[Arch Enemy]

Originally Posted by schmichael

perhaps you should start by explaining your theory of common descent? how can there not be a single common ancestor? are you proposing that for each species there was a seperate ancestor?

There is far more evidence to suggest that all life came from a gene pool of species rather than a single organism.

you have yet to actually provide an example of a mutation increasing genetic info.

I see you ignored what I posted concerning increases.

How very, very convenient.

So here it is again:

increased genetic variety in a population (Lenski 1995; Lenski et al. 1991)
increased genetic material (Alves et al. 2001; Brown et al. 1998; Hughes and Friedman 2003; Lynch and Conery 2000; Ohta 2003)
novel genetic material (Knox et al. 1996; Park et al. 1996)
novel genetically-regulated abilities (Prijambada et al. 1995)

These are observed instances of an increase in genetic information that led to evolution.

A Japanese bacterium that suffered a frame shift mutation that just happened to allow it to metabolize nylon waste is another example. The new enzymes are very inefficient (having only 2% of the efficiency of the regular enzymes), but do afford the bacteria a whole new ecological niche. They don't work at all on the bacterium's original food - carbohydrates. And this type of mutation has even happened more than once!

In order to make room for new information, there have to be types of mutation which make a genome larger. It turns out that several kinds of mutation do this, notably duplication and polyploidy.

If a bacteria becomes penicillin-resistant, it really does contain new information. We know this because researchers have now got to the point where they have read out (sequenced) every last bit of the DNA in some bacteria. This means that it's possible to do before-and-after measurements.

Here's an example. Take a nice fresh culture dish, and place a single bacteria on it. A colony will grow. This is "before".

Take one bacteria from "before", and start a new culture with it. After the culture is well-started, add some antibiotic. Somewhere in the culture, there may be a mutant who is resistant to the antibiotic. If there isn't such a mutant, they all die. In that case, start over. If necessary, you can encourage mutation, maybe with some radioactivity.

Eventually, you will find such a mutant. You will know it's there because it reproduces, and your culture dish will contain a living colony instead of a dead one. This is "after".

Now get the DNA sequences of "before" and "after". Several researchers have done just this, and the DNA sequences have been published. It is definitely the case that "after" can have new genetic information, which is not present in "before".

In the above example, a beneficial mutation allowed the bacteria to survive a negative thing. It is equally easy to get a mutation that allows a positive thing. For example, give your colony a huge supply of some food which they cannot eat. Eventually some mutant will be able to eat the food, and will have a great many descendants. Then wipe out the normals (by withdrawing the normal food) and you have an "after" colony. As one researcher said:

Here's a tested recipe for isolating successful mutations... Grow a batch culture of Salmonella typhimurium strain SK2979 at 37 deg. C on Neidhardt's MOPS-based minimal medium with 0.4% glycerol as the carbon source and 10 mM L-aspartate as the nitrogen source. Dilute and subculture for several days. L-aspartate fast growing mutants will take over the culture in something under 3 days. These typically have a doubling time of 60 minutes on asparate, compared to about 120 minutes for the parental, wild-type strain.
Even better, starting with the fast-growing strain, one can easily isolate secondary mutation(s) which permit growth on aspartate as the sole carbon and nitrogen source -- which the parental strain simply cannot do. This demonstrates how cumulative mutations can arise.

Basically, techniques involving the natural occurrence of spontaneous, beneficial mutations are commonly used by bacterial geneticists.

The above is from a 1995 Usenet posting by Tim Ikeda (timi@mendel.berkeley.edu), UC-Berkeley Plant Biology.

Some Creationists have argued that these beneficial mutations involve simplification of the bacteria, so that some aspect attacked by the antibiotic is no longer present. That idea would rarely explain the ability to consume a new food, since that usually requires new chemical pathways. Before-and-after genetic analysis says that the "simplification" idea is just not always the case. For example, the malaria parasite has become resistant to chloroquine, by learning to make a new protein. Other examples are known from studies of pesticide resistant insects.

It is also illogical that "simplification" always be the case. A mutation is due to a completely random malfunction of the genetic mechanisms. There is simply nothing to prevent a bacteria from occasionally acquiring increased complexity. If the more complex genetic material happens to be useful, then the bacteria has by definition acquired information. It has "learned" what works. As one scientist put it, "evolution is a transfer of information from the environment to the genome."

