In this lecture you will learn about:
|When there is NO SEX and only a
single copy of the genome each generation is identical to the parents.
Good mutations are rare. A good mutation means that more of the progeny of that bacterial "strain" will survive (Aor B on right)
Two good mutations will compete with each
other until one is driven to extinction. So one good mutation will
always be lost. (A and B competing together)
However, sex changes this. For example two strains of bacteria, one for a new food source, gum, the other for motility to get to food. IF the two strains of bacteria had "sex" then some of their progeny would get both good mutations and would be able to "walk" and chew bubble gum at the same time. This is conservation of good mutations.
In order to take advantage of this there needs to be 1N in the gamete going to 2N in the adult.
|"The past decade of research has confirmed
that sex is indeed a potent force. But it's powerful in ways that Darwin
could not have appreciated. Studies in the past few years have demonstrated
that the sexual preference that females have for one kind of male over
another is potent enough to carve an old species apart into several new
ones. In the lakes of East Africa, for instance, sexual selection has driven
the origin of hundreds of new species from fish that live and breed side
|RANDOM AKA INDEPENDENT ASSORTMENT AKA
When genes from parents are randomly and independently sorted into the germ cells it assures maximum variation.
When two germ cells fuse to make a new individual (sex) the good genes of both parents can contribute to better "fitness" and competitiveness.
There is a big evolutionary investment in "sex" where the genes for two sexes need to evolve and and then all the genes to bring the two back together to ensure random assortment and a big mixing of genetic combinations in each generation.
For animation click here
|IN ADDITION, the number of discrete chromosomes
have a big impact on the amount of variation during random assortment.
The more chromosomes, the more different
possible combinations. The equation is
With just 2 chromosomes the ant listed on the right has only 22 possible combinations or 4.
With 8 chromosomes the fruit fly has 28 possible combinations or 2x2x2x2x2x2x2x2 = 256
With 23 chromos (like us) there are 223 possible combinations or 8,8388,6088.4 million different individuals.
|The number of chromosomes is important
for speciation. In GENERAL mismatch in chromosome number prevents
interbreeding, like donkey and horse which produces a mule which is sterile.
"They have trouble making sperm or eggs because their chromosomes don't match up well. And, because of their chromosome number.
A mule gets 32 horse chromosomes from mom and 31 donkey chromosomes from dad for a total of 63 chromosomes. (A horse has 64 chromosomes and a donkey has 62).
To understand why this is a problem, we need to understand how sperm and eggs are made. And to understand that, we need to go into a bit more detail about chromosomes. The mule has a set of horse chromosomes from its mom. And a set of donkey ones from its dad. These chromosomes aren't really matched sets like in a horse, a donkey, or a person. In these cases, a chromosome 1 is very similar to another chromosome 1. It looks pretty much the same and has nearly the same set of A's, G's, T's and C's. But a donkey chromosome doesn't necessarily look like a horse one. And the poor mule even has an unmatched horse chromosome just sitting there.
To make a sperm or an egg, cells need to
do something called meiosis. At the end of meiosis, the sperm or
egg has either mom's or dad's chromosome 1. Not both.
What they think happened click here
V stands for variable region
|"But natural selection is far from the
full story of evolution. Many mutations can spread throughout an entire
species thanks not to natural selection but through lucky rolls of the
genetic dice. This so-called neutral evolution has been particularly important
in shaping the parts of the genome that do not contain protein-coding genes.
Most of the news you read about DNA concerns protein-coding genes, so you
might well think that there's not much of the genome that doesn't contain
them. But just the opposite is true. Some 98.8 percent of the human genome
is this so-called noncoding DNA.
Only in the past few years have scientists started to explore this genomic wilderness in great detail, and they've used evolution as their guide. In the human genome, for example, there are an estimated 11,000 so-called pseudogenes—stretches of DNA that once encoded proteins but no longer do so thanks to disabling mutations. These vestiges of genes once had important functions, such as synthesizing vitamins or allowing us to smell certain molecules. Scientists know that these pseudogenes were once full-blown protein-coding genes, because they can find related versions of them in our primate relatives, in good working order.
While some of your noncoding DNA started out as your own genes, much more of it started out in invading viruses. Certain kinds of viruses can insert their DNA into host cells in such a way that it gets carried down from one generation of host to the next. Eventually these in-house viruses mutate so much they can no longer infect a new host. But they can still make copies of themselves, which get inserted into their old host's genome. About 40 percent of the human genome is made up of this viral DNA. Scientists can trace the ancestry of this virus DNA by comparing its remnants in our own genomes to the ones left in other primates."
Much of this viral DNA has now mutated to such a degree that it has become little more than padding in the genome. But even these inert relicts hold clues to their past. All human beings carry versions of an ancient virus called HERV-K. The differences in those versions evolved after the original virus infected a single human and was then passed down to his or her descendants. French scientists compared these versions of HERV-K, tallying up the mutations in one. Based on those new mutations, the scientists estimated that the virus first infected a human ancestor a few million years ago.
To prove that it had indeed once been a full-fledged virus, the scientists then used the different versions of its DNA to infer what its original genetic sequence had been. They synthesized that piece of DNA and injected it into human cells. The synthesized DNA hijacked the cells and caused them to spew out viruses with the same genetic sequence. The scientists, in other words, had brought a dead virus back to life.
"Sprinkled among the dead virus DNA and
disabled pseudogenes are
Scientists rely on evolution to find these
elements as well. If a piece of