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This paper was originally published in the Proceedings of the Sixth International Conference on Creationism, pp. 73–86 (2008) and is reproduced here with the permission of the Creation Science Fellowship of Pittsburgh (www.csfpittsburgh.org).
Mutations alter the nucleotide sequence of the DNA. They may affect the organism's phenotype, which can play a key role in bacterial adaptation and transformation to changing environments. Some of these mutations even appear to be beneficial to the organism. However, creationists have tended to offer an inconsistent or incomplete perspective of "beneficial mutations" within a creation framework. This includes the frequent denial that mutations can ever provide a beneficial phenotype, and the concept that "beneficial mutations" are merely an evolutionist exaggeration.
In bacteria, a wide range of mutations can be shown to provide a beneficial phenotype to the cell. These benefits are often of sufficient phenotypic affect that they can undergo strong positive selection. But the benefits are generally temporary and limited. Some common examples of beneficial mutations are those involved in bacterial antibiotic resistance. These mutations potentially enable the bacterium to survive exposure to various antibiotics, but the resistance results from loss or reduction of pre-existing activities such as enzymatic, regulatory, or transport systems. Bacteria also can undergo adaptive mutation; a phenomenon used by bacteria to survive very specific stressful conditions. The exact mechanism is controversial because some results suggest a directed mutation specifically enabling adaptation to the environment but at a mutation rate higher than random mutations would produce. Various mutations have also been found that enable bacteria to survive temporary exposure to high temperatures or starvation. Such mutations usually involve loss of certain sigma factors, reduction of DNA repair, or loss of specific regulatory controls. Other examples include several subpopulations of mutant strains of bacteria obtained over a period of up to 20,000 generations. These mutants have a greater "fitness" than the wild-type strain. However, analysis showed that most contained deletion mutations in various genes.
Each of these examples, as well as numerous others, involves certain environmental conditions that make these mutations phenotypically beneficial. However, these mutations frequently eliminate or reduce pre-existing cellular systems and functions. This has been referred to as antagonistic pleiotropy; meaning the cell experiences a trade-off where a temporary benefit for surviving one environmental condition is provided at the expense of systems used for other environments. If the environmental conditions change, the mutation usually becomes less beneficial and perhaps even detrimental. Hence, these mutations do not provide a genetic mechanism that accounts for the origin of biological systems or functions. Rather, they require the prior existence of the targeted cellular systems. As such, beneficial mutations of bacteria fit concisely within a creation model where (a) biological systems and functions were fully formed at creation, (b) subsequent mutations can provide conditional benefits that enable the organism to survive harsh post-Fall conditions even though the mutation is generally degenerative, and (c) most bacteria need the ability to rapidly adapt to ever changing environments and food sources.
All DNA appears to have the potential for mutation. A mutation can be simply defined as a change in the DNA nucleotide sequence compared to a wild-type sequence.1 These mutations often alter the organism's phenotype, which can play a key role in biological adaptation and transformation. Many mutations clearly are deleterious to the organism, probably even lethal. Other types of mutations appear to provide some, albeit, temporary benefit. Creationists have tended to offer inconsistent evaluations of such "beneficial" mutations. Morris2 categorized beneficial mutations as a prediction of an evolutionary model, implying their occurrence is inconsistent with a creation model. Other creationists have denied that mutations ever provide a beneficial phenotype.
However, a wide range of mutations can be shown to provide a beneficial phenotype to an organism. These benefits are often of sufficient phenotypic affect that they can undergo strong positive selection. Such benefits, though, are often temporary and limited.
Bacteria are asexual microorganisms that can rapidly reproduce. While it would appear that bacterial offspring are effectively a clone of the parent, this genetic homogeneity would reduce a bacterial population's ability to quickly respond to changing environments. Instead, bacteria have numerous mechanisms for introducing genetic variation into a growing population.3 These mechanisms, combined with their rapid reproduction and large population sizes, enable bacteria to quickly and effectively adapt to a variety of environmental changes.
Because of these features, bacteria have become a popular system for studying mutations and alleged evolutionary transformations.4, 5 A variety of mutations have been studied in bacteria. Many are clearly deleterious, but examples of advantageous or "beneficial" mutations can also be found.
Many published examples of beneficial mutations are actually proposed historical reconstructions of possible past mutational events. While such reconstructions may accurately represent a mutation's history, it is still a speculated history. In fact, most reconstructions also are based more upon evolutionary supposition than genetic plausibility. Instead, in this paper we will focus upon those mutations where both the wild-type and mutant strain can be empirically compared side-by-side, and the mutation history is clearly documented. Also, some beneficial mutations have resulted from directed genetic engineering. Such engineered alterations do not necessarily represent naturally occurring mutations, rather they are illustrations of theoretical genetic possibilities. In fact, they are genetic possibilities that can result from a guiding intelligence.
Examples of Beneficial Mutations
Mutations during multiple generations
Lenski et al.6 determined that after 10,000 generations in the same cultivation conditions, a population of Escherichia coli contained a diversity of mutant strains. Each of these mutants had an increased adaptation to the cultivation condition, manifesting itself in a 50% greater relative fitness compared to the parental wildtype. Thus, the mutations appeared to be beneficial and were positively selected.
Subsequent genetic analysis of some of these E. coli mutants found that they possessed insertion sequences (IS elements; a small segment of DNA that can insert into numerous sites of the chromosome). These IS elements were indigenous to the chromosome, and their activity did not depend on horizontal transfer from neighboring cells. Movement of these elements produced various insertional mutations in the E. coli chromosome.7 In fact, these types of mutations appear to be the primary function of these IS elements.8 These insertional mutations either create "knockout mutations", disrupting gene function or genetic activity at the point of insertion, or they may carry a promoter or other regulatory segments that activate adjacent genes.9 One specific IS disruption of gene activity in some of the mutants was the loss of the ribose operon.10
No specific explanation has yet been offered of how IS-mediated disruptions are advantageous, but "antagonistic pleiotropy" has been proposed.11 This pleiotropy suggests that a mutation can be beneficial in one type of environment and deleterious for a different environment. Thus, the cell seems to readily sacrifice a system not essential to a given environment, if it in some way helps adaptation to that environment.
After 20,000 generations, additional E. coli mutant strains were isolated that also appeared to be positively selected. Some of these strains had a reduced expression of flagella-encoding (flg) genes.12 Since the parental wild-type was non-motile, maintenance of the unused flagella-encoding genes was likely an unnecessary burden in the cultivation conditions. This provides another example of genomic truncation leading to antagonistic pleiotropy.
A second group of mutants from the same study probably involved a mutation in the regulatory control of spoT.13 This mutation can subsequently result in reduction of ppGpp concentration, a molecule involved in stress response.14 Reduction of ppGpp concentration, in turn, may increase tRNA and rRNA expression.15 Increased RNA can contribute to increased growth rate of the mutants.16
All the E. coli mutants detected within 20,000 generations appear to fit the description of antagonistic pleiotrops. The beneficial mutations are very environmentally specific, and a change in this environment often negates the benefit of the mutation. When repeatedly cultivated in a constant environment, it is not surprising that an organism would reduce its genome of some unused genes and functions. Mutants of E. coli obtained after 20,000 generations at 37°C were less "fit" than the wild-type strain when cultivated at either 20°C or 42°C.17 Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates.18 Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
Stress Survival
Adaptive mutation
In a broad context, adaptive mutation has been defined as that collection of growth-independent mutations that enhance the cell's survival and growth when confronted with stressful and growth-limiting environments.19 As such, various examples of beneficial mutations are a form of adaptive mutation. Interestingly, adaptive mutations appear to be mutations that arise specifically in response to the environment.
