Genetics

Gregor Mendel in the 1860s (the time of the US Civil War) was an Augustinian monk at the abbey in Brno, now in the Czech Republic. Mendel uncovered many important principles of Inheritance of characteristics from one generation to the next.

Because of the heavy math dependence expressed in Mendel's work, the biologists of his day could not appreciate his contributions. He presented the work in person and the scientists in the audience had no idea what he was talking about. Math was not a requirement for becoming a biologist in the 1860s.

Mendel's work was published in a reasonably good journal but the readers of the day did not appreciate it worldwide. His work was essentially "lost" in the library archives for 50 years.

After Mendel had been dead for some years, his work was rediscovered in the early 1900s by three more-modern biologists. These scientists did have some math and statistics background. These scientists knew what had been discovered about cells and tissues in the late 1800s. Discovering Mendel's work in the published journal, these three scientists recognized that these were very important findings. And as biology continued to unfold through the discovery of chromosomes, DNA, and cytology, Mendel came to be much appreciated. He is now often referred to as the "father" of genetics. While perhaps a play on words, it is a reasonable accolade for him.

Let us recall what we know today, but that was unknown to Mendel or any other scientist of his day:

egg (1N) + sperm (1N) syngamy
----------------->
zygote (2N) --> embryo (2N) --> adult (2N)

Mendel did his important work with garden peas (Pisum sativum). This plant is normally self-pollinating...meaning that the reproductive parts of the flower are contained within a petal closed to form a pouch. When a pollinating bee arrives to harvest nectar, the bee's visit vibrates the pouch and pollen is moved from anther of stamen to stigma of carpel all within this pouch. Pollen never gets on the bee. In other words not only are pea flowers bisexual, they only pollinate themselves. There is a common gesture that the vulgar among us show to others indicating that they carry out this same kind of act. But of course that act is impossible for unisexual humans. For peas, self-pollination is a way of life!

I don't think Mendel fully appreciated this fact of life for peas. It gave Mendel a way to collect pea seeds from the worldwide network of the church and grow them in the gardens of the abbey without having the bees mix up all the genetics. The varieties could be grown in common gardens and stay true to their genetic background. Mendel had to specifically intervene to intentionally cross two strains of his pea stocks. He had to tear both flowers open and put the pollen from one flower onto the stigma of the other. So he had to appreciate self-pollination that much. But later in his life, Mendel went to leading scientists of his day to hear their criticisms of his work (which they did not understand), and took their advice to study another plant rather than peas. Mendel tried to repeat his work with hawkweed as suggested, but this plant was actually apomictic...meaning that this plant was not appropriate for genetic work at that time...it reproduces without sex at all! So after Mendel heeded advice none of his later work was productive. He became Abbot of the monastery and did more administrative work than scientific work, assuming wrongly that his work with peas was probably a special case rather than the general case.

Among Mendel's stock peas were some that were tall, requiring a fence for support because they produced long vines. Other stock peas were dwarf that formed knee-high "bush" forms that did not need a fence for support. Today most garden peas come from dwarf stock because they are easier to grow, easier to cultivate, and easier to pick by machines. Mendel wondered how the tall and dwarf characteristics were inherited from one generation to the next. So he decided to cross the two strains.

Let us remember that he has been growing the tall and dwarf stocks in common gardens. Plants from tall stocks always give seeds that produce tall plants in the next generation. We call this true-breeding. Likewise the dwarf plants produce seeds that always grow into dwarf plants in the next generation. In other words both peas parents involved in this first cross are true-breeding. This careful attention to the starting plants was a personal characteristic of Mendel that made him especially well-suited to this work.

So Mendel crossed the tall and dwarf parental peas by tearing open the flowers and cross pollinating them. He let the pods develop and harvested the mature seeds from the pods. He planted them to see how the tall and dwarf characteristic would appear in the next generation (F1). The expectation that scientists of this time would be that he would get some mixture of tall and dwarf, or might get some kind of medium size plants. Mendel found that all of the plants were tall.

