Beneficial MutationS

[mikeynov]

At least you're someone who gives a rational answer (even though I might disagree with it) instead of those who only respond with empty attacks and no explanation. Maybe with you, we I can simply debate the issues instead of hearing only name-calling.

So again, how are these new genes added? Sorry, but you haven't explained how these genes can be added excpept only in our imaginations. If what you're saying is true, then ants could give birth to offspring who could fly. Is that correct?

What you're asking for was already provided. Do you want a peer reviewed example of gene duplication?

If I provide it, will you retract your claim?

 

[Karl - Liberal Backslider]

Please explain how the two can coexist.

Please explain the logical connection between:

"Evolution happened"

and

"God does not exist."

Because there isn't one. If there isn't, then the two can coexist perfectly happily.

 

[Carico]

You might be surprised - ants do give birth to offspring that can fly...

And how do you know that wouldn't be a separate species of ants? Has anyone ever seen two ants who didn't fly give birth to ants who did?

Again, this contradicts the whole reproductive process that offfspring are a product of the genes of their parents. It also does not explain how genes can be added to the DNA of a cell, especially ones that create the billions of neurons present in the human brain that are not present in the brains of primates.

 

[Knees]

OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).

 

[Oliver]

OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).

So you're asking why the textbook never give any example apart from the one(s) they give?

I think part of the answer is that a textbook is not supposed to be an encyclopedia: one example of a specific part of the theory is usually enough, since there is very little time to study it.

 

[rmwilliamsll]

So again, how are these new genes added?

at least two methods you can read about:
gene duplication followed by mutations on the copies, best examples are variant forms of hemoglobin, these number in the hundreds.

second is ERV, obviously the interesting ones are HERV's
check out HERV-W, then HERV-K's

OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).

There are at least two good examples on the molecular level for YECists to look at that show that this "no new information" or "only what is already present" is just not true.

What needs to be present is a piece of DNA.
Look at HERV-W, in particular, look at how a viral protein mediates trophoblast cell fusion in placentals. the source? a virus genome.

look at the nylon bug. the source of the novelty is a frameshift mutation.

the thallesimias(sp) of hemoglobin are the best place to look at a large number of mutations and how they work.

get down into the science, do some googling and reading, this no new information and no beneficial mutations is getting old because the science is there disproving it.


.....

 

[SwampGator]

Please explain the logical connection between:

"Evolution happened"

and

"God does not exist."

Because there isn't one. If there isn't, then the two can coexist perfectly happily.

Your attempt at explanation has nothing to do with the question asked. How do put millions of years into the Bibles 7 day creation?

 

[Carico]

What you're asking for was already provided. Do you want a peer reviewed example of gene duplication?

If I provide it, will you retract your claim?

Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?

 

[Oliver]

Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?

Because the copy of the original gene can then be changed by other mutations into something different from the original gene.

 

[mikeynov]

OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).

You'll have to give examples of these textbooks.

But I will say that the high school level of curricula isn't an appropriate place to discuss complex research, imho, unless it's an AP class or something.

 

[Karl - Liberal Backslider]

And how do you know that wouldn't be a separate species of ants? Has anyone ever seen two ants who didn't fly give birth to ants who did?

Happens every summer in virtually every ant colony. We're actually yanking your chain a bit here - how much do you know about ant reproduction?

Again, this contradicts the whole reproductive process that offfspring are a product of the genes of their parents.

No. A mutation or duplication or whatever happens in a germ cell of the parent, and the offspring that grows from that germ cell will have that feature - straight from the parental DNA.

It also does not explain how genes can be added to the DNA of a cell, especially ones that create the billions of neurons present in the human brain that are not present in the brains of primates.

I suspect that the same gene is responsible in both. The difference is in cranial capacity that allows us to have far more. There isn't a gene for each pair of legs on a millipede, for example, so there doesn't need to be a gene for each neuron.

 

[AnEmpiricalAgnostic]

OK - give us a documented example of a beneficial mutation. While you're at it, why not explain why the text books that try to convince students that evolution is fact never present any such mutations (other than sickle-cell anemia).

Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P<.001), alcohol drinkers (P<.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele(4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P<.001), triglycerides (P<.001), sex (P<.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis.