The initial observed behavior of adaptive mutations suggested they arise from non-random mutations that are directed specifically to adapt to a particular environmental cue or stressor.20, 21 Hence, they were originally termed "directed mutations" because they appeared to be non-randomly generated mutations. However, other mutations often occur concurrently with "directed" mutations that are not directly a result of environmental responses.22
Early work on adaptive mutations involved Lacstrains of E. coli or Salmonella enterica with an F' plasmid containing a copy of the lac operon with a + 1 frameshift (Figure 1). This frameshift renders the operon inactive. While the cells initially remain phenotypically Lac- with this plasmid, after cultivation on medium with lactose as the sole energy source, Lac+ revertants developed at a rate higher than predicted from random mutation.23 In addition, the culture experienced no overall net growth.23
There is some controversy about the nature of adaptive mutations. Are directed mutations specifically arising due to selective pressure, almost in a Lamarckian fashion? Or, are mutations occurring in a more conventional, random manner, and selection processes effectively produce the appearance of "directed" mutations? Focusing on the Lac- mutant experiment described above as the model study system, three models have been proposed for adaptive mutation.
For these Lac+ revertants to occur during a phase of stationary growth (that is, no net growth) requires various recombination enzymes, such as RecA24 and induction of the SOS DNA damage response regulon.25 In particular, the error-prone DNA polymerase IV may have significant involvement. Based on this, one model proposed is the recombination-dependent mutation model (also known as directed mutation).26 This complicated model assumes the mutated lac operon on the plasmid is "leaky," enabling enough lactose catabolism to provide sufficient energy for a low level of DNA replication (Figure 2). Even though conjugation is not occurring, the conjugal origin on the F' plasmid sustains persistent nicks. When the DNA replication fork encounters these nicks, the fork collapses and creates a double-strand end on the plasmid. This double strand end initiates the dsDNA break repair system in the cell involving the recombination enzyme, RecA. RecA catalyzes invasion of a single DNA strand into this double-strand break, priming DNA synthesis. If the error prone DNA polymerase IV is recruited for the DNA synthesis, an increased number of mutations are potentially introduced in the inactive lac operon on the plasmid. This, in turn, increases the probability of a reversion (-1 frameshift) in lac copy.
A second model is the amplification mutagenesis model. This model suggests that the reversion involves gene duplication of the lac region.27, 28 Like the previous model, this model assumes the lac operon on the plasmid possesses enough lactose catabolic activity that some cells can replicate. In some of these replicating cells, the lac region on the plasmid is duplicated. This model assumes that the reversions do not occur in the non-growing parental cells. Instead, some of the growing cells duplicate the lac region, which possesses some weak lactose catabolizing activity. Unequal recombination increases the number of lac copies per cell, enabling even more growth of these cells. This amplified number of lac operons increases the probability of a reversion (-1 frameshift) in the developing clones. No change in either rate or specificity of mutagenesis occurs. But, this model does require the +1 frameshift mutation to be "leaky" and that lactose be present in the selective media.29
The problem for many researchers was that adaptive mutations did not fit their neo-Darwinian paradigm. Eager to dismiss the concept, many geneticists probably found initial comfort in the third proposed model, the hypermutation model.30 This model claims that the revertants resulted from randomly generated mutations in the Lac- mutants. These Lac- mutants underwent a state of hypermutation, which increases the probability of a reversion (-1 frameshift) of the lac operon on the F' plasmid. The hypermutation model was initially supported by claims of 20 to 50-fold increases of nonselected mutations in the revertants.31 However, Roth et al.32 challenged that achieving the observed number of lac revertants would require the overall mutation rate to be implausibly high. It was also found that only about 10% of the adaptive mutants appear to have been hypermutators.33 Thus, hypermutation does not appear to be required for adaptive mutation within this specific F' model.
Helling, Vargas, and Adams34 obtained mutant strains of E. coli following prolonged cultivation under glucose-limited conditions. They found that a stable co-existing population of two different types of mutant strains developed. One mutant possessed a greater rate of glucose uptake v. the wild-type strain. Glucose uptake in the wild-type strain is regulated by a variety of feedback mechanisms, including glucose metabolites. However, this mutant apparently increases glucose uptake by truncating its pathways for glucose catabolism,35 and acetate is a dominant endproduct. Theoretically, this mutant results from a reduction of feedback inhibition, enabling increased glucose uptake.
The second mutant detected in this co-existing population had mutations that reduced the regulatory control of acetyl CoA synthetase, causing over-expression of this enzyme.36 This resulted in an enhanced ability of the mutants to scavenge the exogenous levels of acetate being produced by the other mutant. Thus, together these mutants had a greater survival in the glucose-limited cultivation conditions. However, again, these two mutants are a form of antagonistic pleiotropy. The phenotypic benefit from the mutations was at the expense of a metabolic pathway necessary for more efficient glucose catabolism, and a regulatory system that is necessary for normal genetic control. Also, the second mutant strain is only beneficial in conjunction with the other mutant. Unless that mutant occurs, the acetyl-CoA mutant will not be advantageous.
A different set of bacterial mutants was obtained by cultivating Pseudomonas putida in starvation conditions for a prolonged period in phenol-based minimal medium. An initial population of mutants involved reduced activity of the DNA repair enzyme MutY.37 Oxidation of guanine to 7,8-dihydro-8-oxoguanine is a common type of DNA damage in starving bacterial cells.38 The MutY repair enzyme is involved in repair of this damage. Reduction of this repair activity probably precipitates an increase in C → A transversions.39 As the culture continued to survive the starvation period, the population of transversion mutants was replaced by mutants containing 1-3 bp deletions.40, 39 In addition, prolonged starvation appears to increase the activity of indigenous IS elements in the cells,41, 39 presumably generating an increase of "knock out" mutations as a consequence.
Error-prone DNA polymerase also appears to contribute to survival of E. coli under starvation conditions.42 Loss or reduction of mismatch repair in E. coli43 and Bacillus subtilis44 significantly increases their survival in aging cultures. In fact, decreased DNA repair fidelity and activity is typically associated with nutritionally stressed bacteria.45 Presumably, the decrease of DNA repair enables increased rates of mutagenesis (hypermutation).8 Increased mutation rates provide an increased possibility of a mutation beneficial to survival in a given environment. Thus, hypermutation has been associated with bacterial adaptation to a variety of stressful conditions.8
Severe stress, such as stationary-phase aging of bacterial cells, also selects for a mutation in transcription factors. A mutation in the sigma factor, sS, reduces the factor's regulatory activity, which appears to increase survival of stationary-phase aging cells.46 However, the mutated sS was most advantageous at a high pH, and was detrimental at a low pH.47 Also, a mutation resulting in a three-base-pair deletion of the leucine-responsive regulatory protein (Lrp) eliminates its DNA-binding activity.48 Lrp activates amino acid anabolism and represses amino acid catabolism.49 This mutant form of the lrp gene appears to increase survival of aging cells in stationary-phase.50 Presumably the advantage of either phenotype in aging cells is the loss or reduction of transcription regulation by these factors, although the exact molecular benefit for less transcription control is still speculative.51 Also, inactivation of the tricarboxylic acid (TCA) cycle enzyme, aconitase, enhances survival of cells in the stationary-phase.52
Another mutation of E. coli facilitated amino acid catabolism under starvation conditions, enabling the mutant to outcompete the parental wild-type.53 This increased catabolism resulted from a genomic rearrangement (Figure 3). The first step of this rearrangement was insertion of an indigenous IS5 element between the promoter and a CRP-binding site (catabolite regulatory protein) of the starvationinducible cstA gene.54 The cstA gene encodes an oligopeptide permease.55 Following its insertion, the IS5 undergoes an inversion with a pre-existing IS5 element located about 60 kb distant.56 This second IS element (IS5D) is located upstream of an operon encoding a high affinity ABC-type transporter.57 As a result of the inversion, the ABC-type transport operon is repositioned to close proximity of the CRP-binding site, and cstA is moved away from its regulatory region.56 The cstA gene is inactivated, but the ABC-type transporter operon is activated.57
The adaptive advantage of these mutations under starvation conditions appears to result from an enhanced ability to scavenge amino acids, specifically aspartate and glutamate.57 Simultaneously inactivating oligopeptide uptake and activating increased amino acid uptake helps to serve this purpose. Also, inactivation of lrp enhances amino acid scavenging, but negatively effects amino acid biosynthesis. Hence, these mutants involve a trade-off of resource utilization where amino acid utilization is enhanced and peptide utilization is depressed.