But here again, Mendel is different from the biologists of his day. He is aware of math and statistics. He knows he cannot just collect a few peas in the F1 generation. He knows that he must keep meticulous records of his resulting plants. So he saved and counted hundreds of F1 plants from this cross. All of them were tall...there was not even a single dwarf plant among them! There was not a single medium-size plant there either. All came out tall!

tall x dwarf
all tall

This unexpected result led Mendel to wonder what had happened to the dwarf trait. Was it lost forever? Was it hiding somehow? And while scientists of Mendel's day might have dropped the study here, Mendel was persistent and continued his crossing to the next generation (F2).

F1 tall x F1 tall
F2

So Mendel crossed two of his tall F1 plants to make the F2 generation. Of course this mating really did not involve Mendel. Remember, peas naturally self-cross. So Mendel just let his F1 plants go to seed, saved the seeds, planted them and discovered to his amazement that the F2 generation was NOT uniform in height! In fact 3/4 of the F2 plants were tall and 1/4 of the F2 plants were dwarf. Again there were no plants of medium height. And again, Mendel being meticulous, means that he did the cross several times and counted hundreds of F2 plants to be sure his 3:1 ratio was uniform among the several crosses.

Mendel reasoned that the dwarf trait must have been held in hiding in the F1 plants to allow the trait to reappear in the F2 generation. He was fascinated by the 3:1 ratio that was quite uniform and repeatable. He used his math and probability training to determine how this could happen logically. For the tall and dwarf characteristics to both be held by the F1, then there must have been height contributions from both parentals! In other words, Mendel has elegantly demonstrated that both the male and female parent must provide genes to the offspring. There must be a genetic contribution from both the sperm and whatever the female gives to it. Remember, the Human egg has not been found yet...and neither has the plant egg in 1865! But here is Mendel showing that they MUST exist. The sperm is not some seed...but rather a gamete that joins with a female gamete, the egg to form a zygote! This is ground-breaking! Mendel, without knowing anything of chromosomes or DNA has demonstrated that the pea plant must be diploid (have two genes for every trait!).

Mendel also realizes that if the F1 plants have both tall and dwarf traits but only show the tall height, then the traits must have some kind of relationship that allows one trait to be observed and the other to remain hidden. Today we would call the observed trait "dominant" and the hidden trait "recessive." So Mendel has discovered not only that genes are particles that are inheritted from both parents, but that one gene can be dominant to another when in combination.

Because all of the F1 plants are tall, then tall is the dominant form (allele) of the height gene and dwarf is the recessive allele. When the tall and dwarf alleles go walking the tall gene does all of the talking!.

Mendel wanted to start showing his logic in some symbolic way and to this day we use his method of assigning letters of the alphabet to indicate the alleles for the genes of an organism. Today the convention is to use the letter of the alphabet for the recessive allele in our symbolic logic. In other words, we will use D and d (as in dwarf) rather than T and t (as in tall). We use the uppercase letter for the dominant allele and the lowercase letter for the recessive allele.

D = tall allele
d = dwarf allele

Mendel's plants have received two alleles, one from each parent. So the two parental plants that he started with are represented thus:

P: tall x dwarf
    DD       dd

The tall parent got a tall (D) allele from both of it parents and so it is homozygous (homo-same genes zygous-in zygote) dominant (DD). The dwarf parent got a dwarf (d) allele from both of its parents and so it is also homozygous but is homozygous recessive (dd).

When these parentals were crossed, the resulting F1 generation got a tall (D) allele from one parent and a dwarf (d) allele from the other parent. The F1 plants are heterozygous (hetero-different genes zygous-in zygote) and can be represented thus:

F1 all tall
    Dd

Today we call the look of the plant its phenotype. We call the genetic combination its genotype. So in this symbolic logic we have seen three different combinations of genotype but only two phenotoypes:

GenotypeDDddDd
Phenotypetalldwarftall

Of course Mendel had to extend this logic to the F2 generation to explain his 3:1 ratio of tall to dwarf. He did a masterful job of this using his knowledge of probability and frequencies, etc. But, again, this logic was lost on the scientists of his day. The scientists who rediscovered his work and others who appreciated it developed an easier way to do follow the logic. This way was the use of what is known today as the Punnett square. This simple table could be understood without all of the probability theory behind it. The scientists of the 1900s "got it!"

In a Punnett Square for just one gene, such as height in peas, there are two rows and two columns:

   
   

The heading for each row represents one of the gametes that the female plant gives. Remember that this was all theoretical because no one knew of female contributions in Mendel's day!

