Evolution Research - General Evolution News: 04 February 2007

Saturday, February 10, 2007

Which Genome Variants Matter?

Global Survey of the Consequences of small and large DNA variants in our Genome:

Findings published February 9 2007 in Science (see below) will accelerate the search for genes involved in human disease. The report provides a first genome-wide view of how the unique composition of genetic variation within each of us leads to unique patterns of gene activity.

By defining those genetic variants with a biological effect, the results will help to prioritise regions of the genome that are investigated for association with disease. This is an important step to understanding links between genes and disease for individuals, and across populations.

The Human Genome Project gave us the instruction manual for building a human. The HapMap and Copy Number Variation (CNV) Projects developed indices of where to find differences in the manuals of different people. One of the challenges for research into variation and disease is that most variants have no consequence for our wellbeing.

The new study gives a global view of the consequences of those differences for gene activity. The work shows that activity of more than 1000 genes is affected by sequence variation and is the first map of human populations that identifies the most important fraction of DNA variation, that which directly affects gene activity.

The research was led by scientists from the Wellcome Trust Sanger Institute, together with colleagues from the University of Cambridge, Hospital for Sick Children/University of Toronto and Harvard Medical School/Brigham and Women's Hospital.

Using the HapMap series of cell samples from four populations, they measured the activity of more than 14,000 genes in cells grown in culture. The cell samples provide a snapshot of genetic activity in one cell type. The activity of each gene was then correlated with genetic variation nearby, as defined by the HapMap, an index of single-base changes (single nucleotide polymorphisms, or SNPs) and the new index of copy number variants (CNVs).

"We've been able to look back into our history and find changes that are older and likely to be shared among populations," explained Dr Manolis Dermitzakis, senior author and Project Leader at the Wellcome Trust Sanger Institute. "But we also find many that are newer and less widespread."

"These are part of our recent evolution and a step along the way to understanding the origin and personal consequences of genetic change, not least for our wellbeing. This is a first generation map of biologically important DNA sequence variation."

The understanding of the genetic basis of gene activity will help medical research to provide individuals with information about their personal predisposition to disease.

The study was a massive undertaking: it included HapMap genotype data on 700,000 SNPs located close to genes, as well as 25,000 sites interrogated for potential structural variation to examine copy-number differences, looking at the activity of 14,000 genes in 210 unrelated individuals.

SNP and CNV variation correlated with altered activity in almost 900 and 240 genes, respectively. The HapMap has been invaluable in detecting variants involved in many diseases and these results suggest that the CNV index will prove similarly useful.

"The remarkable finding was that there is such little overlap in the genes found by using the two indices," commented Dr Matthew Hurles, also a leader of the project at the Wellcome Trust Sanger Institute. "Only about 10% of the activity variants associated with a CNV were also associated with a SNP."

"This suggests that we must include CNV studies in our searches for genetic variation associated with disease or we will be missing a lot of the important genetic effects."

The results show that at least 10-20% of heritable variation in gene activity is due to CNVs. The team found associations that included previously known examples, such as UGT2B17, which has been associated with prostate cancer, proving that the new approach works well.

They also showed for the first time that activity of other genes, located close to UGT2B17, was affected. Finding other effects in this way will enhance the search for critical genes within a region of genetic possibilities.

Some associations were not found in all four populations, two-thirds (CNVs or SNPs) being found in only one population. A gene implicated in Spinal Muscular Atrophy showed an association in three populations, but not in Yoruba from Ibadan, Nigeria. Understanding population differences can help us understand our history.

Variation in copy number can affect gene activity by altering the 'dose' of a gene, by disrupting the active parts of a gene that contain the code for protein, or by disrupting the regulatory regions of the genome that control gene activity - the on/off and dimmer switches in our genome.

"Although the simplest model for a CNV affecting gene activity is where the variant is a deletion of a gene or part of a gene, we found examples where activity is affected from a distance," commented Barbara Stranger, first author and post-doctoral fellow at the Wellcome Trust Sanger Institute. "This may occur when the CNV reduces the effectiveness of a region that works to switch the genes on or off."

The survey gives the first global view of the effects of SNPs and CNVs on gene activity. The methods and resources developed will help researchers better understand the link between differences - large and small - in our genome and our health.