Each of these mutant strains has an antagonistic pleiotrophy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a "beneficial" mutation). A gene is inactivated by a process that concurrently activates a silent gene. Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial.
Temperature Stress
Following cultivation of E. coli for 2,000 generations at 41.5ºC, various groups of thermal adapted mutants were isolated.58 Several of these mutants contained at least one duplication near the 2.85 Mb position on the chromosome. In addition, a 12 kb deletion was detected in one line of mutants. These duplication and deletion events were not detected in the parental strain following cultivation for 2,000 generations at 37°C.59
Duplication of certain genes or groups of genes has been suggested as an adaptive strategy for bacteria. Hence, certain environmental conditions seem to favor bacteria with specific genes duplicated.60, 61 This may have provided the organism a temporary increase in gene expression of those duplicated genes, which apparently helped the organism cope with the higher temperature. However, once the duplicated regions no longer provide an advantage, they are likely eliminated by recombination.59
A second study found that after 2,000 generations at 41.5 °C, specific heat-inducible genes were expressed at significantly higher levels that in wild-type cells.62, 63 Not all known heat-inducible genes were affected, and not all lines of the thermal adapted mutants possessed the same level of expression of each gene. While the mutation of regulatory systems presumably was involved, the exact mechanism was not disseminated.
Antibiotic Resistance
When confronted with antimicrobials, such as antibiotics, bacteria frequently will develop resistance to the compound. While this resistance often results from horizontal transfer of pre-existing resistance genes, a significant number also result from point mutations.8, 64 However, as discussed in detail by Anderson,65 these mutations typically reduce or inactivate cellular systems or functions. Thus, the organism develops a resistance to an antibiotic by eliminating certain systems, such as transport proteins, enzymatic activity, and binding affinity. For example, ampicillin resistance can result from an SOS response that halts cell division,66 loss of nitroreductase activity can provide resistance to metronidazole and amoxicillin,67 and kanamycin resistance can result from loss of a specific transport protein.68
Like many of the other beneficial mutations just discussed, mutations providing antibiotic resistance are a trade-off. In fact, they offer a very clear example of antagonistic pleiotropy. The organism sacrifices an existing system with the trade-off that the antibiotic is no longer activated, transported, bound, etc.
Nylon Degradation
Nylon 6 is a synthetic polymer consisting of more than 100 units of 6-aminohexanoic acid. Other forms of cyclic and non-cyclic nylon oligomers are formed as part of nylon 6 synthesis. Because nylon is not a natural occurring molecule, bacteria would not have been exposed to this polymer until the 20th century. The recent appearance of nylon degrading bacteria presents an interesting demonstration of bacterial ability to adapt to an ever changing environment and substrate. It has also lead to a few highly exaggerated claims regarding bacterial evolution.69
At the phenotypic level, the appearance of nylon degrading bacteria would seem to involve "evolution" of new enzymes and transport systems. However, further molecular analysis of the bacterial transformation reveals mutations resulting in degeneration of pre-existing systems. The most studied of the nylon degrading bacteria is Arthrobacter sp. K172 (formerly Flavobacterium sp.70). This bacterium employs three enzymes for nylon degradation, EI (NylA), EII (NylB), and EIII (NylC), which are found on the plasmid, pOAD2.71, 72
EI and EIII (also NylC in Agromyces sp.) have been initially characterized.73, 72 They apparently hydrolyze the cyclic forms of some nylons, which provides a linear substrate for EII. However, no detailed analysis of the mutational changes of EI or EIII has yet been performed.
The mutational changes of EII (6-aminohexanoatedimer hydrolase) have been characterized in detail. This analysis suggests that point mutations in a carboxyesterase gene lead to amino acid substitutions in the enzyme's catalytic cleft. This altered the enzyme's substrate specificity sufficiently that it could also hydrolyze linear nylon oligomers.74, 75 Yet, the EII enzyme still possesses the esterase function of the parent esterase. Thus, the mutational alteration results in a reduction of the parent enzyme's specificity (Figure 4). This enables it to hydrolyze a wider range of oligomers that include nylon oligomers.76
Nonetheless, reduced specificity of a pre-existing enzyme is biochemically degenerative to the enzyme,77, 78 even if it provides a presumed phenotypic benefit. The "beneficial" phenotype of nylon degradation requires the a priori existence of the enzyme and its specificity. Its degeneration is not a mechanism that accounts for the origin of either the enzyme or its specificity.
Also on pOAD2 is a DNA region with a high homology to opp genes.79 These genes are involved in oligopeptide transport. Nylon oligomers have many chemical similarities to oligopeptides, thus genes on this region of the plasmid may be involved in nylon transport into the cell. No analysis of how these genes may have been altered by mutations has yet been preformed. However, it is reasonable to speculate that a pre-existing opp gene or set of genes has been altered sufficiently by mutations so that the transport proteins now have an affinity for nylon in addition to naturally occurring oligopeptides. As with enzymes, reduction of transport protein specificity is biochemically degenerative.
The enzyme and putative transport genes on pOAD2 appear to form a nylon degrading operon.79 As a plasmid based operon, it can be transferred to various bacterial species. Thus, this gives it the potential for widespread distribution in the bacterial world. What is more, the increasing amount of microbial degradation of synthetic material11 may likely involve a similar mutational strategy as found with nylon degradation. This is a testament to the versatility of bacterial adaptation. However, these mutations do not account for the origin of the enzyme or transport protein specificity, merely their degeneration. Thus, this adaptive versatility has imposed limits as well, and this fits well within the types of mutational changes predicted by a creation model.
Horizontal Gene Transfer
Horizontal gene transfer (HGT) is cell-to-cell transfer of genetic material, usually plasmids or transposons. Plasmids are autonomous extrachromosomal segments of DNA. They may posses a variety of genes, including genes for mobilization and antibiotic resistance.
HGT of plasmids merely transfers genetic material from one cell to another. Introduction of specific genes, such as antibiotic resistance genes, via a plasmid can be beneficial for bacterial survival. However, HGT of plasmids does not directly account for the origin of the gene(s) being transferred, merely their movement within the microbial world. The genes' existence is a priori. This is consistent with a creation model where genes, regulatory sites, and other genetic activity were formed at the initial creation event, and are not solely the result of mutational or recombination events. The transfer of pre-existing genes and other genetic activity does not account for the origin of the transferred activity. Also, unless the plasmid incorporates into the host chromosome, it does not result in a mutation. Therefore, the contribution of plasmid HGT to bacterial adaptation is a separate topic outside the scope of this paper.
A transposon is a segment of DNA that can be transferred from cell-to-cell via HGT. The transposon can be maintained on a plasmid, but typically exists autonomous of plasmids, and merely moves from chromosome to chromosome. Most cellular "transformation" by transposons involves (a) incorporation of new genes into the cell from the transposon, (b) activation of "silent" genes, and/or (c) insertional disruption of genes and regulatory sites on the host's chromosome. The introduction of new genes into a cell (such as the antibiotic resistant genes typically found on commonly studied transposons) may provide new genetic capability to the transformed cell. However, as with plasmids discussed above, this does not account for the origin of these genes. Their existence is a priori in the biological world.
By analogy, this is like transferring money from the left to the right pocket. The right pocket now has money that it did not posses before, but you are no richer. This type of mechanism cannot account for the origin of the money, merely its transfer among the population. As applied to the biological world, HGT of genes fails to explain their origin, thus it fails to fulfill the genetic requirements for common descent. However, HGT does fit within the creation model where the transfer of existing genes would be predicted as an adaptive design feature.