F1
tall
Dd
x F1
tall
Dd


possible
gametes
D  
d  

The heading for each column represents one of the gametes that the male plant gives. In the case of Mendel's peas, these are F1 plants that are self-pollinating. So Mom IS Dad...and the column headings are the same as the row headings:

F1
tall
Dd
x F1
tall
Dd
 possible gametes
 Dd
possible
gametes
D  
d  

And now the genotypes of the F1 are filled into the cells of the table by making the combinations of row heading and column heading for each cell:

F1
tall
Dd
x F1
tall
Dd
 possible gametes
 Dd
possible
gametes
DDDDd
dDddd

Knowing how the alleles of the genotypes determine the phenotype, we can now add the phenotype to each cell:

F1
tall
Dd
x F1
tall
Dd
 possible gametes
 Dd
possible
gametes
Dtall
DD
tall
Dd
dtall
Dd
dwarf
dd

The beauty of this Punnett square is that it shows us in proper frequencies how the 3 tall to 1 dwarf ratio was achieved! As you can see above, 3/4 of the F2 plants are tall and 1/4 of the F2 plants in the table are dwarf. And the square shows us these ratios without much knowledge of how the probability logic worked to achieve it. The biologists of the early 20th century understood this easily.

So let's put all of this work onto a single space to be sure we clearly understand the three generations of peas that helped Mendel understand his 3:1 ratio:

P tall
DD
x dwarf
dd

F1 all tall
Dd

F2 = F1
tall
Dd
x F1
tall
Dd

 possible gametes
 Dd
possible
gametes
Dtall
DD
tall
Dd
dtall
Dd
dwarf
dd

But Mendel was, again, not quite satisfied with this. Being a meticulous scientist, he wanted to put this logic to the test. The scientists of his day would never have gone to the next step, but Mendel set it up beautifully to follow the scientific method. If his hypothesis about inheritance of the height genes was correct, then he should be able to distinguish those tall F2 plants from each other. Notice in the final Punnett Square above that there are two kinds of tall F2 plants: 1 of three is homozygous dominant (DD) and two of the three are heterozygous (Dd). He designed what we now know as the testcross to test his hypothesis. He would cross each of his F2 Tall plants which could have either the DD or Dd genotype with a dwarf (dd) plant. He would predict one of two possible outcomes:

If the F2 Tall plant is DD, then the testcross would give these results:

Test Cross = F2
tall
DD
x  
dwarf
dd

 possible gametes
 dd
possible
gametes
Dtall
Dd
tall
Dd
Dtall
Dd
tall
Dd

But if the F2 Tall plant is Dd, then the testcross would give these results:

Test Cross = F2
tall
Dd
x  
dwarf
dd

 possible gametes
 dd
possible
gametes
Dtall
Dd
tall
Dd
ddwarf
dd
dwarf
dd

Notice that these test cross results tell you what the genotype of the F2 Tall parent is. If you get lots of offspring that are all tall then you can be sure that the F2 parent was DD (all tall!). If your testcross gives you a mixture of tall and dwarf, then the F2 parent has to be Dd (half tall, half dwarf). In fact you only need one dwarf offspring to decide that the F2 parent was Dd; you cannot get any dwarf offspring if the F2 parent is DD! See the power of Mendel's test cross?!

So Mendel did test crosses of the F2 tall plants and found that 1/3 of them were DD and 2/3 of those plants were Dd. This result indicated that his hypothesis was correct. This logic was right.

Mendel probably would have been a hero in his own lifetime had anyone been able to understand his work at the time. But it is only recently that scientists have had to take required math, and they now have a lot more biological knowledge to build upon so we can fully appreciate the significance and importance of Mendel's contributions.

Mendel tested the inheritance of other genes too. If you are not yet comfortable with Mendelian genetics, and would like a graphic approach, move on to my page on Mendel's Seed Color Trials. Then, for a more hands-on approach, try also my interactive page on Mendel's Seed Shape Trials.


 

While many gene situations work out this simply, not all do.

Mendel only show the parts of his work that actually fit predicted ratios. Other crosses that didn't fit the model were left out of his articles, but ARE found in his data books. We now know how these worked and why the expected ratios were not observed by Mendel. His work was also extended by the three scientists and then others in organisms other than garden peas.

