 Normally, when plants germinate,
00:04:42.01 if they find themselves in dark conditions
00:04:43.15 — for example, they’re buried under some soil
00:04:45.24 or some leaf litter —
00:04:48.09 they will put all their energy into elongation growth
00:04:50.19 in order to push up through that dark environment they’re in
00:04:54.06 to find the light.
00:04:56.05 And once they find the light,
00:04:57.23 they stop elongating and spread out.
00:04:59.26 And in this population, which segregates for the mutant
00:05:02.29 that can’t see light,
00:05:04.27 you see many wild type plants
00:05:07.04 that have spread out nicely,
00:05:08.24 but the mutants continue to grow tall
00:05:11.00 because they can’t sense as well that they’re in the light.
00:05:13.12 This also is a recessive mutation
00:05:16.23 that’s very easy to phenotype —
00:05:18.29 in other words, to study its growth pattern in the…
00:05:22.29 in the classroom.
00:05:24.29 Another example are mutants that don’t have petals.
00:05:27.15 This is the apetala mutant.
00:05:29.18 Petals, out in nature,
00:05:32.11 typically are used by plants to attract pollinators.
00:05:35.25 Of course, we’re the pollinators of this plant,
00:05:38.03 or your students will be in the classroom,
00:05:39.28 so this mutant does just fine
00:05:42.13 without petals, as long as we pollinate it.
00:05:44.21 And shown here is the wild type plant,
00:05:47.11 where you can see all the color at the top of the plant
00:05:50.05 representing the petals.
00:05:52.18 One last mutant that I want to mention to you
00:05:54.29 is one called abnormal leaf.
00:05:58.05 And I mention this mutant because it’s dominant.
00:06:00.19 And this illustrates an important principle in genetics,
00:06:02.29 that is that mutants aren’t necessarily always recessive.
00:06:07.15 That’s a common misconception.
00:06:09.13 Here’s a particular mutant that’s dominant,
00:06:11.14 and it causes these leaves
00:06:13.18 to form this very shriveled pattern
00:06:17.23 of very abnormal leaves.
00:06:20.28 Shown here is a plant that has one copy of the mutant gene
00:06:23.12 and one copy of the wild type version of the gene
00:06:27.06 that causes this abnormal leaf phenotype.
00:06:31.02 Obviously, there are many important conditions in humans,
00:06:33.24 for example,
00:06:35.15 where dominant genes can play
00:06:38.03 a very negative role.
00:06:40.03 An example is Huntington’s disease,
00:06:42.17 where a dominant version of the…
00:06:44.17 a dominant, mutant version of the gene
00:06:47.13 can lead to disease in humans.
00:06:49.16 So, this plant model is a nice illustration
00:06:53.11 of the types of dominant diseases that can occur.
00:06:55.22 But now, I want to tell you how we can find the genes
00:06:58.24 that are represented by these mutants,
00:07:01.22 and a way that you might be able
00:07:04.17 to bring modern molecular genetics into your classroom.
00:07:08.03 So, I want to go back to that example of segregating mutants
00:07:13.14 and illustrate how we get to a segregating population of mutants.
00:07:17.28 For example, we can have a mutant parent,
00:07:20.07 like one of those albinos
00:07:24.21 or a plant that can’t sense light.
00:07:26.18 It can be crossed to a normal parent,
00:07:29.01 which we’ll call the wild type.
00:07:31.10 And at a particular gene,
00:07:33.07 which is illustrated here on a chromosome
00:07:35.23 of those plants
00:07:37.26 with the letter big A or lowercase a,
00:07:40.04 which I’ll call little a,
00:07:42.11 the various versions of the gene.
00:07:44.21 And the lowercase is typically
00:07:47.08 how we designate the mutant.
00:07:50.03 So, here’s a mutant parent that can be crossed
00:07:52.14 by taking pollen from it and transferring it
00:07:54.16 to a wild type female plant,
00:07:56.22 and this will produce in the next generation
00:07:59.08 an F1 hybrid, a combination of these two parents,
00:08:03.14 a chromosome from each.
00:08:06.27 And I’m just showing one of many of the chromosomes for illustration.