A promoter on a transposon may also be able to serve as a promoter for a "silent" or promoterless gene.80 While this makes for an interesting genetic transformation, it offers no answer to ultimate origin. Both the gene and the promoter are already present in the biological world. What is more, how would a promoterless gene evolve? An evolutionary origin requires an immediate and viable function for any "evolving" gene. Without immediate functionality, the "evolving" sequence would be subject to selective removal. Rather than evolving independent of a promoter and awaiting the arrival of the transposon's promoter, these promoterless genes merely lost their original promoter function at some point. Thus, promoters from transposons can serve as a surrogate.
While promoter surrogacy may provide a beneficial phenotype to the bacterium, it does not account for the origin of either the gene or the promoter, nor does it directly involve mutations. As such, it too is outside the scope of the paper. Also, surrogacy is not a mechanism providing the genetic requirements for evolution's common descent of ancestry, where there must be an accounting of the origin of both the promoters and the promoterless genes. However, such surrogacy is fully consistent with a creation model.
Most relevant to the focus of this paper are transpositional gene disruptions. When inserting into the chromosome of the transformed cell, the transposon may disrupt a previously existing genetic system or function. Transposon mutagenesis normally results in "knock out" mutations. On occasion, transpositional disruptions will inactivate a regulatory system. This can result in a phenotypic change of the host, such as constitutive production of an enzyme81 or activation of a "silenced" gene.82 Even though such disruptions may occasionally result in a "beneficial" phenotype, they are another form of antagonistic pleiotropy. The benefit is achieved at the expense of a pre-existing genetic system. Thus, disruption or "knock out" mutations are fully consistent with the overall genetic degeneration predicted by the creation model. But, these mutations are inconsistent with a mechanism to account for the origin of flight, vision, cognition, or any other biological system required by common evolutionary descent.
Some transposons, known as foldback elements, can undergo specific folding when inserted into the host's chromosome. This folding can subsequently initiate extensive chromosomal rearrangement.83 However, we are not aware that any foldback elements have been identified in bacteria. In addition, while transposon activity can lead to the formation of new transposons (and even plasmids), the genetic activities of the newly formed transposon originated from pre-existing genes, replication sites, etc.84
Implications of Beneficial Mutations for a Creation Model
As these examples demonstrate, there are numerous forms of mutations that can assist bacteria in adapting to various environmental conditions and dealing with adverse environments. Such mutations can be referred to as "beneficial," in that they serve a benefit to the organism. However, the benefit is generally temporary and transient. In fact, identifying many "beneficial" mutations as a form of antagonistic pleiotropy descriptively suggests the limited value of the mutations. Unnecessary or unused systems are eliminated in a manner that provides a phenotype capable of better surviving a specific environment. While this trade-off enables survival, it is at the expense of a pre-existing system or function. Typically the benefit is also temporary. Beneficial mutations for one type of environment often do not serve a benefit in a different environment, and perhaps are even detrimental to survival in an altered environment.85, 86
Rigid flexibility of bacterial mutations
Mutation and natural selection in bacteria, such as in the case of adaptive mutations or antibiotic resistance, are often touted as "evolution in action." As has been shown in the examples given, these mutations do not account for the origin of new systems or functions. Many of the phenotypes result from loss of pre-existing systems. Other phenotypes involve activation of inactive systems, but this activation often involves simultaneous inactivation of another system. As such, they are not examples of mutations originating new cellular systems or activities.
Instead, bacteria give every appearance of having been designed with a sophisticated ability to adapt to a variety of extreme conditions. This should not be unexpected. Bacteria potentially face a wide variety of environmental conditions. Most bacteria need the ability to adapt to ever changing environments and food sources, and have little alternative but to adapt or die. A creating Designer would provide such ability to bacteria. This may also be true for other unicellular organisms such as yeast and protists.
Yet, bacteria also possess a "rigid flexibility." This flexibility allows bacteria the necessary genetic versatility to adapt and survive in ever-changing environments.87 A creation model would predict that bacteria would be designed for rapid and versatile adaptation. But, this change is limited and specific. Bacteria appear to have been created to serve specific ecological roles, such as biomass conversion and organosubstrate degradation. Thus, any adaptive changes would necessarily be limited so that the bacteria will continue to function in these designed roles. The rigidity of possible changes would also limit bacteria to remain within its created baramin (see Frair for a detailed analysis of created baramins88). This conserving or limiting effect of mutations fits with observable evidence of bacterial changes.
The very concept of antagonistic pleiotropy purposes that the mutation creates an antagonistic situation in the cell. A system needed for one set of environmental parameters is sacrificed in order to better adapt to different parameters. However, a change of these parameters may require the cell to reestablish the sacrificed system, and perhaps sacrifice a different system instead. This balance continues through a variety of environmental conditions and stress situations. Yet, at no point has the bacterial cell developed a new system. It is merely managing the systems it already possesses. Instead, these mutations require the prior existence of the targeted systems. As such, beneficial mutations of bacteria fit concisely within a creation model where biological systems and functions were fully formed at creation. Any subsequent mutations may provide conditional benefits that enable the organism to survive harsh conditions, but the mutations are generally degenerative. Thus, antagonistic pleiotropy fits succinctly within a creation model.
The study of advantageous mutations is important for understanding the power and the limitation of mutations for change in bacterial species. A greater understanding of them may assist in developing creation models of speciation and adaptation in the post-Fall and post-Flood world. It may even assist in a better understanding of the development of bacterial pathogenesis from a creationist perspective.
Adaptive mutations are not used by most organisms
Although the differences between prokaryotes and eukaryotes are widely known, they are rarely differentiated in studies of evolutionary change. The mantra seems to be Jacques Monod's statement that, "Anything found to be true for E. coli must also be true of elephants".8 But elephants have choices that bacteria do not. If food becomes scarce, elephants can migrate to areas where food is more plentiful. Although some bacteria are motile, dramatic changes in location are not feasible. If the temperature becomes hostile or the preferred nutrients become scarce, bacteria have three basic options: endospore formation (not possible for all types of bacteria), adapt, or die.
Bacteria have been designed with great genetic diversity that sometimes is only accessible through genetic alterations by mutations. For example, the ebg operon may be part of a complex backup system for the lac operon in E. coli.89 Perhaps it has ultimately degenerated so that it does not serve the original backup function, but certain mutations can reactivate portions of it. Many other bacterial systems also seem to have various "backup" systems.90 Even a complex operation, such as polysaccharide degradation, has very few rate limiting systems.91
There are several genetic and non-genetic factors that distinguish bacteria from humans and animals, and allow the former to be successful in using mutations for adaptation. As Sanford92 states,
For all these reasons, selection in such systems [bacteria] is much more effective, precise, and can have much higher resolution. This means that in bacteria, a much smaller proportion of the genome is near neutral and un-selectable (this is why theorists typically prefer to use microbial examples) (p. 74).
Ploidy and cellularity differ
Humans are diploid, meaning that every cell (except germ cells) contains two complete copies of each chromosome. Bacteria are generally haploid; each cell possesses only one complete copy of its single chromosome. Under laboratory cultivation it is possible for an individual cell to posses multiple replication forks, hence it may be partial diploid; that is, contain more than one copy of portions of the chromosome. But it is unlikely this is a normal state, and cell division naturally begins before two complete chromosomes are formed.
Being haploid is advantageous to the bacteria under conditions where beneficial mutations are generated. There are no dominant or recessive genotypes of a given gene. In humans, beneficial mutations are less frequent since mutations in both chromosomal copies of the gene would likely need to occur for the mutations to result in a phenotypic change.