Source: Wellcome Trust Sanger Institute Press Releases 8th February 2007

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Based on:

Stranger BE et al. (2007) Relative impact of nucleotide and copy number variation on gene expression phenotypes.
Science 9 February 2007: Vol. 315. no. 5813, pp. 848 - 853 DOI: 10.1126/science.1136678
Matthew Hurles and Manolis Dermitzakis are corresponding authors.

Extensive studies are currently being performed to associate disease susceptibility with one form of genetic variation, namely, single-nucleotide polymorphisms (SNPs). In recent years, another type of common genetic variation has been characterized, namely, structural variation, including copy number variants (CNVs). To determine the overall contribution of CNVs to complex phenotypes, we have performed association analyses of expression levels of 14,925 transcripts with SNPs and CNVs in individuals who are part of the International HapMap project. SNPs and CNVs captured 83.6% and 17.7% of the total detected genetic variation in gene expression, respectively, but the signals from the two types of variation had little overlap. Interrogation of the genome for both types of variants may be an effective way to elucidate the causes of complex phenotypes and disease in humans.

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Friday, February 09, 2007

Professor Contends Biological Underpinnings Of Darwinian Evolution Not Valid

(Jeffrey H. Schwartz and Bruno Maresca's approach is consistent with a proposed testable 'Model of an Internal Evolutionary Mechanism' based on an extension to homeostasis - see [2])

Summary: Jeffrey H. Schwartz's most recent article, "Critique of Molecular Systematics," is the next step towards a counter evolutionary theory that takes a critical look at the theory of cellular and molecular change.

Pittsburgh - Jeffrey H. Schwartz, University of Pittsburgh professor of anthropology in the School of Arts and Sciences, is working to debunk a major tenet of Darwinian evolution. Schwartz believes that evolutionary changes occur suddenly as opposed to the Darwinian model of evolution, which is characterized by gradual and constant change. Among other scientific observations, gaps in the fossil record could bolster Schwartz's theory because, for Schwartz, there is no "missing link."

In an examination that further challenges the Darwinian model, Schwartz and cowriter Bruno Maresca, a professor of biochemistry at the University of Salerno, Italy, examine the history and development of what the writers dub the "Molecular Assumption" (MA) in the article "Do Molecular Clocks Run at All? A Critique of Molecular Systematics," [1] to be published in the Febuary 9 issue of Biological Theory. [Molecular Clock]

The MA became a veritable scientific theory when, in 1962, biochemists Emil Zuckerkandl and Linus Pauling demonstrated species similarity through utilizing immunological activity between the blood's serum and a constructed antiserum. Upon observing the intensity of the serum and antiserum reactivity between human, gorilla, horse, chicken, and fish blood, Zuckerkandl and Pauling deduced "special relatedness"-the more intense the reaction, the more closely related the species were supposed to be.

Fish blood was most dissimilar, so it was assumed that the fish line diverged long before the other species. Human and gorilla blood were the most similar, meaning both species had the least amount of time to diverge. Ultimately, the Darwinian model of constant evolutionary change was imposed upon the static observation made by Zuckerkandl and Pauling.

To date, the scientific community has accepted the MA as a scientific truth. It is this assumption, which Schwartz is contemplating: "That always struck me as being a very odd thing-that this model of constant change was never challenged." Schwartz has his own theories regarding evolution, which are backed by recent developments in molecular biology.

Multicellular animals have large sections of genomes, the genetic material of an organism, which control their development. Schwartz argues that the structure of the genome does not keep changing, based on the presence of stress proteins, also known as heat shock proteins. These proteins are located in each cell, and their main function is to eliminate the potential for cellular error and change via maintaining normal cellular form through protein folding.

This regular cellular maintenance is what Schwartz points to regarding his refutation of constant cellular change. "The biology of the cell seems to run contrary to the model people have in their heads," says Schwartz, and he contends that if our molecules were constantly changing, it would threaten proper survival, and strange animals would be rapidly emerging all over the world. Consequentially, Schwartz argues that molecular change is brought about only by significant environmental stressors, such as rapid temperature change, severe dietary change, or even physical crowding.