00:08:09.20 This F1 hybrid can undergo self-pollination
00:08:12.08 and in its next generation, as you know,
00:08:15.01 these traits will segregate.
00:08:17.18 As I showed earlier for the albino trait,
00:08:19.26 this will segregate three to one,
00:08:24.02 where we have three wild type for every one mutant.
00:08:26.18 And of course, the mutants are where that mutant gene
00:08:29.22 is homozygous,
00:08:32.02 as illustrated by the individuals in this segregating population
00:08:35.10 with the box and the asterisks.
00:08:39.01 So, how can we use a segregating population
00:08:42.08 to find a gene?
00:08:44.05 I want to introduce the concept of DNA polymorphisms,
00:08:47.26 and that is, if you have two parents
00:08:50.06 creating these populations,
00:08:52.05 that have differences in their DNA sequence
00:08:55.03 throughout their chromosomes,
00:08:57.02 these can be used as addresses
00:08:59.26 for where genes are on the chromosome.
00:09:02.17 We call them molecular markers.
00:09:04.20 And any difference in DNA sequence
00:09:06.21 is potentially a molecular marker.
00:09:10.12 Shown here are just some of the chromosomes
00:09:12.11 of Brassica rapa
00:09:13.27 showing that we have a rich set of markers
00:09:16.19 that cover the chromosomes very thoroughly.
00:09:21.22 And there are various ways
00:09:24.09 we can look at those polymorphisms.
00:09:26.16 One way that’s commonly used nowadays,
00:09:29.13 because of lowered cost and increased efficiency,
00:09:32.05 is just to sequence the entire genome of organisms
00:09:35.19 to find which have one version of a gene versus another.
00:09:39.09 But a technique that’s very amenable to the classroom
00:09:42.23 is a technique called gel electrophoresis,
00:09:45.14 where we can amplify,
00:09:47.20 with a technique called polymerase chain reaction, or PCR,
00:09:50.26 various pieces of these chromosomes
00:09:53.26 and ask, what’s…
00:09:57.06 whether the one parent or the other parent’s version
00:10:00.18 is present,
00:10:02.10 because we’ve chosen regions where there’s a slight size variation
00:10:05.11 in the version from one or the other parent.
00:10:07.28 And so, those PCR products
00:10:10.15 can be run on gels.
00:10:12.05 This is a typical gel electrophoresis setup,
00:10:14.21 and this is from the University of Nebraska.
00:10:17.23 And what’s being detected are these DNA polymorphisms.
00:10:21.06 So, shown here, for example,
00:10:23.07 on the far end is one parent that has the F genotype.
00:10:27.10 And amplifying a bit of its DNA
00:10:29.29 — an address on one of its chromosomes —
00:10:32.07 gives a band of a certain size
00:10:34.08 on that gel electrophoresis.
00:10:36.04 The other parent, indicated R here,
00:10:39.11 is actually a bit larger fragment,
00:10:42.22 so it migrates to a higher position on the gel.
00:10:46.25 A F1 hybrid between both parents
00:10:49.07 is shown in lane H, there,
00:10:51.12 where you can see it has one copy of the F gene
00:10:54.16 and one copy of the one marked R.
00:10:57.05 And then, in a segregating population
00:10:59.28 from that F1 hybrid or heterozygote self-pollinating,
00:11:03.29 you can see at that particular locus
00:11:06.14 in the offspring all different types.
00:11:09.06 Some get one of each copy.
00:11:11.13 Some get only the one from the F parent,
00:11:13.12 others only the one from the H parent.
00:11:18.22 And so, how can we use this, then,
00:11:22.26 to determine the location of a mutant gene?
00:11:25.16 Well, again, if we get…
00:11:28.00 have a situation where we can pick out the mutants…
00:11:30.03 in many cases…
00:11:31.29 in cases of recessive mutants, they’re 1/4 of the population…
00:11:34.17 we can make DNA just from those recessive mutants.
00:11:39.03 And so, if we’re tracking, for example,
00:11:40.29 a gene that causes dwarfism,
00:11:43.00 which we have done,
00:11:44.26 we take all the DNA from all of the dwarf plants.
00:11:47.14 And because they’re homozygous for the mutant