In addition, because of the multicellular composition of humans, altering the function of a particular tissue or organ would require the beneficial mutation either to occur in multiple cells or the mutated cell would have to replace all existing cells. For bacteria, the adaptive mutations need only to occur in a single cell. Sanford93 states in regards to bacteria, "Perhaps most importantly, every cell is subject to selection, independently, every cell division." (italics in original) (p. 74). This situation is not true for a multicellular organism. A particular tissue or organ would be selected for as a whole, not at the individual cell level. In addition, tissues and organs do not function in isolation. They are part of organs and organ systems that are interconnected. These organ systems must work together properly to allow an organism to maintain homeostasis. The complexity of multicellular organisms makes the applicability of most types of beneficial mutations found in bacteria unlikely.
In particular, adaptive mutations would not be expected in humans since the mutations would likely occur in somatic cells, which are not inherited by their offspring. It is difficult to imagine how adaptive mutations could occur in germ cells since these cells would not be faced with any of the same selective pressures as the somatic cells. Such a situation would revert back to a Lamarckian type evolution—a position with no genetic basis in humans. What is more, even if the adaptive mutations occurred in germ cells, there is no guarantee that offspring will exhibit the trait caused by the mutation. Two germ cells (that is, sperm and egg) must combine to form the zygote, and it is unlikely they would have the same adaptive mutations. On-the-other-hand, the unicellular nature of the bacteria ensures that the mutation is passed to subsequent generations.
Degree of functionality within the genome differs
An increasing proportion of the DNA within the genomes of humans is being found to be functional (that is, "junk" DNA is not junk).94 This makes it difficult to perceive how humans and animals could utilize many of the types of "beneficial" mutations found in bacteria. There are many sequences known as pyknons throughout the human genome that do not code for proteins but appear to have some function (possibly structural or regulatory).95 Also, transcriptional regions have been found within exons of known human genes.96
This overlapping nature of genes and regulatory functions in human and animal DNA means that a mutation has a distinct possibility of affecting multiple aspects of the genome. Some of those affects may be beneficial, but most would be detrimental. Bacteria need more genomic flexibility for survival, so they are unlikely to have these types of sequences or suffer multiple effects from a single mutation. Mutations in the human genome may have many side effects, whereas those in bacteria are likely to have one specific effect. Beneficial mutations in bacteria are more likely to have a phenotypic impact and undergo stronger positive selection.
Population sizes and generation times differ
Bacterial populations reproduce much faster and produce more offspring than humans. This rapid generation time and large population size means that bacteria can afford the "cost" of selection. When a bacterial population faces adverse environmental conditions 99.999% of the cells may fail to adapt and subsequently die. However, the small percentage that do survive are sufficient for the population to survive. It can rapidly replenish the population back to the original population size. The surviving bacteria may have multiple deleterious mutations throughout their genome (that is, such as a result of being in a hypermutable state), however, they can compensate by reversion or suppression mutations. Humans (and vertebrates) have much longer generation times and much fewer offspring than bacteria. Consequently, an accumulation of multiple mutations will ultimately lead to genetic decay.93 The "cost" of selection becomes more than the population can pay.97
Amount of "noise" differs
In population genetics, noise is a combination of genetic and non-genetic factors that affect the heritability of a trait within the population. Human genomes are more affected by noise than bacterial genomes. For example, the human trait of "fitness" is extremely complex and greatly affected by noise.93 This may be because most contemporary humans do not consistently face life threatening situations where speed or strength become vital attributes. So, fitness levels of humans are not under a strong selective pressure. Thus, fitness in humans has a low heritability factor.93 However, bacterial fitness is frequently under strong selection, as it is a necessary aspect of their constant life-death struggle. Bacteria that are "fit" will be able to adapt and survive, whereas those unable to adapt will die.
Adaptive mutations in humans may lead to cancer
Multiple mutations are characteristic of cancer cells. The number of mutations in cancer cells cannot be sufficiently accounted for based on the spontaneous mutation rate alone, even if these cells have been exposed to carcinogens.98 It has been suggested that possible developing cancer cells are much more like E. coli cells under non-lethal selection.99 The quickly dividing cells would soon need a well-developed blood supply in order to continue their rapid divisions. The blood supply will take time to develop and it is plausible that early cancer cells would have limited nutrients available. Spontaneous mutations in cells that lead to a mutator phenotype may be the first step.100 The mutator phenotype would be similar to the hypermutable state in E. coli wherein mutations are made but not repaired because of a faulty DNA repair system (discussed previously).
Adaptive mutations that allow the cancer cells to grow better under these conditions may occur. It has even been shown that tumor cells with mutations in DNA repair systems have normal mutations rates when growing and higher mutation rates when not growing. This suggests these cells are in a type of hypermutable state when under nonlethal selection.101 Hall102 also points out the problematic nature of adaptive mutations for multicellular organisms, such as humans, and he states,
The machinery that produces adaptive mutations would be very useful in single-cell organisms but might be deleterious in multicell organisms where the requirement for organizing cells into tissues means that programmed growth constraints must be applied to most cells. In multicellular organisms the activation of that adaptive-mutagenesis machinery, which would be advantageous to the individual cell in that it would allow that cell to divide rapidly, would be very disadvantageous to the organism, where the rapidly growing population would be described as a tumor. (p. 5673)
Bacteria frequently develop mutations that enable them to survive and adapt to a variety of environmental conditions. These mutations are generated by many different mechanisms, and provide a wide range of phenotypic modifications. However, most of these mutations can be classified as a form of antagonistic pleiotropy. Some existing systems are sacrificed as a means for surviving certain environments.
Antagonistic pleiotropy is a useful feature of a creation model. Bacteria face a variety of environmental conditions and stressful situations. However, in order to survive, they must contend with any environmental condition that confronts them. Antagonistic pleiotropy provides them genetic mechanisms where they can make specific (and potentially detrimental) genetic changes that will then serve in a particular environment. If the environmental conditions change, the mutation usually becomes less beneficial and perhaps even detrimental. Hence, these mutations do not provide a genetic mechanism that accounts for the origin of biological systems or functions. Rather, they require the prior existence of the targeted cellular systems. As such, beneficial mutations of bacteria fit concisely within a creation model where (a) biological systems and functions were fully formed at creation, (b) subsequent mutations can provide conditional benefits that enable the organism to survive harsh conditions even though the mutation is generally degenerative, and (c) most bacteria need the ability to rapidly adapt to ever changing environments and food sources.