If an organism's stress proteins are unable to cope with a significant change, the genomic structure can be modified. However, Schwartz notes, a mutation also can be recessive in an organism for many generations before it is displayed in its offspring. Whether or not the offspring survives is another matter. If it does in fact live, the presence of this genetically modified organism is not the product of gradual molecular change but a sudden display of the genetic mutation, which may have occurred myriad years prior.

However, it is not only the current molecular theory that intrigues Schwartz, but the failure of the scientific community to question an idea that is more than 40 years old: "The history of organ life is undemonstrable; we cannot prove a whole lot in evolutionary biology, and our findings will always be hypothesis. There is one true evolutionary history of life, and whether we will actually ever know it is not likely. Most importantly, we have to think about questioning underlying assumptions, whether we are dealing with molecules or anything else," says Schwartz.

Schwartz, who forensically reconstructed three life-size images of George Washington that are on display at Mt. Vernon, is a Fellow of the prestigious American Association for the Advancement of Science and the World Academy of Art and Science. He is the author of several books, including "The Red Ape: Orang-utans & Human Origins" (Westview Press, 2005) and "Sudden Origins: Fossils, Genes, and the Emergence of Species" (Wiley, 2000). He has spent more than 20 years contemplating the methods, theories, and philosophy of taking data and trying to interpret it for purposes of reconstructing evolutionary relationships.

Source: University of Pittsburgh News February 9, 2007

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[1] "Do Molecular Clocks Run at All? A Critique of Molecular Systematics,"
Jeffrey H. Schwartz and Bruno Maresca

Currently available as a PDF file from Orangutans and human origins at the Buffalo Museum of Science.

Abstract

Although molecular systematists may use the terminology of cladism, claiming that the reconstruction of phylogenetic relationships is based on shared derived states (synapomorphies), the latter is not the case. Rather, molecular systematics is (largely) based on the assumption, first clearly articulated by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness. This assumption derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change. Review of the history of molecular systematics and its claims in the context of molecular biology reveals that there is no basis for the "molecular assumption."

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[2] Maresca, Bruno and Schwartz, Jeffrey H.
(2006) "Sudden Origins: a general mechanism of evolution based on stress protein concentration and rapid environmental change." The Anatomical Record, Part B: The New Anatomist, Vol. 289B: 38-46.

Abstract

A major theme in Darwinian evolutionary theory is that novelty arises through a process in which organisms and their features are gradually transformed. Morgan provided Darwinism and the evolutionary synthesis with the idea that minor mutations produce the minuscule morphological variations on which natural selection then acts, and that, although mutation is random, once a process of gradual genetic modification begins, it becomes directional and leads to morphological, and consequently organismal, transformation. In contrast, studies on the role of cell membrane physical states in regulating the expression of stress proteins in response to environmental shifts indicate the existence of a downstream mechanism that prevents or corrects genetic change (i.e., maintains "DNA homeostasis") (homeostasis). However, episodic spikes in various kinds of environmental stress that exceed an organism's cells' thresholds for expression of proper amounts of stress proteins responsible for protein folding (including stochastically occurring DNA repair) may increase mutation rate and genetic change, which in turn will alter the pattern of gene expression during development. If severe stress disrupts DNA homeostasis during meiosis (gametogenesis), this could allow for the appearance of significant mutational events that would otherwise be corrected or suppressed. In evolutionary terms, extreme spikes in environmental stress make possible the emergence of new genetic and consequent developmental and epigenetic networks, and thus also the emergence of potentially new morphological traits, without invoking geographic or other isolating mechanisms.

See "The Internal Evolutionary Mechanism: Basic Concept" (blog post - includes fibonacci analogy) and "Model of an Internal Evolutionary Mechanism" (original webpages).

And:

"An Error In Associating Lamarck With 'Adaptive Mutations'?"

