mikelepore said:
Please explain something I don't understand about the evolution of animals that have sexual reproduction.
I thought that being a separate species means an animal will have sexual intercourse resulting in fertile offspring only if the partner is of the same species.
I shall cite the giraffe as an example because of an explanation about its evolution that was once taught to me.
If I understand correctly, the giraffe with a long neck probably came into existence because at one time a mutation occurred inside in a shorter-neck parent, such that the offspring had a longer neck.
Am I correct in saying that the new long neck animal will continue as a distinct species only if does not mate with short neck animals? But why? Would two animals, which are otherwise sexually attracted to each other, stop and think, "I'm unwilling to mate with you because I can see that your neck is too long (or short)"? Or did the mutation that made the offspring's neck longer also make the reproductive cells or organs physically incompatable with those of the short neck animals?
You are incorrect. The new long neck animal could become a new species even if it mated with short necked individuals. The new long necked animal may not even be a separate species, technically. The new species would develop over time, after many mutations.
mikelepore said:
In either case, how did that long neck animal find a mate, so that the new species could survive?
A hybridization barrier is not a toggle. There are gradations to hybridization barriers. Many times, two populations within the same species can hybrids with a slightly decreased viability. Some small genetic difference makes the hybrid individuals slightly more vulnerable, but the "pure" individuals with a gene slightly more fit.
My favorite example occurs within the human population. Human beings have at least two Rh blood types: Rh positive and Rh negative. You agree that we are the same species, regardless of our Rh blood type. You agree that this is merely a small variation in the same species. Yet, there is a very slight hybridization barrier between the two populations.
There is an allele in most primates, including that contains genes that determine the blood type. If a person has two copies of either type of gene, then the baby will be the same blood type as both parents. However, a hybrid baby may be a different blood type then the mother. Then, there is a chance that the mothers immune system will attack the baby during childbirth. This is called blue-blood syndrome.
I have heard the argument that "Rh baby syndrome" is a minor problem because modern hospitals know how to handle it. Just use prenatal blood transfusions! However, it probably was close to lethal before the 17th century.
Here you see a hybridization barrier within a species (human beings) which can not be eliminated by dilution. Furthermore, it has not been eliminated by natural selection.
If an Rh woman mates with an Rh positive man, the second and third babies may be sick with Rh baby syndrome. I doubt this will lead to a new species of human now that medicine can treat it. However, it is an interesting hybridization barrier.
http://en.wikipedia.org/wiki/Rh_disease
“Rh disease (also known as Rhesus isoimmunisation, Rh (D) disease, Rhesus incompatibility, Rhesus disease, RhD Hemolytic Disease of the Newborn, Rhesus D Hemolytic Disease of the Newborn or RhD HDN) is one of the causes of hemolytic disease of the newborn (HDN). The disease ranges from mild to severe, and typically occurs only in some second or subsequent pregnancies of Rh negative women where the fetus's father is Rh positive, leading to a Rh+ pregnancy. During birth, the mother may be exposed to the infant's blood, and this causes the development of antibodies, which may affect the health of subsequent Rh+ pregnancies. In mild cases, the fetus may have mild anaemia with reticulocytosis. In moderate or severe cases the fetus may have a more marked anaemia and erythroblastosis (erythroblastosis fetalis). When the disease is very severe it may cause haemolytic disease of the newborn (HDN), hydrops fetalis, or stillbirth.”
http://www.marchofdimes.com/baby/birthdefects_rh.html
“The Rh factor is an inherited protein found on the surface of red blood cells. Most people have this protein and are called Rh-positive. However, some people don't have protein; they are called Rh-negative. Rh-negative pregnant women are at risk of having a baby with a potentially dangerous form of anemia called Rh disease. Fortunately, treatment usually can prevent Rh disease.”
mikelepore said:
Did there have to be at least two mutations in the same geographical area, in both cases having the effect of causing short-neck parents to have long-neck offspring, so that the long neck animal could find a mate?
No.
“Diluting” a mutated gene does not destroy it. Meiosis does not destroy mutated genes, it only mixes them up. Natural selection follows copies of a mutated gene, not the individual that has the gene. Unless the mutated gene is instantly lethal, natural selection can not destroy a mutated gene in one generation.
Hybridization and reproduction barriers come in many forms. Mating behavior is only one way to keep populations separate. Other changes restrict gene flow between populations. There is a large number of such changes. “Dilution” by cross breeding can’t destroy a gene. Only natural selection can totally eliminate a gene and only after more than one generation.
These hybridization barriers are seldom toggles. One mutation does not automatically make the population different. Even using Mendelian laws, it is easy to see that genes don’t get destroyed by cross breeding populations. Most important genes have more complicated dynamics then are indicated by Mendelian laws. Even in those cases, cross breeding doesn’t eliminate the existence of a gene.
In the case of the giraffe, the first mutation that first made the neck longer didn’t need a hybridization barrier to propagate. Genes don’t get diluted continuously. If a giraffe with a slightly longer neck mates with a giraffe that doesn’t have the gene, then the gene for a longer neck will pass on to some of the offspring. The gene doesn’t have to be protected from contact with its opposite allele.