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text:
Yoga Shouldn't HurtIf you practice yoga, no doubt you're aware of its health benefits. But like any physical activity, it's not completely risk free. If you've been practicing for long, you or someone you know has probably pulled a hamstring, tweaked a sacrum, or experienced some injury while on the mat. Close to 9,000 Americans received medical treatment for yoga-related injuries in 2004 and 2005, according to the U.S. Consumer Product Safety Commission. Still, there are only two yoga injuries reported for every 10,000 times it is practiced, according to American Sports Data. Injuries can be great teachers. They invite you to uncover your yoga demons—misalignments or overzealous attempts to force your way into poses—and make corrections. But it's smart to learn proper technique, especially when it comes to your inner knees, hamstring tendons, and sacroiliac joints. These parts are vulnerable to damage and take time to mend. But if you understand what causes trauma to these areas, it's easy to adjust your practice to avoid or help heal injuries. Here's a primer on each. Inner KneeThe Road to Injury: Have you always found it difficult to get into Padmasana (Lotus Pose) and felt tempted to force your legs into the position to join your serene-looking classmates for meditation? If you are thinking of traveling down this road, please reconsider. You may have discovered that rather than leading you to the blissful land of the Lotus, pushing yourself in this way dead-ends with a sickening "pop" in the knee, followed by years of pain and limited mobility. When you hurt your inner knee doing yoga, it's usually because you've tried to force a leg into Padmasana or one of its variations. Sometimes the injury occurs after one or both legs are already in Lotus position and you attempt a pose that adds a back-bending movement, such as Matsyasana (Fish Pose), or a forward-bending movement, such as Ardha Baddha Padma Paschimottanasana (Half-Bound Lotus Seated Forward Bend). To understand how Lotus can hurt your knee, visualize lifting your right foot up and placing it atop your left thigh. To get into this pose safely, your thigh will have to rotate outward about 115 degrees. For many of us, though, the thigh cannot turn out that much, either because of its bone structure or because tight muscles and ligaments inhibit its movement. If your thigh stops rotating but you keep lifting the shin and foot, you'll bend the knee joint sideways, which will pinch the inner-knee bones together—the upper inner end of the shin-bone pressing against the lower inner end of the thighbone. Between these bones lies the medial meniscus, which is a protective rim of cartilage that pads the knee joint and guides its movement. When you lift your foot, you are using your same-side shinbone as a long lever. If the thighbone doesn't rotate enough, you'll apply tremendous pinching pressure to the meniscus—as if your shinbone and thighbone were a giant pair of pliers. Forcing this lift even moderately can do serious damage. Similarly, if you are in Lotus and your top knee is not on the floor, pushing that knee downward can apply enormous damaging force to the meniscus. Prevent and Prepare: To prevent this injury, the first rule is to never force your legs into any Lotus variations—either by pulling the foot strongly upward, pushing the knee downward, or thrusting your body forward or backward. Don't let your yoga teacher push or pull you into any of these poses either. Janu Sirsasana (Head-of-the-Knee Pose) and Baddha Konasana (Bound Angle Pose) can cause similar (though usually less severe) pinching of the inner knee, so practice them cautiously, too. Stop going deeper and back off if you feel pressure or pain in the knee. The structures that need to loosen up in these poses are all located around the hip area, so that's where you should feel stretching or releasing sensations as you go deeper. The safest way to practice Padmasana and related poses is to strongly rotate your thigh outward at the hip and not go deeper into the pose when you reach the limit of your outward rotation. This means that you'll have to stop lifting your foot when your thigh stops rotating, so you may not get your foot on the opposite thigh. (Remember the upside: happy, functional, pain-free knees.) You can use your hands or a strap to help rotate your thighbone outward. Whether using your hands, a strap, or a cloth, if your knee ends up dangling in midair, support it with a folded blanket so you do not inadvertently force it downward as you turn the thigh outward. The Path to Healing: If you have the misfortune of hurting your inner knee in Padmasana or a related pose, the first thing to do is leave it alone. You need to rest, ice, elevate, and compress it for a few days to reduce swelling and inflammation. If the injury seems serious, seek medical attention. It's a good idea to reintroduce knee range of motion as early as you can by gently flexing and extending the knee to the extent possible. A yoga program for recovery needs to be individualized to your needs and supervised by a qualified instructor. But the general pattern is to promote alignment and strength with basic standing poses, such as Trikonasana (Triangle Pose) and Virabhadrasana II (Warrior Pose II). If necessary, support your body with a chair to take weight off the knee. In addition, increase range of motion by doing Virasana (Hero Pose) with the pelvis supported on a prop, and eventually reintroduce outward rotating movements like Baddha Konasana (and perhaps Padmasana) using a rolled cloth behind the inner knee.
Upper-Hamstring TendonsThe Road to Injury: Say that you're a flexible yoga teacher. Each day you wake up and practice hamstring stretches, then demonstrate deep forward bends in your classes. When you notice a pain just below one of your sitting bones, you stretch it more, thinking that will promote healing. But when the pain increases, you decide to rest it. After the pain diminishes, you stretch again and reinjure the area. The pain comes back, and the cycle repeats. This process can go on for years. The hamstrings are three long muscles that cover the back of the thighs. At the top of them, tendons attach all three to the sitting bones. A nagging sensation just below the sitting bone is caused by a tear in the upper-hamstring tendon, near where it connects to the bone (called the attachment). To stretch hamstrings in forward-bending poses like Uttanasana (Standing Forward Bend), you straighten your knees while lifting your sitting bones. Any time you stretch a muscle, it pulls on its tendons, creating microscopic tears in them. If you wait 24 to 48 hours between practice sessions, these tiny tears heal. But the upper-hamstring tendons can take longer to heal because they are poorly supplied with blood. When you don't give your hamstrings time to rest, you set up a scenario for injury. Alignment can also be an issue. Teachers often tell beginners to lift their sitting bones in forward bends because beginners tend to round their backs in such poses, which can lead to disk compression and lower-back injuries. But people with loose hamstrings can lift their sitting bones so high that the tendon starts to wrap around the bone. This can weaken the tendon. To recap: If you produce new tears in your upper-hamstring tendons faster than your body can repair the old ones, you'll end up with an injury. If you rest and start to heal, the partially healed tissue may still be too weak to withstand the pose and you'll tear it again, ending up with more pain than before. If you repeat this cycle often enough, scar tissue will eventually develop in the torn area—and rehabilitating scar tissue is typically a slow, difficult process. Often hamstring injuries that seem to occur suddenly are set up by a gradual weakening of the tendon over time, caused by overstretching and insufficient rest. The weakening can culminate in one powerful stretch that leads to injury. Prevent and Prepare: To prevent an upper-hamstring injury, you need to approach straight-leg forward bends gradually and with awareness, taking any pain near the sitting bone seriously. Never force a forward bend (or any pose), and if you feel discomfort at or near the sitting bone while bending forward, stop stretching that hamstring immediately. If the discomfort recurs in a future practice, avoid any action that causes it for at least several days. This usually means you should avoid practicing forward bends over that leg or you can bend the injured-side knee in all forward bends. Bending the knee protects the hamstring tendons by taking some of the stretch off of them and giving them time to repair themselves before a significant injury develops. Reintroduce straight-leg forward bends on the affected side only when the discomfort is completely gone for at least a few days, and then do so gradually. Another important preventive measure is to include plenty of hamstring-strengthening poses, such as Salabhasana (Locust Pose), Purvottanasana (Upward Plank Pose), and Virabhadrasana III (Warrior Pose III), in your asana practice. Building muscle strength also strengthens the tendons of these muscles. However, if you have an existing hamstring injury, be sure to introduce these poses gradually. The Path to Healing: If your injury is new, especially if you experience a dramatic injury such as a sudden tearing sensation during a hamstring stretch, rest and ice the area immediately. Be sure to avoid stressing it in any way for several days before introducing any recovery exercises at all. Recovering from an upper-hamstring tendon injury typically takes at least a year. There are different schools of thought on how to recuperate. Some people suggest that you avoid all stretching for about six weeks while slowly reintroducing very mild strengthening exercises such as tiny preparatory movements for Salabhasana and Dhanurasana (Bow Pose). You systematically build up strength over the next several months, eventually adding powerful strengtheners like Purvottanasana and exercises that combine strengthening and stretching, such as Supta Padangusthasana (Reclining Hand-to-Big-Toe Pose), against resistance. The key is to avoid any stretching that causes pain to the injured tendon while systematically introducing stronger hamstring-strengthening exercises, including those that strengthen the muscle in the stretched position, for several months. You shouldn't reintroduce any maximum-power hamstring stretches, such as Paschimottanasana (Seated Forward Bend), for at least a year after your injury.
