The genetic variety caused by two unrelated people mating is easy to understand. Blond dad and redhead mom are going to have different DNA strands interacting to produce variety. OK.
But why aren’t all of one mans sperm the same? Aren’t they being copied off of the same “template?” How is the variety between sperm introduced so that brothers from the same parents are not identical? I guess this question also applies to ova.
Roughly speaking, your DNA template is a bunch of paired chromosomes. For each chromosome, the two ‘halfs’ have different genes in a bunch of places… sometimes one gene is dominant and the other recessive, sometimes they’re ‘co-dominant’ and both express themselves to a certain extent.
In the process of creating sperm, testicular cells (and ovary cells) divide in such a way that the results of division only have one from each chromosome pair. Thus, there are an enormous number of ways the split can happen, and few if any sperm are exactly identical.
When the sperm and the egg combine, their unpaired chromosomes join back up to form pairs again for the new zygote.
Does that help explain things??
Great 2000th post!
You have 23 pairs of chromosomes. You donate 23 unpaired chromosomes to each gamete (as does anyone else). That gives you 2[sup]23[/sup] (8,388,608)different possibilities to combine with your partner’s 8,388,608. In other words, 70,368,744,177,664 possible different Hypno-Toads and it had to be you. 
So, out of the 70,368,744,177,664 possibilities, what is the percentage of viable offspring?
You’ve got to remember you have 23 pairs of chromosomes. Your sperm, OTOH, have 23 chromosomes - one of each pair. It’s pretty much random which chromosome out of the pair each sperm will get.
Look at it this way:
Each cell in your body has the following configuration of chromosomes:
X Y
1A 1B
2A 2B
3A 3B
4A 4B
5A 5B
Etc.
One sperm might get: (determined by coin flips)
Y
1B
2A
3A
4B
5B
Another might get:
X
1A
2B
3A
4A
5B
And so on.
Because you have 23 pairs, there are 2^23 (8,388,608) possible combinations.
Even beyond that, during the production of eggs or sperm (in the kind of cell division known as meiosis) the two chromosomes comprising each pair can swap sections of genetic material, in a process called “crossing-over.” So not only are the chromosomes themselves shuffled, so is the genetic material on each individual chromosome. So the potential for genetically different sperm is far higher than even the calculations above suggest.
Depends on what you might call the couple’s “genetic health”. If neither of them is carrying any “bad” genes, it’s at least possible in theory that all 70 trillion plus combinations could result in healthy offspring. In practice, well, one need only look at congenital mortality statistics.
70 trillion Hypno-Toads? Who do you think I am, Wilt Chamberlain?
I think I get it now. Although my 23-letter “alphabet” is always the same, the letters can be put into different combinations to produce endless variations of the glory that is the Hypno-Toad.
And now that I see Colibris post, it seems that even the “letters” in my alphabet may become transformed into new letters.
Tricky. You’d have to calculate the odds of recessive genes combining to give the offspring an inheritable diseases like cystic fibrosis, tay-sachs, sickle-cell anemia, hemophilia or any of several thousand others (not all of which render a person non-viable in the sense they can’t live long enough to reproduce on their own). I gather if both parents are completely free of genetic disorders, expressed and recessive, the offspring will be, too, barring random mutation. Whether or not there’s anyone on Earth who meets this rather stringent condition is something I’ll wait for a geneticist to explain. The wikipedia pages on “genetic disorder” and “recessive gene” might be a good place to start.
Also depends on your definition of viable… I would think that a number of egg-sperm pairs are incompatible enough that they could never fertilize. That wouldn’t be ‘viable’ in my interpretation… not because either of them are problematic in themselves, just too chemically or biologically different. That’s a WAG though.
The process of fertilisation is not really a function of the genes themselves, but more of a physical penetration of the egg by the sperm and an electrochemical transformation of the egg’s cell membrane to preclude other sperm from penetrating (hehe, penetrating). I’m a little confused by your post. Certainly there are many combinations of egg and sperm that will never lead to a viable zygote/embryo/fetus, but those tend to be trisomies or other gross genetic anomolies. As far as I know, barring genetic mutations, any 23 chromosome egg can be successfully combined with any 23 chromosome sperm.
In addition to the above descriptions, during meiosis the pairs of genes can exchange segments of DNA so that 1A and 1B can recombine some segments to become 1A’ and 1B’. So the number of possibilities can increase exponentially. This is called Chromosomal Crossover
“Gross” genetic anomalies? Unless you’re defining as a gross genetic anomaly “anything that would lead to a fetus not being viable” I find that somewhat exagerated. A female fetus with two homophilia genes would not be viable; a male fetus with (only can have one) homophilia gene would be viable; a female fetus with one hemophilia gen would be viable.
hEmophilia, in all three cases. Dang. Sorry.
Yes, and to complicate things even more, every chromosome contains many, many genes. You are carrying around genes from generations ago that didn’t play a part in mapping out the finished Hypno-Toad. Your offspring might have Great Granddad’s mismatched ears that you don’t have, or maybe not.
Genetic selection is not as simple as Mendel’s charts said it was, back in the monastery garden.
You have the details wrong. In all cases the fetus is viable, in that a living baby will probably be born. The problem is that a child that has hemophilia will likely die from the condition at an early age.
Since the allele of the gene that governs hemophilia is on the X-chromosome and recessive, a male with a single dose, or a female with two doses, will have hemophilia. A female with a single dose will usually not have the condition (but can sometimes have it in a milder form).
That is, was likely to die before treatments were developed.
I recall seeing suggestions that there were “helper sperm” that attempt to assist their brethren in the face of competition. Is my memory correct?
Sorry, that’s the information I was taught. I stand corrected (although the majority of the sources I’ve googled still don’t even talk about hemophilic women).
I always thought the reason why some of my relatives have had such skewed gender relationships for their kids was something like what I was taught about hemophilia, though. I’m talking about things like “14 births, 12 f and 2m”… it’s possible that there wasn’t any kind of gender-linked genetic disease but it that case the husband sure had some fast female spermatozoid!
But not as high as a purely random process would predict, right? Genes that are further located apart on the chromosome are more likely to end up on different chromosomes during the cross-over process than are genes that are closer together. Genes that are very close together and tend not to separate from each other are said to be linked.
Also, the X and Y chromosomes in males can’t cross over during meiosis, except at the very tips, so they don’t exchange much genetic material. In particular, the SRY gene (sex-determining region Y), cannot swap with the X chromosome-- for good reason, since an embryo with this gene will become male (under normal conditions). In the rare cases when this gene does swap, you can get an XX “male” (though infertile).