The Official Perfection KOs Creationism Thread Part Three: The Return of the KOing!

[sanabas]

I may be talking entirely out of my bum here, as I don't have enough background in cell biology. But El Mac's question seems to go:

1. Mitochondrial DNA comes only from the female line
2. Females' eggs degrade over time, which can make it harder to conceive later in life, and also lessen the chance of pregnancies being successful.
3. Newborns get their mitochondrial DNA, and the mitochondrial DNA in their eggs, from the egg they were conceived from.
4. The process, and the degradation repeats.
5. None of those 4 steps offer anything but degradation ofthe DNA, so why don't we have much worse DNA now?

Why would step 3 involve a newborn having degraded DNA, because the mitochondria in the egg was degraded? Aren't new cells, new mitochondria, etc produced to make the newborn's egg supply? Mitochondria in cells degrade over time, eggs degrade and are less productive over time, and that degradation can effect whether an egg can fertilise. But why would a fertilised egg produce already degraded mitochondria? I thought the degradation was due to time since production, not underlying code.

Children of older parents may be less healthy on average, but have any studies been made of the quality of those children's eggs?

 

[Neonanocyborgasm]

Well, I have a question. When Michael Behe says that the probability of getting one protein molecule (which has about 100 amino acids) by chance would be the same as a blindfolded man finding one marked grain of sand in the Sahara Desert three times in a row. And one protein molecule is not life. To get life you would need to get about 200 protein molecules together!

What do you say? Your answer is crucial to me as to whether I want to attempt to tackle something in the question I asked in my To athiests and agnostics thread.

I have several answers to that.

1) How in the world does Behe come up with these crazy probabilities? They sound like they're made up as he goes along.

2) Living things contain more than just protein, so the point makes no sense at all.

3) To suggest that "life" requires 200 protein molecules (again, I'm assuming you're getting this from Behe, who seems to be making this up as he goes along) is another fantastic number that he seems to pull out of nowhere, and is based on nothing. Some forms of life are more complex than others, and may require more than 200, or less. Which life? Bacteria? Viruses? Shrimp? Chimpanzee? Lions? Tigers? Bears? (Oh my!)

4) This is, anyway, a classic ploy of creationists. They assume that the lay public will be (1) too stupid to know the difference between evolution and abiogenesis (he's arguing the later, not the former) and (2) that the public believes that life sprung up fully formed the way it is today, without any intervening steps. The scenario that's being argued never existed, so it's a form of strawman argument. Life did not suddenly appear with all the component parts ready to live.

 

[ironduck]

Let's hope you are not being serious.

I'm just as serious as diablodelmar.

 

[Boris Godunov]

From the other thread:

If I built a house out of old trees, but told you the house was created in six days and was made last year.

Would I be lying?

"The rings on that tree say the logs are 100 years old!"

So? The house is only 1 year old.

This was in response to my pointing out that God making the universe appear billions of years old by all measurements and "planting dinosaur bones" was deceitful. I'll let the response stand as an example of a baffling horrible analogy.

 

[Birdjaguar]

Before Perf formalized the evolution vs creation threads, I wonder how many thread/posts there were? We must be up to 5,000 by now.

 

[Dr Tiny]

Hmm hope I have understood the question about the mitochondria correctly.

I would have thought with mitochondria in oocytes that to prevent the build up of deleterious mutations over generations there is some sort of 'quality control' mechanism built into the system to ensure , I will have a look on pubmed during my experiments today and see what I can find out.

Plus I would think that selection would act against inheritence of mutant mtDNA so that oocytes with a deleterious mtDNA mutation would be less likely to form viable embryos. Thus only cells with non mutated (or mutations that confer a benefit) would form embryos and thus the deleterious mtDNA is not inherited in a homoplasmic fashion.

For example,
http://www.biolreprod.org/cgi/content/full/71/6/1936
this paper shows that mouse embryo formation is inversly proportional to the ammount of damage to the mitochondria.

 

[The Last Conformist]

Women consistently having children in their 30s IS fairly new. Where is a line of women who all had children in their 30s? There isn't one, or at least one that is very old.

You'd not need them to all have children in their 30s - just one every few generations add up quickly. My own ancestry over the last few centuries provides plenty examples.

 

[sanabas]

I wrote a reply to Diablodelmar this morning, on the speed of light, coral reefs and star formation, but it seems to have been eaten. Bummer. Hopefully he proves me wrong on some more stuff soon.

 

[El_Machinae]

Aren't new cells, new mitochondria, etc produced to make the newborn's egg supply?

The egg that you came from was one cell, and the mitochondria in that cell were partially (genetically) degraded. There aren't magic 'new' cells - there are cells that are daughters of your zygote (PS: I know Sanabas knows this, I'm just being aggressive). As you divided, the mitochondria would reproduce and migrate into dividing cells. Those mitochondria would contain the genetic defects that your mother's egg suffered, and pass them on during reproduction.

Now, with females, we have a transition. Sperm undergo a strict 'survival of the fittest' regimen in your gonads - so whatever mutations occur are selected against. But with females - their eggs are made at a very young age, and are a fixed number. So - those eggs were made containing the mother's damaged mitochondria, and contain damaged mitochondria. Over the next many years, random event will conspire to degrade that DNA.