Lipoprotein lipase (LPL) is the rate-limiting enzyme in the lipolysis of triglyceride-rich lipoproteins, and the gene coding for LPL is therefore a candidate gene in atherogenesis. We previously demonstrated that two amino acid substitutions in LPL, the Asn291-Ser and the Asp9-Asn, are associated with elevated triglycerides and lower HDL cholesterol and are present with greater frequency in coronary artery disease (CAD) patients than in normolipidemic control subjects. Conversely, a third frequent mutation in this gene, the Ser447-Stop, is reported by some investigators to underlie higher HDL cholesterol levels and would represent a beneficial genetic variant in lipoprotein metabolism. We therefore sought conclusive evidence for these allegations by investigating the effects of the LPL Ser447-Stop mutation on LPL and hepatic lipase (HL) activity, HDL cholesterol, and triglycerides in a large group of CAD patients (n = 820) with normal to mildly elevated total and LDL cholesterol levels. METHODS AND RESULTS: Carriers of the Ser447-Stop allele (heterozygotes and homozygotes) had significantly higher postheparin LPL activity (P = .034), normal postheparin HL activity (P = .453), higher HDL cholesterol levels (P = .013), and lower triglyceride levels (P = .044) than noncarriers. The influence of the Ser447-Stop allele on LPL activity was pronounced in patients using beta-blockers (P = .042) and not significant in those not using them (P = .881), suggesting a gene-environment interaction between the Ser447-Stop mutation and beta-blockers. CONCLUSIONS: We conclude that the LPL Ser447-Stop mutation has a significant positive effect on LPL activity and HDL cholesterol and triglyceride levels and that certain subgroups of CAD patients carrying the Ser447-Stop mutation will have less adverse metabolic effects when placed on beta-blockers. The LPL Ser447-Stop mutation therefore should have a protective effect against the development of atherosclerosis and subsequent CAD.

To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study (n = 1273). The possession of this mutation associates with protective lipid and lipoprotein profiles. Subjects possessing the mutation have significantly higher HDL-C (p = 0.002) and apo AI (p < 0.04) levels, lower triglycerides (p = < 0.04) and total cholesterol/HDL-C ratios (p < 0.02); all established previously to reduce risk of CAD. We also find that this mutation is significantly less frequent amongst CAD subjects (p < 0.05). These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD..

Congenital factor XIII (FXIII) deficiency is potentially a severe bleeding disorder, but in some cases, the symptoms may be fairly mild. In this study, we have characterized the molecular mechanism of a mild phenotype of FXIII A-subunit deficiency in a Finnish family with two affected sisters, one of whom has even had two successful pregnancies without regular substitution therapy. In the screening tests for FXIII deficiency, no A-subunit could be detected, but by using more sensitive assays, a minute amount of functional A-subunit was seen. 3H-putrescine incorporation assay showed distinct FXIII activity at the level of 0.35% of controls, and also the fibrin cross-linking pattern in the patients clotted plasma showed partial gamma-gamma dimerization. In Western blot analysis, a faint band of full-length FXIII A-subunit was detected in the patients' platelets. The patients have previously been identified as heterozygotes for the Arg661 --> Stop mutation. Here we report a T --> C transition at position +6 of intron C in their other allele. The transition affected splicing of FXIII mRNA resulting in low steady state levels of several variant mRNA transcripts. One transcript contained sequences of intron C, whereas two transcripts resulted from skipping of one or two exons. Additionally, correctly spliced mRNA lacking the Arg661 --> Stop mutation of the maternal allele could be detected. These results demonstrate that a mutation in splice donor site of intron C can result in several variant mRNA transcripts and even permit partial correct splicing of FXIII mRNA. Further, even the minute amount of correctly processed mRNA is sufficient for producing protein capable of gamma-gamma dimerization of fibrin. This is a rare example of an inherited functional human disorder in which a mutation affecting splicing still permits some correct splicing to occur and this has a beneficial effect to the phenotype of the patients.

We have recently described a C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins. The 825T allele is associated with a novel splice variant (Gbeta3-s) and enhanced signal transduction via pertussis toxin (PTX)-sensitive G proteins. fMLP-induced chemotaxis, but not O2- generation, was increased in neutrophils with the TC/TT (EC50 = 1.5 +/- 1.3 nM) genotypes compared to the CC genotype (EC50 = 5.9 +/- 1.5 nM). Maximal fMLP-induced increase in [Ca2+]i was significantly reduced in neutrophils from individuals with TC/TT genotype vs. CC genotype (212.9 +/- 10.1 nM vs. 146.4 +/- 24.2 nM). Gbeta3-s appears to be associated with enhanced immune cell function in humans.