You might wonder how a change could fail to be damaging. If all of a bacteria's genetic information is useful, then any change must have removed something useful. This is half-true, because bacteria do indeed run a tight ship. ("Higher" creatures are different, and carry around lots of genetic junk.) However, the chemical mechanisms which use genes do not really understand the idea of dosage. That is, if a creature needs twice as much of one chemical as another, there is no way to tell the mechanism "make twice as much". (I'm simplifying. Actually, hemoglobin has "enhancers" and "promoters".) The obvious trick for solving this problem is to simply have two copies of the gene. Therefore, creatures carry around two or more copies of some genes. If one copy is changed by a mutation, the creature can get along fairly well on the other one(s).

Gene duplication is a fairly common mutation. Having an extra copy doesn't "cost" much, so a creature with such a mutation isn't at any great disadvantage. Extra copies are actually fairly common in the genetic material of "higher" creatures. And of course a mutation that changes an extra copy is not the same problem as a mutation that changes an only copy.

Some idea of what geneticists are up to can be obtained by poking around at BIONET. Or, if you read Usenet newsgroups such as bionet.journals.contents, you can see what's being published in, say, Journal of Molecular Evolution or Molecular & General Genetics.

Evolution of cis elements in the differential expression of two Hoxa2 coparalogous genes in pufferfish (Takifugu rubripes).

Stowers Institute for Medical Research, Kansas City, MO 64110.

Sequence divergence in cis-regulatory elements is an important mechanism contributing to functional diversity of genes during evolution. Gene duplication and divergence provide an opportunity for selectively preserving initial functions and evolving new activities. Many vertebrates have 39 Hox genes organized into four clusters (Hoxa-Hoxd); however, some ray-finned fishes have extra Hox clusters. There is a single Hoxa2 gene in most vertebrates, whereas fugu (Takifugu rubripes) and medaka (Oryzias latipes) have two coparalogous genes [Hoxa2(a) and Hoxa2(b)]. In the hindbrain, both genes are expressed in rhombomere (r) 2, but only Hoxa2(b) is expressed in r3, r4, and r5. Multiple regulatory modules directing segmental expression of chicken and mouse Hoxa2 genes have been identified, and each module is composed of a series of discrete elements. We used these modules to investigate the basis of differential expression of duplicated Hoxa2 genes, as a model for understanding the divergence of cis-regulatory elements. Therefore, we cloned putative regulatory regions of the fugu and medaka Hoxa2(a) and -(b) genes and assayed their activity. We found that these modules direct reporter expression in a chicken assay, in a manner corresponding to their endogenous expression pattern in fugu. Although sequence comparisons reveal many differences between the two coparalogous genes, specific subtle changes in seven cis elements of the Hoxa2(a) gene restore segmental regulatory activity. Therefore, drift in subsets of the elements in the regulatory modules is responsible for the differential expression of the two coparalogous genes, thus providing insight into the evolution of cis elements.

PMID: 16569696 [PubMed - as supplied by publisher]

Is that enough? I can go on and on. You can continue ignoring what I post, for whatever reasons, and I continue to make you look like a fool while you protest that I have not provided any evidence for increases in information while anyone with a set of WORKING eyes can see that I have.

why do you say that. beneficial mutations can arise from either no change in the genetic info or from a loss of info.

As weel as an INCREASE IN GENETIC INFORMATION. See above. Here's another example:

Diversity and duplication of DQB and DRB-like genes of the MHC in baleen whales (suborder: Mysticeti).

School of Biological Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand, cs.baker@auckland.ac.nz.

The molecular diversity and phylogenetic relationships of two class II genes of the baleen whale major histocompatibility complex were investigated and compared to toothed whales and out-groups. Amplification of the DQB exon 2 provided sequences showing high within-species and between-species nucleotide diversity and uninterrupted reading frames consistent with functional class II loci found in related mammals (e.g., ruminants). Cloning of amplified products indicated gene duplication in the humpback whale and triplication in the southern right whale, with average nucleotide diversity of 5.9 and 6.3%, respectively, for alleles of each species. Significantly higher nonsynonymous divergence at sites coding for peptide binding (32% for humpback and 40% for southern right) suggested that these loci were subject to positive (overdominant) selection. A population survey of humpback whales detected 23 alleles, differing by up to 21% of their inferred amino acid sequences. Amplification of the DRB exon 2 resulted in two groups of sequences. One was most similar to the DRB3 of the cow and present in all whales screened to date, including toothed whales. The second was most similar to the DRB2 of the cow and was found only in the bowhead and right whales. Both loci showed low diversity among species and apparent loss of function or altered function including interruption of reading frames. Finally, comparison of inferred protein sequence of the DRB3-like locus suggested convergence with the DQB, perhaps resulting from intergenic conversion or recombination.