00:11:49.15 — in other words, they’re little a little a at both chromosomes —
00:11:52.12 they have to have the same genotype there.
00:11:54.28 In other words, it’s all the green chromosome,
00:11:58.00 if you will,
00:11:59.18 that’s present in the plants that are homozygous mutant.
00:12:03.06 And then we can query all of the chromosomes
00:12:06.02 in these mutants
00:12:07.25 that have segregated in the population
00:12:09.14 and ask, do we find a co…
00:12:11.28 something called linkage to that mutant?
00:12:14.18 Linkage is a genetic concept
00:12:16.17 that indicates something is tightly associated
00:12:18.20 with something else,
00:12:20.10 so we’re looking for a type of DNA,
00:12:22.20 a type of address of a particular region of a chromosome,
00:12:26.16 that’s always associated with the mutant gene.
00:12:31.11 And of course, due to recombination events,
00:12:33.16 the chromosomes are a mixed-up pattern
00:12:36.16 of green and blue segments.
00:12:38.27 And imagine we took one of those polymorphic DNA markers
00:12:42.11 from the M1 part of the chromosome.
00:12:45.17 If we ran that type of gel that I showed,
00:12:47.23 we wouldn’t see any particular pattern.
00:12:50.02 We’d see a mixture of sometimes homozygous for the big A,
00:12:53.28 shown here in blue,
00:12:55.23 or homozygous for the little a,
00:12:57.28 shown in green,
00:12:59.12 and often a mixture.
00:13:01.10 Or if we took an address of a chromosome
00:13:03.24 down in the lower region of this chromosome,
00:13:06.16 we’d see a similar mixture.
00:13:08.10 But imagine we had a marker
00:13:10.14 that was very close or perhaps part of the gene itself.
00:13:13.14 Now what we’ll see is only a particular band,
00:13:16.21 only one band,
00:13:20.06 the band that’s the size of that region
00:13:23.06 from the one parent that contained the mutation.
00:13:26.21 And that tells us we’re getting very close to the gene.
00:13:29.16 And by doing this process repeatedly,
00:13:31.14 we can narrow into an interval
00:13:33.22 that often contains just one or a few genes,
00:13:35.15 and discover the gene.
00:13:37.11 And in fact, if you don’t have the capability in your classroom
00:13:40.26 to do this type of gel analysis,
00:13:43.20 we’re creating a system that lets students
00:13:46.09 choose random locations of chromatin…
00:13:48.04 of chromosomes
00:13:50.08 and determine if they can find linkage,
00:13:52.10 because we have software that will simulate these gels
00:13:55.04 to create sort of virtual gels,
00:13:57.16 where students can do these types of experiments
00:14:00.13 on the computer in the classroom.
00:14:05.09 So, these types of polymorphisms,
00:14:07.00 I wanted to end by saying,
00:14:08.20 enable certain things.
00:14:10.12 As I mentioned,
00:14:12.19 they enable us to find the genes responsible for various traits
00:14:14.23 like an albino or dwarfism or an abnormal leaf.
00:14:18.17 But once we know the difference in a particular gene
00:14:21.26 — a copy that’s a mutant versus wild type —
00:14:24.12 we can use that difference also to track versions of genes,
00:14:28.16 and versions of genes are known as alleles.
00:14:31.05 So, we can track either the mutant version,
00:14:34.08 that leads to an albino or a dwarf, or the wild type.
00:14:40.08 And examples of this in use in various realms are,
00:14:44.27 for example, marker-assisted breeding in plants and animals,
00:14:48.03 where those breeding new varieties of,
00:14:50.27 for example, cows or corn plants
00:14:53.09 will look at the offspring of a cross
00:14:56.26 and they’ll know that certain offspring will have certain traits
00:14:59.01 even before those animals or plants reach adulthood.
00:15:01.16 So, if you’re a plant breeder,
00:15:03.11 you can take only those plants you want
00:15:06.06 and advance them in your breeding program.
00:15:08.17 And of course, DNA polymorphisms are critical
00:15:11.11 in many tests of whether humans are carriers
00:15:15.28 of certain versions of genes
00:15:18.13 that might contribute to disease.