Evolutionary theory states that the DNA does not degrade sufficiently during the ages, and in fact (partially) states that the mtDNA strengths (adapts). This conflicts with data that the mtDNA degrades in older people. If it degrades in older people, it degrades in younger people - but due to repair mechanisms (repair can approach 100%, but does not reach it) mtDNA degrades more slowly.

The reason I focus on mtDNA is because it is under a LOT more stress than nuclear DNA. Mainly due to Reactive Oxygen Species (ROS) being generated really near it (nuclear DNA is insulated from ROS).

 

[Dr Tiny]

I was under the impression that oocytes in humans are produced in anaerobic conditions and kept quiescent (lit suspended/slowed animation) in order to minimise exposure to ROS. In addition some 8-10 million oocytes are made during development and this number drops over time thus there is selective competition between follicles and eggs, only 400 are ever released during ovulation, in addition it is less likely that an oocyte with defective mitos will form an embryo if it is fertilized. All these processes will slow the turning of Muller's ratchet. I am sure that in time there will be a better scientific explanation, oocyte biology seems to be quite a developming (no pun) area especially given IVF etc

Good review article
Jansen and Burton (2004) Mitochondrion 4 pp577-600
Mitochondrial dysfunction in reproduction

 

[The Last Conformist]

Can I see the entirety of that pubmed article? The Abstract mentions only damage to membranes and the like, not to mtDNA.

 

[Dr Tiny]

Sure
Pubmed ID is 16120416
If you are in an institution that has a subscription to the journal then you should be able to see it, if not I have the pdf and can send it out via email (most likely Monday when I am back in work)

Link to science direct version
http://www.sciencedirect.com/scienc...d=494590&md5=6b65072d7d91cacd540a01670d75b23c

 

[The Last Conformist]

Er, sorry, I was refering to El Mac's pubmed link.

 

[El_Machinae]

Locomotor functional decline and loss in muscle mass with age is virtually a universal characteristic that has been documented in several species, including worms, fruit flies, rodents, non-human primates and humans. The age-related loss of muscle mass and strength (sarcopenia) represents an important risk factor for disability and mortality in older subjects and has been linked with cellular energy deficit and increased apoptosis at old age. Many key theories on aging describing the mechanisms underlying sarcopenia are now focused on the mitochondria because of their dichotomous role in controlling life and death processes within myocytes. Mitochondria represent the main producers of cellular energy in the form of adenosine triphosphate, but are also considered a key regulatory center of apoptosis. Unknown factors leading to a decrease in aerobic energy efficiency are linked with mitochondrial mutations which may result into apoptosis. Moreover, deregulation of autophagy (degradation and recycling of long-lived protein and organelles, such as the mitochondria) in post-mitotic tissue might also be responsible for the age-associated cellular energy failure. Alterations in specific signaling pathways, such as AMP-activated protein kinases, play a role in both cell survival response and apoptotic response depending on energy depletion. Evidence supports that apoptosis occurring in aging skeletal muscle may be due, in part, to the progressive decline in mitochondrial function and the resulting energy depletion within the cell. In turn, mitochondrial dysfunction is partly due to the accumulation of oxidative damage to macromolecules, including mitochondrial DNA, RNA and proteins, essential components for optimal functioning of mitochondria. Evidence concerning these series of events leading to energy depletion and apoptosis are discussed.

pubmed

Really, there is oxidative damage to mtDNA. Pubmed is full of links.

 

[Dr Tiny]

double post, sorry

 

[Dr Tiny]

Oh I agree ROS will damage the DNA of oocytes, but there would appear to be mechanisms in place to reduce the effect on oocyte DNA and subsequent embryo formation eg anaerobic conditions during embryo formation, oopause, DNA repair enzymes, competition between eggs and follicles, reduced chance of embryos with damaged mitos being viable (thus reduced fertility). All these processes will slow/prevent the turning of Muller's ratchet.

edit - finally getting to go home from work so wont be able to reply until Monday

 

[ironduck]

Interesting discussion. Can it be established whether there actually is a degeneration of mtDNA through the generations? Even if we set up an ideal scenario of only very young women having children that would still mean some assumed degeneration and if the degeneration accumulates the result is the same, just takes longer to get there.

But is this true? Have we found evidence on this in tests of mice? Because our data from human history is obviously sporadic, but I can't think of data that would support it..

 

[The Last Conformist]

The fact the human race is still around is powerful evidence we don't see a gradual degradation of mtDNA from generation to generation.

 

[El_Machinae]

That's not proof. That's not proof at all.

My evidence fits the hypothesis that originally the DNA was 'better' and now it's gotten 'worse' (though still acceptable), since it's certainly partially degraded (junk DNA, etc.) now.

You're disregarding evidence because it doesn't fit your theory.

 

[The Last Conformist]

That's not proof. That's not proof at all.

Learn the difference between "proof" and "evidence".

My evidence fits the hypothesis that originally the DNA was 'better' and now it's gotten 'worse' (though still acceptable), since it's certainly partially degraded (junk DNA, etc.) now.

There's next to no junk in mtDNA.

All your evidence for degradation is at rates that, if they applied to germ cell lines (which you haven't showed), would've killed off humanity within recorded history. The conservative conclusion is that they don't apply to germ cell lines.

If you want anyone to take your objection seriously, at the very least you have to find a ref for people born of older mothers having worse mtDNA than those of younger.