Here is an example that was observed in the early 1900s in snapdragons. The flower petal colors were easily observed and put into study. True-breeding (homozygous) stocks of red and yellow snapdragons were available. When these were crossed the predicted results did not match up with Mendel's work!

P red x yellow
F1 all orange

Obviously this is a case where the dominant/recessive relationship is different. When red and yellow alleles go walking they both do some of the talking! In other words, they are co-dominant! Because both yellow and red pigment is being made, we are seeing orange flowers in the F1 plants.

In trying to write down our symbolic logic we are faced with the dilemma: shall we use R/r or Y/y for our symbols? Well clearly neither red nor yellow is recessive so neither choice would be conventional. So we move to a third choice...perhaps P/p for petal color. Of course since both red and yellow are dominant, we will use superscripts to tell the two dominant alleles apart:

P   red phenotype = PRPR   x   yellow phenotype = PYPY
F1   all orange phenotype = PRPY

OK so now things will get interesting again when we move on to cross two of these orange F1s to make an F2 generation:

F1
orange
PRPY
x F1
orange
PRPY

Here is the expected outcome from this cross shown in a Punnett square. Notice how we are allowed only one base symbol and one superscript at the heading for each row and column:

 possible gametes
 PRPY
possible
gametes
PRred
PRPR
orange
PRPY
PYorange
PRPY
yellow
PYPY

As you can see, Mendel's rule of a 3:1 ratio fails here in one sense. However, this exception UPHOLDS the rules of how genes are inherited from one generation to another. You can see that the 3:1 ratio is instead a 1:2:1 ratio but this is only because the alleles involved are co-dominant. So the world is not just recessive and dominant...we obviously got over it!

But you might also notice that thanks to the fact of codominance there is no need to test cross any of our F2 plants in the Punnett Square! The genotypes give unique phenotypes so all of the F2 plants have known phenotypes! So while we may have altered Mendel's simple world, the new dimension in this case is actually making life easier for the geneticist!

But wait! There's more! No, not any Ginsu knives, but more alleles are coming along. It turns out that there is a sort of recessive...white! So this new wrinkle gives us more options for diploid genotypes for snapdragons:

PRPR = red
PRp = pink
PYPY = yellow
PYp = cream
PRPY = orange
pp = white

Now whether you call white recessive, or maybe a diluting co-dominant, or that Red and White are "incompletely dominant" is kind of up to you. Is your glass half-full, half-empty, or just fine with you? Regardless, this three-allele system is perhaps the simplest explanation for the color range we observe in snapdragons!

On the Human Affairs side of our course, human blood types work something like this with three alleles controlling the blood type you have.

IAIA = Type A
IAio = Type A
IBIB = Type B
IBio = Type B
IAIB = Type AB
ioio = Type O

Another human example is the base color for human hair color. Again there may be several genes contributing to hair color, texture, and absence(!) but the simplest explanation for base hair color works something like this:

Alleles:

HBd = blonde
HBr = brown
hR = red
hbl = black

Possible Genotypes and Phenotypes:

HBd HBd = blonde
HBd HBr = mousy brown
HBd hR = strawberry blonde
HBd hbk = blonde
HBr HBr = brown
HBr hR = auburn
HBr hbk = brown
hR hR = red (orange)
hR hbk = red (orange)
hbk hbk = black

Important!: Please note that the double recessive hblhbl is the most MOST common genotype in world! It is critical for you to learn from this that dominant does not mean common! The fact that most of the people have black hair does not mean that black is dominant! Frequency and dominance are NOT the same thing. I want to be sure you understand this.

To drive the point home that frequency and dominance are not the same concept from a plant perspective here is something you have learned in your studies of garden peas. The most common pea on this earth is dwarf with white flowers that produce wrinkled green pea seeds. You should realize that dwarf stature requires double-recessive, white flowers require double-recessive, wrinkled seeds require a double-recessive, and green seeds require a double-recessive. In other words, the most common pea in the world is a quadruple-double-recessive (dd aa gg rr)! It is hardly rare!

It is also true that a particular trait can be influenced by multiple genes...not just multiple alleles for just one gene. We sometimes call this kind of inheritance quantitative inheritance.

