Favorable Mutations? Help me!!

I know that there are many people debating if there is such thing as a "positive mutation." I have been researching this topic for only an hour for a class, and I have been able to learn only a few things, which seem to be opinions...1.Mutations may have favorable traits but are there are never any completely positive mutations.2.The traits of mutations may be favorable or unfavorable depending on the environment that the mutations have occurred in.I was wondering if anyone would be willing to help me out by giving your opinions here. I would also love any examples of "positive mutations" if you believe there is such a thing, or if you don't tell me why there aren't pos. mutations!So far I have gotten very vague information about sickle cell, Lactose tolerance, and Resistance to atherosclerosis.I just started biology 3 weeks ago, so try to keep it simple for now!!THANKS!!!!!!!------------------
I'm just a little girl--teach me more!!

Out of curiosity, what grade are you in?

I'm a freshman

At Patriot University?

quote:

---

I know that there are many people debating if there is such thing as a "positive mutation." I have been researching this topic for only an hour for a class, and I have been able to learn only a few things, which seem to be opinions...
1.Mutations may have favorable traits but are there are never any completely positive mutations.

​

2.The traits of mutations may be favorable or unfavorable depending on the environment that the mutations have occurred in.

---

The second statement is more accurate, and it contradicts the first. Don't you think so? If fitness is relative to the environment of the organism, it's impossible to make an absolute statement about mutations being positive or negative.The qualifier "completely" is just a way to hedge the bet if one's agenda requires maintaining that belief. Almost every trait has its drawbacks - for example, large human brains drastically increase our energy requirements. We would be, in many ways, better off without them. Despite this, the fossil record shows that their size has increased steadily. The benefits outweight the cost.If you want more short-term, observable examples of positive mutations, there are some that have occurred in your lifetime (or at least the lifetimes of the old farts here ). One of the best examples of positive mutation is a type of bacterium observed in Japan that feeds off waste from the production of nylon. This race thrives in an environment that didn't exist a few decades ago, due to a mutation that allows them to digest the waste. We can also do experiments with bacteria where they mutate over generations and develop resistance to parasites or toxins.[This message has been edited by zephyr, 09-06-2003]

No, at West Virginia University------------------
I'm just a little girl--teach me more!!

Does that bacterium that eats the waste in Japan actually help get rid of the waste completely?Thanks for the examples, keep em comin! ------------------
I'm just a little girl--teach me more!!

I couldn't find specific info on what's left over. Obviously, there will be some kind of byproduct from the digestion. If you want to read more, here's a decent page describing the nature of the mutation and its effects on the enzyme used in digestion:http://www.nmsr.org/nylon.htm

Great link! Thanks! I was actually looking at the pos. mutations stuff for my anthropology class, but that cleared up a few things for me that we are studying in biology. Again, thanks!!------------------
I'm just a little girl--teach me more!!

Also, that link had a link at the bottom of the page with information on "pos mutations"------------------
I'm just a little girl--teach me more!!