If the gene was a classic Mendelian type gene, with one major phenotype tied to one site on one chromosome chromosome, crossing can never get rid of it. An animal either has one copy, two copies or no copies. If the trait involved several alleles, then natural selection only occurs in those hybrids that have the correct gene on all alleles. The effect of these genes would then be additive. However, hybridization would still preserve the gene whether or not it is advantageous. The animal with the gene would have to be killed by natural selection to eliminate the gene.
This is especially true if the associated phenotype is recessive. The first mutation probably has a gene of only one allele, so the trait isn’t even expressed in the first mutation. The recessive gene won’t be expressed until it has already passed on to quite a few descendents. Then, the animal would need the same recessive gene in two alleles to express itself. If the trait is advantageous, then natural selection will favor animals with two genes. So the natural selection will actually act on the population, not the individual. There is a statistical favoring of the traite.
In your giraffe example, how do you know that the first giraffe with the mutation for longer neck even had a longer neck? The gene could have been recessive. Thus, it wouldn’t express itself in the first generation. If the species isn’t inbred, then it may be a few generation before the gene for a longer neck is expressed. So the selection wouldn’t act on it until long after the mutation had occurred. The population would gradually increase the fraction of animals with a gene for a longer neck. Then another mutation occurs, which could be a duplication of the allele on a chromosome. That duplicate gene could make an even longer neck. The contribution to neck length of the two alleles could add. Pretty soon one would have multiple copies of the long neck gene. The number of such multiple copies would vary in the population, but natural selection would favor more copies of the original allele.
The hybridization barrier, whatever it is, won’t be useful until a few animals already have this gene. Once the advantageous gene has spread through the population, natural selection would favor those animals which cross with those animals that have the advantageous gene. A second mutation, favoring animals which mate with those animals which show the trait, could occur randomly much later. Natural selection would then favor such animals.
Note that in your giraffe case, there is a type of geographical isolation. The short necked giraffe would find food most easily in a jungle or place with short plants. The okapi is an extant animal that lives in a jungle which is like a giraffe in many ways. However, the mutant with the slightly longer neck would find food at the edge of a forest, or any place with long trees. They would graze in the regions where they were the most comfortable. These regions would overlap but have areas outside the overlap. This would not separate the two species completely. However, it would reduce the amount of cross breeding slightly.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0469.1999.tb00979.x/abstract
“The frequency of the occurrence of hybrids between Chironomus thummi thummi and Chironomus thummi piger is estimated to be 0.047% in the wild. The rare hybridization events are the consequence of the sexual isolation mechanism of different swarming behavior of thummi and piger. Under laboratory conditions hybrids are easily obtained.”http://ukpmc.ac.uk/abstract/MED/12782734/reload=0;jsessionid=zOfty1718zCKvs7waG8r.12
“The success or failure of interspecific crosses is vital to evolution and to agriculture, but much remains to be learned about the nature of hybridization barriers. Several mechanisms have been proposed to explain postzygotic barriers, including negative interactions between diverged sequences, global genome rearrangements, and widespread epigenetic reprogramming. Another explanation is imbalance of paternally and maternally imprinted genes in the endosperm.”
One example with marine animals. More on this mating.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338553/
“Sympatric assemblages of congeners with incomplete reproductive barriers offer the opportunity to study the roles that ecological and non-ecological factors play in reproductive isolation. While interspecific asynchrony in gamete release and gametic incompatibility are known prezygotic barriers to hybridization, the role of mating system variation has been emphasized in plants. Reproductive isolation between the sibling brown algal species Fucus spiralis, Fucus guiryi (selfing hermaphrodite) and Fucus vesiculosus (dioecious) was studied because they form hybrids in parapatry in the rocky intertidal zone, maintain species integrity over a broad geographic range, and have contrasting mating systems. We compared reproductive synchrony (spawning overlap) between the three species at several temporal scales (yearly/seasonal, semilunar/tidal, and hourly during single tides).”
Here is an article concerning a hybridization barrier based on mating preferences. Note that this is an example of a saltation. Natural selection acts on the mutation over only a few generations. This fast type of evolution is rare. They call it a saltation. Notice that even in this case, the natural selection takes more than one generation to make an effect. So even with the saltation, using a Mendelian type allele, the mutant gene spreads over more than one generation.
http://www.la-press.com/redirect_file.php?fileId=604&filename=EBO-2-Norrstrom-et-al-(2)&fi...
“Coevolution of exploiter specialization and victim mimicry can becyclic and saltational
Darwin’s Principle of Divergence explains sympatric speciation as gradual and directional. Contradicting evidence suggests that species’ traits evolve saltationally. Here, we model coevolution in exploiter-victim systems. Victims (resource population) have heritable, mutable cue phenotypes with different levels of defense. Exploiters have heritable, mutable perceptual phenotypes. Our simulations reveal coevolution of victim mimicry and exploiter specialization in a saltational and reversible cycle. Evolution is gradual and directional only in the specialization phase of the cycle thereby implying that specialization itself is saltational in such systems. Once linked to assortative mating, exploiter specialization provides conditions for speciation.”