Crop yield in plants is a good example. Obviously how well a plant deals with light, water, fertilizer, pests, temperature, etc. are probably controlled by different genes. But all of these genes would ultimately influence the yield of the plant per acre of crop field. If we assume that the dominant alleles provide some positive impact on yield, then a plant with the genotype, AABBCCDDEE, would be our highest-yielding genotype. A plant with the genotype, aabbccddee, would be the lowest-yielding genotype. If these two mate, the F1 would be AaBbCcDdEe with some kind of moderate yield. But if we cross two F1 plants we could get anything from AABBCCDDEE to aabbccddee with lots of differences among the progeny! The yield per plant would probably follow some kind of distribution curve with AABBCCDDEE and aabbccddee being rare extremes and genotypes near the middle (e.g.: aaBbCCDdEe) being far more common.

Popping back to Human Affairs, human skin color appears to be a case of quantitative inheritance too. The best explanation for our base skin color is based on shades of brown caused by dominant alleles among five genes. So AABBCCDDEE would be a person of very dark brown color (in fact, the skin color of this person might be described as "blue" because of some interference caused by the surface skin cells backed by the extremely dark skin color). The opposite extreme aabbccddee would be a person who is such a pale brown color that you can see the blood coursing in the capillaries within the skin. The resulting color is described as "pink" because of this. But most of the human population is found between these extremes rather than at these extremes. A person of medium skin-tone (perhaps an African American thanks to combined genes from African and European ancestors) would have a genotype of AaBbCcDdEe. Again, when two such people mate:

AaBbCcDdEe   x   AaBbCcDdEe

...the children can be just about any color from very pale (aabbccddee) to the deepest brown (AABBCCDDEE) but with most of the children falling in between these extremes. Because people do not understand this, they often falsely accuse the wife of infidelity. I'm sure you have seen this on Maury and Jerry...lots of speculation because two "typical" people have a baby with an extreme color. But that can be explained with complete fidelity!

Our discussion of human skin color reminds us that there is yet another factor that can impact the phenotype...the environment. The color of our skin is not only influence by the number of dominant alleles we have among five genes (the genotype)...but is also impacted by sunlight! What we see is the product of the genotype and the environment working upon that genotype.

Phenotype = Genotype + Environment

So as we expose our skin to the Ultraviolet light from the sun or certain kinds of lamps we have invented, our skin can change color from our base tone to even darker colors. So the expression of some of these five genes is increased by light exposure and more brown pigment (melanin) is made. This fact, of course, is the basis for tanning salons and beach bunny businesses. It is interesting that our society has made such stigma of dark skin colors while people pay to darken their skin. Hmmm...sounds like a social science study! On the biological side, just about every genotype can deepen the base color by UV exposure. The palest genotypes will mostly burn and peel. The darkest genotypes are already at maximum production and so respond less well to UV. Intermediate genotypes will respond strongly to sun exposure because they CAN produce melanin but are not normally producing as much as they could.

Back to plants, again yield is impacted by genotype and environment. Obviously having the right seeds for your crop is important...but getting soil nutrients, light exposure, and water levels right, and controlling pests and weeds will impact how well even the best seeds can perform in terms of crop yield!

Who mates with Whom?

One other feature of genetics has to do with negative characteristics that are found in each organism's genome. Our family has passed along to us some alleles that are defective and could lead to disease. This are typically inherited as recessives, so you don't have the disease because your other parent gave you a functional allele. You are heterozygous for this disease but do not suffer.

But with whom will you mate? If you pick a close relative, the chance is that this person also has inherited the family allele for the disease and there will be a 1/4 chance that one of your children will have the disease! This problem was noticed way before Mendel and has long been called inbreeding depression. So society produced taboos or laws decreeing that you must mate outside your family to some extent.

We all know that one of the best dogs is that mongrel that is some strange mix of the various breeds of dogs in the neighborhood. It is smart, tough, disease free, and has great temperament. But people go to great lengths to inbreed just certain dogs to "stay true" to certain breeds...like dachshunds and sharpeis. Of course these "pedigreed" dogs are expensive...and may have some problems due the inbreeding of their types. So dachshunds can have back problems, German shepherds can have hip dysplasia, and Dalmatians often go blind. So we haven't quite learned the lesson of inbreeding depression.