00:15:20.24 One example that’s not a DNA test
00:15:23.05 with which you might be familiar
00:15:25.20 is that all newborns are tested for a particular disorder
00:15:29.16 called phenylketonuria.
00:15:31.26 And that’s a disorder that can be controlled by diet,
00:15:34.05 so it’s important to find that genetic alteration
00:15:38.16 early after a child is born,
00:15:40.28 because then diet can be modified
00:15:43.08 so the disease is not manifest.
00:15:46.13 In the same way, we could look through our plants
00:15:49.04 and find those that, for example,
00:15:51.06 have the gene for dwarfism.
00:15:53.00 And I wanted to end by showing you
00:15:56.08 how we could correct that dwarfism, if we wish to,
00:15:58.02 because the plants that we have that are dwarf
00:16:00.11 are deficient in a particular plant hormone called gibberellin.
00:16:03.16 So, in this video I’m about to show,
00:16:05.06 we simply add gibberellin to the plants on the left
00:16:08.19 but not to those on the right.
00:16:12.03 And so, I’ll run this video,
00:16:14.14 and you can see how rapidly adding back
00:16:16.26 this critical growth hormone
00:16:19.06 can allow the plant to grow normally again.
00:16:23.24 And the hormone was just added.
00:16:26.13 Now you can see the time lapse going.
00:16:29.16 And within a day or so, you can start to see a striking difference
00:16:32.15 in those treated plants.
00:16:35.14 They’re now recovering from that dwarfism.
00:16:54.16 So, over just five or six days,
00:16:56.11 you can see the remarkable difference
00:16:58.00 between the untreated plant and the treated plant.
00:17:02.22 And this illustrates that we’ve developed these resources
00:17:06.16 that can be used to look at simple things like Mendelian segregation,
00:17:10.14 if you have the capabilities to do modern molecular biology in the lab
00:17:15.16 and molecular genetics
00:17:17.11 — or even if you don’t,
00:17:19.21 we have ways you can do it on a computer simulation —
00:17:21.28 as well as do physiological experiments with various mutants.
00:17:25.24 There’s an illustration of how to rescue a mutant,
00:17:28.26 how to restore a normal growth pattern to a deficient plant.
00:17:33.26 So, I’d like to end by thanking
00:17:36.12 the Plant Genome Program at the National Science Foundation,
00:17:40.05 as well as the Howard Hughes Medical Institute,
00:17:42.27 for funding our development of these classroom tools.
00:17:46.18 And I want to invite you to visit our website,
00:17:48.15 which is FPsc,
00:17:52.07 for Fast Plants, self-compatible,
00:17:54.08 dot wisc (for Wisconsin) dot edu.
00:17:58.01 And there’s much more material at the website
00:18:01.24 than I’ve had time to tell you about today.
00:18:04.00 Thank you.

This Talk

Speaker: Richard Amasino

Audience:

Educators of H. School / Intro Undergrad
Educators of Adv. Undergrad / Grad

Recorded: October 2014

Talk Overview

Richard Amasino explains that plants are great tools for teaching genetics in K-12 classrooms, because they are easy and inexpensive to grow and have mutant traits that can be visualized with the naked eye. He and his colleague, Scott Woody, developed a self-fertilizing plant from Brassica rapa, a small flowering plant with a very fast lifecycle. Amasino demonstrates how easily this Brassica rapa model can be applied in different ways to teach Mendelian genetics. Visit the FPsc Genetics Resources website (http://fpsc.wisc.edu/) to learn how to order these self-fertilizing Brassica rapa seeds and obtain lesson plans and experimental protocols for the classroom.

Speaker Bio

Richard Amasino

Richard Amasino is a Distinguished Professor of Biochemistry at the University of Wisconsin-Madison and a Howard Hughes Medical Institute Professor. His lab uses genetics and biochemistry to study plant development and the regulation of flowering. Amasino also encourages undergraduate students to explore genetics through experiments with Brassica rapa. Amasino has been honored with numerous awards for… Continue Reading