High blood levels of coagulation factor VII are associated with a risk of ischemic vascular disease. Although factor VII levels may be genetically determined, the relation between genetic polymorphisms of factor VII, factor VII blood levels, and the risk of myocardial infarction has not been established. METHODS: We performed a case-control study of 165 patients with familial myocardial infarction (mean [+/-SD] age, 55+/-9 years) and 225 controls without a personal or family history of cardiovascular disease (mean age, 56+/-8 years). The polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene were studied. Factor VII clotting activity and antigen levels were also measured. RESULTS: Patients with the QQ or H7H7 genotype had a decreased risk of myocardial infarction (odds ratios, 0.08 [95 percent confidence interval, 0.01 to 0.9] and 0.22 [95 percent confidence interval, 0.08 to 0.63], respectively). For the R353Q polymorphism, the RR genotype was associated with the highest risk, followed by the RQ genotype and then by the QQ genotype (P<0.001). For the polymorphism involving hypervariable region 4, the combined H7H5 and H6H5 genotypes were associated with the highest risk, followed in descending order by the H6H6, H6H7, and H7H7 genotypes (P<0.001). Patients with the QQ or H7H7 genotype had lower levels of both factor VII antigen and factor VII clotting activity than those with the RR or H6H6 genotype. Patients with the lowest level of factor VII clotting activity had a lower risk of myocardial infarction than those with the highest level (odds ratio, 0.13; 95 percent confidence interval, 0.05 to 0.34). CONCLUSIONS: Our findings suggest that certain polymorphisms of the factor VII gene may influence the risk of myocardial infarction. It is possible that this effect may be mediated by alterations in factor VII levels.

SOURCE: http://www.gate.net/~rwms/EvoHumBenMutations.html

 

[Karl - Liberal Backslider]

Your attempt at explanation has nothing to do with the question asked. How do put millions of years into the Bibles 7 day creation?

Again, http://freespace.virgin.net/karl_and.gnome/genesis.htm

It's all in there.

 

[Governed Apology Exploded]

Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?

NO GENE IS SUPERIOR TO ANOTHER GENE! All genes are made of the same four nucleotides. It is the proteins they code for that can be superior. Simply changing one nucleotide can make a proton superior or useless. Of course, as I've already said, "superior" depends on the environment.

 

[mikeynov]

Gene duplication is not at all producing genes superior to itself. It is simply duplicating the original gene. So how would that show evolution?

Evolution isn't about "going from less to more perfect."

Do you understand that? If you don't, no conversation about this subject is ever going to help, because you don't understand the basic evolutionary model.

This would be like me telling you "there's no evidence for Jesus, because England has no record of a Jesus living 500 years ago!" In other words, the entire assertion is framed on something nobody is claiming is true. So there's nothing to refute.

But the answer was already given - a duplicated gene can diverge to produce a new protein product. Do you also want examples of gene families that arose in this manner?

But honestly, I'm not sure that would help. Like I said before, you're asking to have a graduate+ level discussion with a pre-high school understanding of biology.

 

[mikeynov]

NO GENE IS SUPERIOR TO ANOTHER GENE! All genes are made of the same four nucleotides. It is the protons they code for that can be superior. Simply changing one nucleotide can make a proton superior or useless. Of course, as I've already said, "superior" depends on the environment.

proton=protein

 

[Heather S.]

OK - give us a documented example of a beneficial mutation.

There are several in humans that have to do with cholesteral and some other issues that I can't remember off the top of my head (I'm no doctor). However there is a beneficial mutation in the algae C. taxifolia. It's a uni-cellular algae with a gene that mutated due to UV radiation. The mutation enabled the plant to survive in the cold waters of the Mediterranean, where it has been introduced. It is now causing a lot of harm to native plants. The new, mutated strand of C. taxifolia is much different from the harmless original.

A similar mutation has been seen in the Nothern snakehead, which has recently been introduced into US waters.

That's all I can remember without looking anything up. Do a Google search, for goodness sake.

Please explain how the two can coexist.

http://www.theisticevolution.org/


Heather

 

[Governed Apology Exploded]

proton=protein

Oops, it was a typo (no idea how I did that)

 

[Kripost]

Most creationists do not say there are no positive mutations - absolute statements are never a good idea - but it is possible to say that evolutionists have never documented any good examples of postitive mutations. The only one most of the literature presents is the example of sickle-cell anemia because people of African descent who have this disease are less likely to get malaria.

The underlined section above is misleading.

Sickle-cell anemia is a recessive trait, meaning your need to have two genes inherited from both parents in order to have that trait. When a person has only one copy of that gene, the person does not only have sickle-cell anemia, but also resistant from malaria.

Also, you are underestimating how serious malaria is. Many children die from malaria before reaching puberty.

 

[Oliver]

Sickle-cell anemia is a recessive trait, meaning your need to have two genes inherited from both parents in order to have that trait. When a person has only one copy of that gene, the person does not only have sickle-cell anemia, but also resistant from malaria.

Didn't you mean something like "the person not only doesn't have sickle-cell anemia"? I mean if it is a recessive trait.. then again, English's not my mother tongue, so I may well have misunderstood this sentence...