In fact we haven't even learned it from a human point of view! Our society in addition to incest taboos and laws nevertheless urges young people to "marry your own kind." That's a very mixed message! It has been taken to the extreme in the monarchies of Europe and some other places. Monarch families were just "too good" to mate with "commoners" and so marriages were arranged among cousins who sat on the thrones in various places. Queen Victoria (England) apparently had a mutation for hemophilia on her X chromosome. This passed unnoticed to her many daughters and granddaughters. The gene then popped up in the next generation of crown princes! The famous example was when her granddaughter Alexandra married Nicholas II of Russia. The tsarevich, Alexis, was born a hemophiliac and there were no other sons. So the succession of the Tsar was obviously going to be a problem...that and corruption and social problems in the country led ultimately to the Russian Revolution and the execution of the royal family. Tay-Sachs disease occurs at high frequency among inbred Jewish populations. Bipolar disorder occurs at high frequency among inbred Irish populations. Polydactyly occurs at high frequency among inbred Hutterite populations.

So I guess the take home lesson is: DON'T marry your own kind.

OK so there is some advantage to mating outside the family and religious and ethnic group. Is there a name for that? Yes, it is known as hybrid vigor. Just as we observed in the mongrel dog, the outcrossing covers up the recessives of one family with dominant alleles from another for a good outcome. Does this explain why the US does so well in Olympic games? OK there's another social science project for someone to do.

From a plant point of view, we have understood hybrid vigor quite well. The best example comes from a sad period of human history. Europeans arrived in North America and brought with them weapons technology and biological diseases against which the native peoples had virtually no defense. The Europeans took the land and the seeds (the germplasm) that belonged to the native peoples. Some of our most important crop plants today were derived from the germplasm taken from those peoples. Our example here is corn. Various tribes of native peoples had different strains of corn unique to those tribes. As Europeans displaced these tribes and collected the seeds, they grew the various kinds of corn in common fields. Because corn is wind pollinated, these strains of corn cross-pollinated and hybrid strains were produced.

wild corn A
low yield
    x     wild corn B
low yield
hybrid corn
high yield

This hybrid corn had much taller plants with more vigorous defense against pests and diseases, the extra leaves produced more and larger ears of corn. The ears had more kernels and larger kernels than either of the strains of wild corn from the different native peoples. Today much of our agriculture depends upon hybrid seeds that possess hybrid vigor.

If it is desirable to out-cross rather than in-breed, then how did plants evolve to enhance outcrossing rather than inbreeding?

The most extreme form of forced outcrossing was the evolution of unisexuality (dioecious) in whole plants. In many species the sexes are found in flowers on separate plants. If you want to grow Kiwi fruits, for example, you need both male vines and female vines growing near each other. The pollinator takes the pollen from flowers of the male vine to the flowers of the female vine. Obviously all of the Kiwi fruit will be formed only on the female vines.

Of course this fact escapes people when planting holly bushes in their home landscapes. Again holly is dioecious. So it too has male plants that produce pollen but never any fruit...and female plants that must receive pollen to produce the fruit. Obviously one needs to plant at least one male in the home landscape to pollinate all of the females if you like the red berries to form on the bushes. But I have seen people landscaping new homes go to the nursery and load the truck only with females with fruits showing. Next year they will have nice bushes with no red berries. Similarly I have known people who noticed one of the holly bushes in their landscape was producing no berries, so they cut it down...their only male plant! Ouch!

Other plants are spatially bisexual but separate their male and female functions in time. So the bisexual flower may produce its pollen first (protandry) and when all of it has been removed, then grow out the carpel and open the stigma to receive pollen from elsewhere. Alstroemeria which may have been dissected in lab is an example. Of course there are other plants that use the opposite sequence (protogynous) and open the stigma for outcrossing and later grow out their own anthers when foreign pollen tubes are already growing into the ovary.

Perhaps the most bizzarre life history is in the cucumber family where the vine produces male flowers first, then later makes bisexual flowers, while still later produces female flowers, and then at the end of the year makes female flowers that are parthenocarpic (literally virgin-fruits that need no pollination). So this plant is multiply- transgendered!

One of the most cryptic forms of avoiding self-pollination or inbreeding is found in many tree fruits (sweet cherry for example). In these species, the flowers are bisexual and the timing is the same for both pollen and embryo sac. However, if their own pollen gets on the stigma, it is prevented from participating in syngamy at one of several levels:

Obviously for these species you need two trees near each other to cross pollinate successfully. Reputable nurseries will advise gardeners of this situation when they attempt to purchase just one tree of these species (sweet cherry, pear, filbert, almond, etc.).

