Can random mutations cause an increase in information in the genome?

That is tantamount to saying that a pile of sand conveys meaning.

1. Mutations that the organism has no control over2. Mutations that can no be predicted using any current methodologies.I think we call the mutations random because we have no way to predict what they will be.

So you believe just mentioning "God" means one loses a debate, eh?

I am not sure though that these definitions are helpful. First, just because the organism has no control over does not rule out the mutation being part of an embedded design, or actually being the result of direct intelligent action.

Garret writes:As to why a species can't acquire information...it's because no known natural process can create specified complexity. In other words, no unintelligent process would know how to arrange the strand in an order that had any meaning to the translator.

In a sense, you are right. DNA, in and of itself, conveys no meaning. However, the specified complexity of the DNA does have meaning

the actual trigger that prevents malaria is the fact that the mutation causes the hemoglobin to form in the wrong shape and fail to carry oxygen.

Garrett writes:The granules of sand on the beach have no specified complexity to their order, therefore carry no meaning to be interpreted even if there was a strange beach-side translator to do so.

It is hard to understand how anyone could make this claim, since anything mutations can do, mutations can undo. Some mutations add information to a genome; some subtract it. Creationists get by with this claim only by leaving the term "information" undefined, impossibly vague, or constantly shifting. By any reasonable definition, increases in information have been observed to evolve. We have observed the evolution of* 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)If these do not qualify as information, then nothing about information is relevant to evolution in the first place.# A mechanism that is likely to be particularly common for adding information is gene duplication, in which a long stretch of DNA is copied, followed by point mutations that change one or both of the copies. Genetic sequencing has revealed several instances in which this is likely the origin of some proteins. For example:* Two enzymes in the histidine biosynthesis pathway that are barrel-shaped, structural and sequence evidence suggests, were formed via gene duplication and fusion of two half-barrel ancestors (Lang et al. 2000).
* RNASE1, a gene for a pancreatic enzyme, was duplicated, and in langur monkeys one of the copies mutated into RNASE1B, which works better in the more acidic small intestine of the langur. (Zhang et al. 2002)
* Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further. (Brown et al. 1998)The biological literature is full of additional examples. A PubMed search (at PubMed) on "gene duplication" gives more than 3000 references.# According to Shannon-Weaver information theory, random noise maximizes information. This is not just playing word games. The random variation that mutations add to populations is the variation on which selection acts. Mutation alone will not cause adaptive evolution, but by eliminating nonadaptive variation, natural selection communicates information about the environment to the organism so that the organism becomes better adapted to it. Natural selection is the process by which information about the environment is transferred to an organism's genome and thus to the organism (Adami et al. 2000).# The process of mutation and selection is observed to increase information and complexity in simulations (Adami et al. 2000; Schneider 2000

While it is true that most mutations are either harmful, as suggested by the creationists, or neutral, the creationists gloss over a crucial fact: beneficial mutations do occur, though they are very rare. Can a beneficial mutation that occurs once in million individuals ever really contribute to evolution? Yes it can, since a rare beneficial mutation can confer a survival or reproductive advantage to the individuals that carry it, thereby leading -- over several generations -- to the spread of this mutation throughout a population. Beneficial mutations occurring in several different individuals in several different genes can simultaneously spread through a population, and can be followed by successive rounds of additional mutation and selection.Does the fact that we know many human detrimental mutations but essentially no clear beneficial ones mean that there are have been no beneficial mutations in human history? Not at all, since there is a clear bias in what medical scientists have studied. The human mutations we know most about are detrimental because medical scientists preferentially study illnesses that cause significant morbidity and mortality. Consider the theoretical possibility that a beneficial mutation has occurred in a particular human gene; even if this mutation were identified by a comparison of the mutated gene in a child versus the unmutated version of the same gene in both parents, there is no way that this mutation could ever be recognized as beneficial. If the mutation increased intelligence, strength, longevity or specific disease resistance, this would never be apparent without long-term breeding experiments that could obviously never be done on humans. Therefore, since such beneficial mutations in humans could never be recognized in humans, our ignorance of examples cannot be taken as evidence that they don't exist. However, the experiments necessary to demonstrate a beneficial mutation can be done with laboratory organisms that multiply rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance. In this case (in contrast to the situation with the peppered moth populations described above) origin of the population from a single bacterium allows comparisons of the mutated genes with the corresponding genes from the original bacterium, verifying that the variant sequences were not present before the culture with antibiotics and therefore arose as de novo beneficial mutations.

While a detailed mathematical consideration of information theory is beyond the scope of this article, none of the creationist arguments based on information theory that I am aware of adequately address the obvious increase in information that can occur when a gene duplicates and the two copies undergo independent mutations leading to two genes with somewhat different functions. Gene duplication, mutation and selection are all known to occur due to natural biochemical processes in a variety of organisms studied in the laboratory. Many gene families are known with members that encode proteins having related structure and related but distinct function. Each family can be explained by multiple gene duplications followed by random mutation and differentiation of the functions of the individual gene copies. Clearly the expansion from a single primordial gene to a large family of genes with distinct functions represents an increase in genetic information.An example that I have already mentioned in another posting on Talk.Origins is the hemoglobin/myoglobin family. The gene for a primordial oxygen-carrying protein is thought to have duplicated leading to separate genes encoding myoglobin (the oxygen-carrying protein of muscle) and hemoglobin (the oxygen-carrying protein of red blood cells). Then the hemoglobin gene duplicated, and the copies differentiated into the forms known as alpha and beta. Later, both the alpha and beta hemoglobin genes duplicated several times producing a cluster of hemoglobin-alpha-related sequences and a cluster of hemoglobin-beta-related sequences. The clusters include functional genes that are slightly different, that are expressed at different times during the development of the embryo to the adult, and that encode proteins specifically adapted to those developmental periods. Other examples of gene families that appear to have developed by such duplication and differentiation include the immunoglobulin superfamily (comprising a large variety of cell surface proteins), the family of seven-membrane-spanning domain proteins (including receptors for light, odors, chemokines and neurotransmitters), the G-protein family (some members of which transduce the signals of the seven-membrane-spanning domain family proteins), the serine protease family (digestive and blood coagulation proteins) and the homeobox family (proteins critical in development). A large part of the increase in information in our genomes compared with those of "lower" organisms apparently results from such gene duplication followed by independent evolution and differentiation of duplicated copies into multiple genes with distinct function. If an information theory analysis claims that random mutation cannot lead to an increase in information but the analysis ignores gene duplication and differentiation through independent mutations, such an analysis is irrelevant as a model for gene evolution, regardless of its mathematical sophistication.

It is unreasonable to believe something could begin to exist without a cause.The universe therefore requires a cause.