PMID: 16568262 [PubMed - as supplied by publisher]

example. shrivelled-eyed cave fish or flightless beetles on windswept islands, where the changes still involve loss of sight or flight.

See above. Here's another example of an INCREASE IN GENETIC INFORMATION:

Molecular evolution of the major outer-membrane protein gene (oprF) of Pseudomonas.

LMDF (Laboratoire de Microbiologie Du Froid), UPRES 2123, ABISS (Atelier de Biologie, Informatique, Statistique et Sociolinguistinque), Universite de Rouen, 76821 Mont Saint Aignan, France.

The major outer-membrane protein of Pseudomonas, OprF, is multifunctional. It is a non-specific porin that plays a role in maintenance of cell shape, in growth in a low-osmolarity environment, and in adhesion to various supports or molecules. OprF has been studied extensively for its utility as a vaccine component, its role in antimicrobial drug resistance, and its porin function. The authors have previously shown important differences between the OprF and 16S rDNA phylogenies: Pseudomonas fluorescens isolates split into two quite separate clusters, probably according to their ecological niche. In this study, the evolutionary history of the oprF gene was investigated further. The study of G+C content at the third codon position, synonymous codon usage (codon adaptation index, CAI) and genomic context showed no evidence of horizontal transfer or gene duplication. Similarly, a robust likelihood test of incongruence showed no significant incongruence between the oprF phylogeny and the species phylogeny. In addition, the ratio of nonsynonymous mutations to synonymous mutations (K(a)/K(s)) is high between the different clusters, especially between the two clusters containing P. fluorescens isolates, highlighting important modifications in evolutionary constraints during the history of the oprF gene. Since OprF is known as a pleiotropic protein, modifications in evolutionary constraints could have resulted from variations in cryptic functions, correlated with the ecological fingerprint. Finally, relaxed constraints and/or episodic positive evolution, especially for some P. fluorescens strains, could have led to a phylogeny reconstruction artifact.

PMID: 16549671 [PubMed - in process]

ah, a classic arguement. use a hypothetical situation where you have actually provided some evidence (like that's ever going to happen!), and then assume what my response will be. very clever.

Read what I posted, sparky. The evidence for my arguments is drowning you. Here's ANOTHER example of an INCREASE IN GENETIC INFORMATION:

Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans.

Physiological Genomics and Medicine Group, MRC Clinical Sciences Centre, Imperial College, London W12 0NN, UK. t.aitman@csc.mrc.ac.uk

Identification of the genes underlying complex phenotypes and the definition of the evolutionary forces that have shaped eukaryotic genomes are among the current challenges in molecular genetics. Variation in gene copy number is increasingly recognized as a source of inter-individual differences in genome sequence and has been proposed as a driving force for genome evolution and phenotypic variation. Here we show that copy number variation of the orthologous rat and human Fcgr3 genes is a determinant of susceptibility to immunologically mediated glomerulonephritis. Positional cloning identified loss of the newly described, rat-specific Fcgr3 paralogue, Fcgr3-related sequence (Fcgr3-rs), as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats. In humans, low copy number of FCGR3B, an orthologue of rat Fcgr3, was associated with glomerulonephritis in the autoimmune disease systemic lupus erythematosus. The finding that gene copy number polymorphism predisposes to immunologically mediated renal disease in two mammalian species provides direct evidence for the importance of genome plasticity in the evolution of genetically complex phenotypes, including susceptibility to common human disease.

PMID: 16482158 [PubMed - indexed for MEDLINE]

Had enough yet? I'm kind of getting tired of posting massive amounts of evidence of INCREASES IN GENETIC INFORMATION while you ignore them and say the words aren't even there on the screen, myself.