Alright, we need to outcross and we have mechanisms to prevent inbreeding. But how far out can we outcross? And what happens if you go out too far? Obviously bees are not sterile and carry pollen from multiple species and this gets on stigmas of the "wrong" species. The problem is worse for wind-pollinated species because you don't have a magic bullet with a brain to know which flowers are rewarding them.

So plant species obviously have ways to detect wildly foreign pollen that is just not compatible and can probably stop it from germinating, growing, shedding sperm, or the sperm joining with the egg successfully. But these barriers to way-out crossing are probably not sufficient to completely prevent species from crossing that are more closely related.

I know of no human examples of successful breeding with other species. But it is commonly known that a male donkey (a Jack) will mate with a female horse (a Mare) that is in heat if he gets half a chance. These are different species...but conception does occur and the offspring animal is known as mule. While there are male and female mules, they generally do not mate and are considered to be usually sterile. Of course there are some reports...

In plants, crossing the species lines is a rather common occurrence and the outcome is NOT always sterile! In fact some of our important crops arose this way in prehistoric times under early human cultivation. In other words some of our "normal" crops are really GMOs (Genetically Modified Organisms)...it is just that the modification was achieved before people knew much about science or genetics. The example I will use here is bread wheat. This plant is a hybrid with genetic information from three different natural grass species!

Prehistoric humans started cultivating various grasses to eat the seeds as food. These wind-pollinated species were being grown side by side and so some "unnatural" crosses happened. As best we can tell Triticum urartu and Aegilops tauschii crossed at some point. The resulting hybrid was, like the mule, sterile. This is because the Triticum and Aegilops chromosomes do not pair up properly to form egg and sperm...they are too different to match up. But while this would be a dead-end for a mule, this is not a dead-end for a plant. Plants at some frequency are able to prepare for a cell division but then fail to go through with it...doubling the chromosomes without separating them. After that there are two sets of Triticum and two sets of Aegilops chromosomes available in the cell. Because the chromosomes are doubled you now have a fertile tetraploid (four sets of chromosomes). This new species, created by human agriculture, had properties of both the Triticum urartu and the Aegilops tauschii. But this was not the end of the story...people were still cultivating multiple species of grasses in their fields. Another species being grown was Aegilops speltoides and this allowed another strange combination of pollen and embryo sac. In this case a gamete from the hybrid...with one set of Triticum urartu and one set of Aegilops tauschii chromosomes...joined with a gamete with one set of Aegilops speltoides. This syngamy produced a plant with three sets of chromosomes (triploid) but again because these do not match up properly, they were sterile. However again plants sometimes can double their chromosomes spontaneously. This happened in prehistory so that the sterile triploid became a fertile hexaploid. This GMO (Genetically Modified Organism) is what we call bread wheat today. It does not occur in the wild...just like corn does not occur in the wild...because it is a species that we humans created at a time estimated to be about 7500 BC.

In the diagram below, the pathway by which ancient humans created a species is diagrammed. Please notice that the symbols used in the logic do not represent alleles of a gene...instead they represent an entire set of chromosomes for a particular natural species.

Triticum urartu
diploid wheat
AA
x Aegilops tauschii
diploid grass
DD

sterile diploid
AD

spontaneous doubling

fertile tetraploid
AADD
x Aegilops speltoides
diploid grass
BB

sterile triploid
BAD

spontaneous doubling

Triticum aestivum
(bread wheat)
fertile hexaploid
BBAADD

Today we have discovered a range of drugs that help us create GMO species more easily. Perhaps the most famous of these is a chemical made by the corm of autumn crocus to poison herbivores. The crocus is called Colchicum autumnale and the drug it makes is called colchicine. That drug prevents cells from finishing cell division, so that the chromosomes double in the herbivore. For virtually all mammals, adding even one extra chromosome is lethal so this doubling of all the chromosomes is a potent toxin. But when we have a sterile diploid or triploid from some strange cross we make, we can use colchicine to double those chromosomes so that fertility is restored. There are a range of newer drugs that also work this way.

 

This page © Ross E. Koning 1994.

 

 

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