For additional examples and explanations of chromosomal changes, click on:
FOR USEFUL, GRAPHIC EXPLANATIONS,
CLICK ON CAUSES OF CHROMOSOMAL SPECIATION
In the following material, a number of technical terms are used.
To see definitions and explanations of these, click here: DEFINITIONS.
CHROMOSOMAL SPECIATION: FURTHER EXPLANATIONS
Responses to Questions
From Rebecca, an ENSI-using teacher:
Dear Dr. Nelson (ENSI co-director),
I read with interest the discussion (Chromosomal Speciation Models) about chromosomal speciation and the "conflict" between the idea of reproductive isolation and speciation via changes in chromosomes. While I haven't read the articles suggested in the discussion, I don't understand one sentence that is highlighted in the discussion:
"I hope that the number of fairly severe assumptions in that model make it clear why this form of speciation is not the commonest form in animals."
This doesn't really make sense to me since we know chromosome changes do in fact occur and we see the variations in chromosome number, inversions, translocations etc. in differently related species, so why isn't it a common form of speciation? I had assumed it was one of the major forms of speciation even in animals, given that it’s the genetic material and related species do in fact have these visible variations and they had to get different and be preserved through generations somehow. If this isn't considered to be common, can you tell me then what IS the most common form of speciation in mammals? Also, how did they get different? Or am I misunderstanding your argument? I wasn't sure why flowers were used in this instance as an example since they as you say, don't have the reproductive barrier, and the grasshopper story makes it look like it can only occur in very small populations (basically incest)....well, there must be some other way, unless all speciation is a result of brother sister mating......... thanks for clarifying as I was wondering about this "teaching dilemma" myself and wondering who had an easy enough answer for students to understand.
Good question. Let's see if I can help.
The key point is that for a new species to be isolated by chromosomal rearrangements, those rearrangements must strongly reduce fertility in heterozygotes. Otherwise, they can spread (or not) by natural selection.
Animals have to cross with other individuals, so any new arrangement cannot easily become homozygous except when there is a lot of close inbreeding. Moreover, in the original mutant, only a very small proportion of the gametes will typically carry the mutation.
If you look at variegated plants, you will see that entire branches can show a new color form (ignore for now that these are usually chloroplast changes). Each branch is derived from a small bud with a few cells, and each successive branch arises again from a small number of cells etc. right through to the germinal bud that gives rise to each flower. Thus, new somatic variation is plated-out. This is economically important. When a branch of a fruit tree bears superior fruit, that variation can be propagated by grafting buds from it on to other plants.
This plating out is very helpful for speciation. At the extreme, a diploid plant can give rise to a tetraploid somatic cell by failure of meiosis. This then can come to be the only kind of cell in branch and hence in all of the flowers on that branch. In meiosis, each chromosome will have a perfect match (two full diploid sets), and all of the derived gametes will have exactly the diploid set of the original plant. Add self fertilization and all of the seeds derived from that branch will be tetraploids. But if these cross with the diploid plants around them, there will be much triploid sterility. So a single mutant branch can give rise to a new species. And because so much of morphology is affected by chromosome number, these will be ecologically different too (survival will depend on an available niche). Instant speciation.
Animals also have a lot of somatic polyploidy (and aneuploidy, an abnormal number of chromosomes). Your liver cells are mostly hexaploid and many of your skin cells are tetraploid. (Teachers are sometimes stunned to realize that we are somatic diploids only for a bit after we become zygotes. Thereafter we become predictably ploidy mosaics.) But since the germ line is isolated, this is usually not heritable (no ovules from your skin cells, etc.). And even when it affects the germ line, since animals cannot self fertilize, it is difficult to produce a new uniform population (new diploid sperm usually must fertilize haploid eggs giving rise to largely sterile triploids). The best away around this in animals is very small populations. All very small populations are automatically highly inbred. Sib matings are ideal (both sibs carry same new arrangement heterozygously by inheritance from one parent). And only very small populations allow the new form to rapidly stabilize.
Real life has lots of further interesting ways around these problems. Articles and books on chromosomal speciation will lead you through these.