Sacroiliac JointThe Road to Injury: Suppose you're one of those people who finds that yoga comes easily to you. You can bend into most poses without stress or strain. One day, while coming out of Janu Sirsasana, you notice that something feels a little off down where your lower back joins your pelvis. From that day on, you frequently have a nagging ache in that area. It's usually more annoying than disabling, and periodically it goes away altogether, only to mysteriously reappear days or even weeks later. These are some of the symptoms of an unstable sacroiliac joint alternately moving out of alignment and back in again. The sacrum is the bone that is shaped like an upside-down triangle at the base of the spine. On each side of the sacrum, a roughened surface makes contact with the corresponding surface of the left and right ilium bones, or the "wings" of the pelvis. These are the left and right sacroiliac (SI) joints. Strong ligaments hold the SI joints together to prevent the sacrum from tipping forward between the ilium bones. To get an idea of where your SI joints are, trace your thumb over the top rim of your pelvis on one side, moving backward until you find the rearmost bony prominence of the ilium (this is called the posterior superior iliac spine or PSIS). If it were possible to press your thumb forward an inch or two, deep into your body, you would be touching one of your SI joints. Yoga students frequently develop a specific pain pattern that's characterized by a dull ache over an area about the size of a quarter and is centered on the PSIS on one side of the body only. Sitting, forward bending, and twisting movements often make it worse, and back and sidebending can also be painful. Although not all experts agree and other injuries must be ruled out, many yoga teachers and health professionals believe that this pain pattern is caused by the misalignment of one of the sacroiliac joints. According to one theory, yoga practice (especially if it emphasizes forward bends, twists, and poses that stretch the inner thighs) can loosen the supporting ligaments of the SI joints over time, until one side of the upper sacrum slips forward relative to the ilium on that side. Because the two irregular surfaces no longer sit properly on one another, pressing them together tightly (as occurs strongly while sitting) causes pain. Prevent and Prepare: To prevent this problem from happening, be mindful of your alignment in different types of poses. In forward bends, be careful to move your sacrum and ilium forward as a unit. For example, in Janu Sirsasana, move into the pose by tilting the iliac crest (pelvic rim) of the bent leg forward toward the foot of the straight leg. This makes the ilium push the sacrum along so that the two bones move as one. When your ilium stops moving, don't tilt your sacrum any deeper into the pose. Likewise, in twists, experiment with letting the pelvis turn along with the spine instead of keeping it fixed, so the sacrum and ilium move as a unit. In forward bends, twists, and any pose that stretches your inner thighs, try contracting the pelvic-floor muscles. These muscles help hold the sacrum in place by pulling the sitting bones toward one another, thereby squeezing the ilium bones inward against the sacrum. Finally, strengthening muscles of the back with poses such as Salabhasana, and strengthening the deepest abdominal muscle (transversus abdominis) with pPranayama practices such as Kapalabhati (Skull Shining Breath), help stabilize the SI joints. The Path to Healing: If you already have a sacroiliac misalignment, the key is to adjust the joint back into its proper position and keep it there. Some health professionals know how to manually manipulate the SI joint back into place, but it often pops back out soon afterward. Therefore, it's helpful to learn how to reset your own SI joint using asana techniques, but it's best to learn these techniques from a qualified instructor. The golden rule for SI-adjusting postures is that a correct pose should immediately feel good on the injured area while you practice it. Enter each pose slowly, and if it causes any discomfort near the PSIS, come out of it right away. Not all poses work for all people, but you need only a single one that works for you. Two examples of poses that help some people are the Salabhasana and Virabhadrasana I (Warrior Pose I) variations shown here. Either side of the Virabhadrasana I variation may be helpful. Once you have learned to put your SI joint back into place, make sure it is properly located before each yoga practice and follow the preventive steps above to keep it there. At the end of practice, use your technique again, if needed, to firmly reset the joint. Some teachers find that taking special care to keep the SI joint in place at all times over a period of months or even years can make it more stable.
Roger Cole, PhD, has practiced yoga since 1975 and taught since 1980. He is a certified Iyengar Yoga teacher trained at the Iyengar Yoga Institutes in San Francisco and Pune, India. He teaches at Yoga Del Mar in Del Mar, California. For more information, visit http://www.rogercoleyoga.com.Popular Asana Columns ArticlesRecent Practice Articles
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Wednesday, March 05, 2014
... and (hopefully) out like a lamb. In light of our recent mini ice storm, here's an illustration we did for the kid culture page for the march issue for Dallas Child Magazine.
Wednesday, March 05, 2014
... and (hopefully) out like a lamb. In light of our recent mini ice storm, here's an illustration we did for the kid culture page for the march issue for Dallas Child Magazine.
Saturday, December 07, 2013
Major bummer, but because of the weather and the roads are still a bit crunchy, we are postponing our 4th Anniversary Soul Train Party to next week, Saturday, Dec. 14th. Just want everyone to be safe and to have a happy holiday. Bishop Arts District is still hosting the Jingle Bells on Bishop if you're getting stir crazy! Stay warm and have a great day and hope to see you next week to party!
Sunday, December 01, 2013
Here's our new letterpress workshop schedule for 2014! We've added a new workshop in the mix! Here's the schedule listed out. You can sign up on our online store or in person at both shop.
Click here (1,2,3) to see some photos from our Typesetting Poster Workshop.
We are super excited about our new FROM THE DESK OF... WORKSHOP. Students will have the opportunity to print 150 one-color personal letterpress business cards, 50 folded (A1 size) notecards on Crane Lettra Pearl White 110#C and line 50 envelopes from French Paper; we'll have various colors of envelopes for students to choose from.* Students can pick from three templated design options that we provide or student can produce their own design. Once you've signed up for the workshop, we will send you an email within 24 hours for you to complete so that we can fill in the relevant personal information to the design that you chose. Please send artwork and forms back immediately, we send off for polymer plates, which you can keep and reuse, and want to make sure that they are delivered to us in time for the workshop. THIS WORKSHOP IS VERY DATE SENSITIVE to make sure that we get your plates in time for the workshop. Please take notes of the dates in the individual workshops.
Students can pick from these design options:
See the examples below. Because of the complexity and time sensitive nature of this workshop, please feel free to email us at firstname.lastname@example.com or come by to either shops if you have any questions.
Option A. Students will mix their own inks from the color they choose..
Option B. We will be printing on the either the Challenge or the Vandercook...
Option C. Students keep the polymer plate with their design.
Option D. All Artwork MUST be submitted and approved by us by specified date. And MUST be sent in Adobe Illustrator EPS file with vector artwork only and outlined type. There is more information on the workshop page.
Sunday, December 01, 2013
FOURTH YEAR ANNIVERSARY PARTY on SATURDAY NIGHT, DECEMBER 7th, 2013!!!
To celebrate, we're throwing a huge Soul Train themed party at the Henderson Shop. We're gonna come dressed up, but absolutely no pressure (but, if you need wardrobe inspiration, click here!), just come out, have a drink, and hang with us as we celebrate four years. As usual, we'll have all sorts of yummy food and drinks. Our good friend, DJ Cj DeMarx will be providing the grooves. The three of us feel so amazingly lucky and this is such a happy time for us, we cannot wait to celebrate this milestone together.
With this in mind and in light of the recent typhoon that hit Tacloban in the Philippines, we will be donating 10% off all our sales that night to the Red Cross Disaster Relief. Also, you can also directly donate to the Red Cross on their fundraising page.
Tuesday, November 12, 2013
Hope y'all can come out for Candlelight on Henderson on Wednesday, November 13th, 2013 from 6-9pm. We're joining our Henderson Avenue neighbors in celebration of the twenty plus years of this event and the upcoming holiday season with some drinks and food.
AND, it was exactly four years ago that we opened our shop down here! To celebrate our FOURTH ANNIVERSARY, we're having a STOREWIDE 10% OFF SALE ON EVERYTHING this evening. All jewelry, prints, frames, stationary, ornaments... EVERYTHING is on sale!!!!!!
* ALL SALES ARE FINAL. NO REFUNDS OR EXCHANGES.Discount only applies on this date and time at our Henderson shop.
Here's some pics of some of the new deliveries we've been getting. Glitter Deer!
Amethyst Diarama from Becky's Buttons and Things from Colorado
Ceramic vases and vessels from Bean and Bailey in Tennessee
New Rings from Brooklyn's Digby and Iona
Handmade eyewear from Masanuga of Japan.
Friday, October 25, 2013
Derek and Jully doing their best Magnum. These SUPER PURPLE FOIL shirts are printed by the mega
talented Shamsy and Scot.
Think this might be one of the coooooolest project we've ever worked on. A few weeks ago, we were thinking about our shop and what it meant (we get asked almost daily), and thought it would be really great to do a Chinese version of it. So after a few calls to Toronto, our badass Grandmother agreed to do a few versions for us. Not only is she a strong matriarch, but she's also an amazing scholar and beautiful calligrapher. She runs this family.