To lift a post of my own from a different forum, where the canarn of "no new information" is actually the subject of the thread, but the example is one of my favorites. I think of Hemoglobin C as sort of a "sickle-cell lite."
------------
Ref: Nature, vol 414, pp 305-308 (2001) - "Haemoglobin C protects against clinical Plasmodium falciparum malaria" , by D Modiano et al. It's not online, to my knowledge, except by paid subscription.Normal human hemoglobin ("HbA") is coded for by DNA which reads, as the 16th through 18th positions of a certain gene, GAA. This codon tells a cell's protein factory to put the amino acid glutamate at the sixth spot along the peptide that will become the beta chain of your or my hemoglobin. However, in a large number of West Africans, particularly the Mossi of Burkina Faso, this speck of DNA reads AAA. The distribution of folks with this variant looks like a bull's-eye: lots of the gene in one area of Burkina Faso, and fewer and fewer people with it as you move away from that center. The distribution is consistent with the idea that one person had the mutation about a thousand years ago, and that it spread through his or her descendants since. (Most people weren't terribly mobile in that area until nearly modern times - at least until the slave trade started.)Now this DNA change alters that sixth amino acid on the beta chain of hemoglobin to lysine, making HbC. Most people with hemoglobin C never know it - some have mild anemia, gallstones, or spleen problems. But Modiano's paper documents that Mossi children that have both genes for HbC are 7% as likely to develop malaria as their classmates who have boring old HbA. 7% as likely to get the disease that kills a couple of million kids in West Africa every year. And that's because their genome has the information to make a protein that has one amino acid that's different from the one in their neighbors, and in their ancestors, too, if you go back a ways. New information. Useful new information. (You will agree that being able to make two different proteins is "more information" than being able to make only one, won't you? Kids in the study that had the AC genotype - that had both HbA and HbC in their blood - had a 29% reduction in their chance of getting malaria.) New, useful, "information" from a mutation.Now a footnote: if your DNA reads GUA instead of GAA in this position, you get a valine in position 6 and have sickle-cell trait - the result of a different mutated hemoglobin called HbS. This protects against malaria, too, but the side effects can be severe, including fatal, especially if you have both genes for HbS. This, too, is "new information" - a different protein is being made.

On the sickle cell anemia mutation, is is also noteworthy that it appears to have happened in four different locations and three different forms (in two of the locations the mutation is identical). See this site for information. Ther's an animated map showing the spread near the bottom.Another favourable mutation is described here. This mutation confers immunity to arthritis, and has, indeed been traced to a specific 18th Century couple.

The pertinent question to ask is, what evidence exists where the mutated type is more viable than the parent type in a normal environment?Does the nylon example qualify? A quick read of the link and you will see it doesn’t. A huge cost is incurred in efficiency, and thus in a normal environment the mutated strain could not last long (AiG also argues plasmid xfer, but the enzyme effeciency loss alone in the article cited by zephyr is sufficient to dismiss mr. nylon as a hero of the evolutionary faith). Does sickle-cell qualify? Of course not. I really can’t believe the number of evolutionists who use a DISEASE as evidence of evolution!!!

quote:

---

Also, that link had a link at the bottom of the page with information on "pos mutations"

---

I need not go further than Robert Williams' first citation (why bother with the rest when the first one out of the gate is specious). Robert's source claims: By the end of the experiment, the lines cultured at 32 C were shown to be 10% fitter that the ancestor population (at 32 C), and the line cultured at 42 C was shown to be 20% more fit than the ancestor population.This is in reference to this article:Bennett, A.F., Lenski, R.E., & Mittler, J.E. (1992). Evolutionary adaptation to temperature I. Fitness responses of Escherichia coli to changes in its thermal environment. Evolution, 46:16-30.Let’s check what the article actually states:

Within Abstract: In the novel environments, the 42 group generally produced yields higher than the 37 group (and marginally higher than the ancestor), but we found no differences in competitive fitness among the 37 and 42 groups and the ancestor.

Within conclusion (emphasis mine):

It appears that, whereas biovolume yield provides a measure of the efficiency
of growth and as such can be regarded as a fitness component,
it is clearly not equivalent to Darwinian fitness when genotypes
compete with one another for resources. Indeed, in a
mass-action environment, there is no direct selection on
growth efficiency, only on growth rate (Vasi et al. 1994).
However, it is possible that increased biovolume yield might
be advantageous under conditions other than those measured
here. For example, given opportunities to colonize stressful
but uninhabited environments, populations with greater total
biovolume may be better able to establish new populations.
Alternatively, greater biovolume may make populations better
able to survive more extreme environmental challenges
than those used in our experiments. However, these possibilities
are merely speculative.

Uh, where in this study is compelling evidence that the mutated type is more viable than the wild type in a normal environment? Missing in action again. Yet evolution demands a virtually countless number of these mutations if we truly share a common ancestor with a banana!

Is West Africa, with its high incidence of malaria, a "normal environment?"