But the essence is that very small populations are usually needed in animals, just as you wrote. And that somatic plating out and self-fertilization (and often, very small breeding populations) make chromosomal speciation much easier in plants.
In animals, geographic isolation [allopatry] has been the driver of much speciation, most clearly in vertebrates. Geographic isolation has also been important in plants. Climatic shifts have driven many cycles of geographic isolation and reconnection, especially since the Pliocene. Continental fragmentation and migration to islands involves much geographic isolation also. [Click Here for a Quick Speciation class participation activity demonstrating allopatry.]
Geographic isolation often involves small founder populations and may involve frequent population crashes. Different places also select for ecological differences and may select for other important differences (as in mating call systems).
From Tom, another ENSI-using teacher:
I was aware of the variegated plant story, but unaware that polyploidy extended to somatic cells of mammals. In retrospect this makes great sense as a defense against cancer. Given cancer occurs after the occurrence of 5 distinct categories of genetic mutation (according to old classic mutation studies), it makes sense that skin and liver cells would have some sort of defensive mechanism to up the ante as it were, as skin and liver are under greatest "mutagen attack".
My question is as follows: I am most curious whether there is any evidence that either epidermal or hepatic stem cells are aneuploid (have abnormal numbers of chromosomes)?
Regarding the chicken-egg question of chromosomal aneuploidy vs. speciation - I was flumoxed to discover that William Bateson the founder of modern Genetics actually addressed this question first! How many modern textbooks actually even mention this great man's name? These insights are summarized as the Bateson-Dobzhansky-Muller Model.
According to my glib and naive understanding of the Bateson-Dobzhansky-Muller Model, hybrid inviability is a genetic phenomenon and not a chromosomal aneuploid incompatibility problem. For example - the classic inability of mule-horse hybrids to produce gametes occurs by some breakdown in prophase and not due to irresolvable mess-ups at the metaphase plate.
My own "AHA! moment" only occurred when I realized that the karyotype of the domestic horse (2n = 64) differs from that of Przewalski's horse (2n = 66) by an extra chromosome pair either because of the fission of domestic horse chromosome 5 in Przewalski's horse, or fusion of Przewalski's horse chromosomes 23 and 24 in the domestic horse.
This is the clincher! Przewalski's Wild Horse and the domesticated horse can be crossed and do produce fertile offspring, with varying karyotypes! This is significant to a correct understanding of Evolutionary theory and why I constructed the attached worksheet (The Chromosome Shuffle).
Theoretically, Mule-Horse hybrids could form trivalents just like Przewalski-Horse Hybrids, but they do not - something else must be going on along with the Bateson-Dobzhansky-Muller line of reasoning.
The story of Przewalski's Wild Horse and the domesticated horse hybrids indicate that chromosome rearrangements may perhaps reduce fertility but do not constitute an immediate barrier to interbreeding.
However, accumulated chromosome rearrangements would eventually constitute a reproductive barrier to inter-breeding.
I explain this to my students along these lines: Population A gives rise to Population B accompanied by some chromosomal rearrangement. Population B gives rise to Population C accompanied by a different chromosomal rearrangement. A can still interbreed with B and B can still interbreed with C but A cannot interbreed with C.
What about single chromosomal rearrangements that do result in reproductive isolation? The new mutant is repulsive or somehow physically incompatible for sexual reproduction with members of the ancestral population. Such events do exist, and as Craig has mentioned, intra-familial incest easily slices through that Gordian knot.
Consider the genetic diversity of Chimpanzees and Bonobos, our nearest relatives. The number of these animals is small compared to ours, but their genetic diversity is much larger than that of our species. In fact, the entire 7 billion member human species has a level of genetic diversity that is on the order of a large chimpanzee population. Genetically, humans appear to be a very inbred subset of the chimpanzee species.
If you would like copies of the original activities for your students to do - please go to my quia site. and click on:
Zimmer's Chromosome Shuffle.pdf
Human Chimp DNA.pdf
The strange case of Oliver the Chimpanzee.pdf
[For reasonable responses to these, send your reguest (from your school email address) to the Webmaster.]