The Chinese language is not just technically complex, but each word, each grouping of words, has a multitude of meanings. It's considered visual and symbolic poetry. The semantics are so important. So, after multiple calls between ShopDad, ShopUncle, and our Grandma these are all the versions she came up with. Like how are shop can mean and be so many things, she provided us with thoughtful and beautiful versions to choose from. So far, we've got the new shirt and some new letterpress cards and shop tags. Looking forward to using all of her work on more projects.
Close up.
Printed in-house.
love yellow and black on chipboard.
Our classy version.
Heart Eye patch.


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Chancellorsville Visitor Center Closed Beginning Dec. 23
The Chancellorsville Battlefield Visitor Center will be closed for renovation work until March 15, when we expect to open on a limited basis. The information desk, restrooms, and bookstore will open then, but exhibits will be closed as we install new.
Exhibit renovations at Fredericksburg Battlefield Visitor Center
The Fredericksburg Battlefield Visitor Center will be closed Friday, March 7, and exhibits will be unavailable as we work on dismantling existing exhibits and prepare for new. The bookstore will remain open.
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Did You Know?
Both Ellwood and Chatham were owned by the Lacy family during the Civil War. Both houses are part of Fredericksburg and Spotsylvania National Military Park.


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Duck Crossing Holds Up Traffic Can you notice the duck that doesn't fit in? 8/10/2011 12:00:00 AM 15,217
Duck Ride Malfunction This ride was made for little kids, not some teenagers trying to spin into oblivion. 7/21/2011 12:00:00 AM 28,080
Ducks vs Wind A big gust of wind sends the little ducklings rolling away leaving mother duck to chase after them. 3/13/2011 12:00:00 AM 68,608
Gravity Duck Gravity Duck needs your help! Help him gather all the golden eggs in all of the 40 levels. Use your arrow keys to move and hit X to invert the gravity! 11/1/2010 12:00:00 AM 11,135
Duck Hunt Behind The Scenes You just press start and enjoy, but there is a lot going on behind that fence. 5/27/2010 12:00:00 AM
Surfing Duck makes news headlines in Australia This news piece is about all the recent duck clips seen in Australia. Bizarre! 2/12/2008 12:00:00 AM 39,064
Ducks on an Escalator Check out all the ducks trying to climb an Escalator in the mall. 1/29/2008 12:00:00 AM 88,816
A Surfing Duck This duck wanted to get in on the surfing action as well! 1/22/2008 12:00:00 AM 63,887


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After drought: How much N credit for next year?
The dry conditions and reductions in yield in many fields this season have resulted in lots of questions about plans for next year. Are nitrogen (N) rate adjustments needed for the 2013 corn crop?
First, the easy answers. In areas where corn yields were somewhat reduced but overall production practices have been normal, there should be no need to adjust the typical practices for next year's crop. For corn following corn, use the maximum return to nitrogen (MRTN) or profitable N rate range calculated with the corn N rate calculator. Similarly for soybean fields, even if they yielded nothing or very little, no special change should be made in nitrogen-management decisions. The corn N rate calculator has the option to select soybean as the previous crop when calculating MRTN for the corn crop in rotation. The reason you should not worry about adjusting the MRTN value according to the condition of the soybean crop is that soybeans do not leave excess N in the soil. Corn following soybean often needs less nitrogen because, among other factors, the quantity and quality of soybean residue compared to corn residue reduce the amount of immobilization and increase the amount of nitrogen mineralization from crop residue and the soil. Using nitrogen response data for corn following soybean, the calculator already adjusts for what we used to call an "N credit." Compared to corn following corn for Illinois, the calculator shows that the N rate for corn following soybean for the north, central, and south regions of the state can be reduced approximately 50, 30, and 20 lb N/acre, respectively.
Now let's talk about the difficult answers--those for fields where the corn crop was severely affected by drought and the amount of N taken up was reduced. In these situations it is likely that large amounts of unused nitrate-N would be left in the field. What is hard to know is how much of that nitrate to consider available for next year, and thus how much to adjust N rate applications. While there is no simple guideline, it is possible to approximate how much N would be available either indirectly, by determining how much was removed in grain, or directly, by measuring soil nitrate-N (NO3-N) levels.
The indirect measurement using grain yield is easier, but I believe it provides less certainty. On average, a bushel of corn removes 0.66 lb N. Multiplying this removal rate by the bushels produced per acre and subtracting it from the amount of N applied per acre would give an idea of how much N remains in the field. Of course, not all that N will be plant-available the next growing season. Under low N-loss potential (normal precipitation or drier conditions during the time between harvest and next spring), one should anticipate approximately 50% of the total remaining N to be available for the 2013 crop. For example, if a field received 180 lb N/acre and only yielded 70 bushels/acre, then the remaining N would be 180 - 46 (N in grain: 70 x 0.66) = 134 lb N/acre. Multiplying that difference by 0.5 (50% availability) equals 67 lb N/acre that could be subtracted from the nitrogen rate for next year.
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Originally Posted by CyclonesRulzzz game over Really?
Originally Posted by mhalb Why didn't Moody start? late for practice
and we scored!? wtf is this scoring thing?
***King of Diplomacy***
Big Ten Network
yay we scored. there goes the shutout.
5 turnovers in first 7 minutes. They are pressing too hard.
Settle down ladies...things will come.
I think theyre forgetting there is a court between the basket in the 3 point line
When you dig a hole this deep, you just try to crawl back to within several points by half. It's not over folks. Sometimes getting off to such a fast start isn't the best thing (fools gold). That said, I wish it was us who was up by 11.
We always seem to fall to pieces in Iowa City.
Originally Posted by cyowan Rulzzz 3:16 says I just liked your post!
We have to win this on the defensive end.
Slowly starting to crawl back into the game.
10-2 run. They are starting to settle down and play ISU ball. Defense still needs to stiffen up.
Its 16-10 and its a ball game.
My goodness the turnovers are terrible. bad, bad, bad.
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- FrontPage Magazine - http://www.frontpagemag.com -
Pause Before You Play, Says Bristol Palin
Posted By Suzanne Venker On April 9, 2010 @ 6:00 am In NewsReal Blog | No Comments
Bristol Palin has a message for America — and it's a good one. Essentially, she tells young people to stop and think before they have sex. Or, better yet, just don't have sex at all. Naturally, the left — like the foolish readers over at Huffington Post — are doing their best to dismantle Palin's message. They simply refuse to accept that Miss Palin offers something of value to society. Instead, they make silly claims like these:
"She wants to promote no sex, yet she was screwing when her mom was a goofy elected governor."
"Okay…so if Palins have children out of wedlock, the child is totally worth the trouble and expense, but anyone else's child will only present problems."
This is standard leftist logic. To a lefty, a person who made a mistake and speaks out in an effort to help others avoid her fate is a hypocrite. Ridiculous. If we can't learn from one another, what's the point?
In the second quote the reader hears elitism where there isn't any. Bristol Palin is conceding that being a teen mom is difficult regardless of class but is also stating a fact that without money and a support system (i.e. family/friends to help care for the child), teen motherhood will become more difficult than anyone can imagine.
"I don't think anyone realizes how difficult it really is until you actually have a screaming baby in your arms and you're up all night," said Palin. "It changes literally every aspect of your life, and if girls realized how hard it was to be a teen mom, they would think twice about having sex without the proper education and proper knowledge."
By "proper education and knowledge," Palin isn't just referring to the politically correct safe sex message of making sure people use birth control. She's talking about having all the knowledge one needs — including the uncomfortable fact that teen motherhood is neither fun nor glamorous.
Palin's ad is harsh — but honest. Which is the best approach to solving any social ill.
Suzanne Venker is an author, blogger, and former teacher. You can read more from Suzanne at www.suzannevenker.com and No Bull Mom.
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