"Why research an 'Internal Evolutionary Mechanism'? (1)"

"An Internal Evolutionary Mechanism and 'Direction in Evolution': Preliminary Notes"

"Common objections to 'Internal Evolutionary Mechanisms' (1)"

"Researcher gives hard thoughts on soft inheritance"

"Mother's Diet during Pregnancy can affect Grandchildren (Epigenetics)"

"'New Science' to be created at Florida State University Workshop"

"Evolution's 'Driving Force' Shifts Based on Behavior, Study Says"

Technorati: model, internal evolutionary mechanism, homeostasis, molecular, systematics, theory, change, darwinian, evolution, school, arts, anthropology, scientific, gaps, fossil, record, missing link, clock, biological, blood, human, gorilla, genome, offspring, history, origins, ape, fossils, genes, science, lamarck, evolutionary, mechanism, research, epigentics, dna

Permanent Link posted by John Latter @ 7:36 PM 0 comments

Wednesday, February 07, 2007

Human proteins evolving slowly thanks to multi-tasking genes

Many human proteins are not as good as they might be because the gene sequences that code for them have a double role which slows down the rate at which they evolve, according to new research published in PLoS Biology.

By tweaking these dual role regions, scientists could develop gene therapy techniques that produce proteins that are even better than those found in nature, and could one day be used to help people recover from genetic disorders.

The stretch of DNA which codes for a specific protein is often interrupted by sections of apparently useless DNA - known as introns - which need to be edited out in order to produce a new protein.

Recently it has been discovered that some of the instructions on where to splice and re-splice the DNA in this editing process are contained in the coding section, or exon, of the DNA itself.

So, as well as spelling out which amino acids are needed to produce a specific protein, the part of the exon immediately next to the intron contains information that is essential for the gene editing process.

This means that these parts of genes evolve particularly slowly, making the proteins they encode for not as good as they could be had evolutionary processes been more able to improve them over time.

"Our research suggests that a gene with many exons would evolve at under half the rate of the same one that had no introns, simply owing to the need to specify where to remove introns," said Professor Laurence Hurst from the University of Bath (UK), who worked with colleagues from the University of Lausanne (Switzerland) on the project.

"This is one of the strongest predictors of rates of protein evolution known, indicating that this dual coding role is vastly more influential than previously believed."

The finding could have major implications for medicine and the development of gene therapy techniques in which people with a defective gene are given the correct version.

"Our results suggest that we could make the replacement gene even better than the normal version," said Professor Hurst, from the Department of Biology and Biochemistry at the University of Bath.

"We would just need to remove the introns and tweak the protein at the sites that were dual coding.

"We also found that genes that have lost their introns many millions of years ago evolve especially fast near where the introns once resided.

"This indicates that this tweaking of the dual role sections of genes is also what evolution does when introns are removed."

The research was funded by the Biotechnology and Biological Sciences Research Council, the Swiss National Science Foundation and the Center for Integrative Genomics at the University of Lausanne.

Source: University of Bath 6 February 2007

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Based on the paper "Splicing and the Evolution of Proteins in Mammals"

Citation:

Parmley JL, Urrutia AO, Potrzebowski L, Kaessmann H, Hurst LD (2007) Splicing and the Evolution of Proteins in Mammals. PLoS Biol 5(2): e14 doi:10.1371/journal.pbio.0050014

Excerpts:

Authors Summary

Most of the DNA in our genes is actually not involved in the specification of proteins. Rather, the bits with the protein-coding information (exons) are separated from each other by noncoding bits, introns. Before a gene can be translated into protein these introns are removed and the exons are spliced back together to be translated into protein. While information about which DNA to remove is largely in the introns themselves, parts of the exons near the intron - exon boundary can, for example, function as splice enhancer elements. In principle, then, these parts of exons have two functions: to specify the amino acids of the resulting protein and to enable the correct removal of introns. What impact might this have on a gene's evolution? We show that near intron - exon boundaries, amino acid usage is biased towards nucleotides involved in splice control. Moreover, these parts of genes evolve especially slowly. Indeed, we estimate that a gene with many exons would evolve at under half the rate of the same gene with no introns, simply owing to the need to specify where to remove introns. Likewise, genes that have lost their introns evolve especially fast near the former intron's location. Thus, human proteins may not be as optimised as they could be, as their sequence is serving two conflicting roles.

Abstract

It is often supposed that a protein's rate of evolution and its amino acid content are determined by the function and anatomy of the protein. Here we examine an alternative possibility, namely that the requirement to specify in the unprocessed RNA, in the vicinity of intron - exon boundaries, information necessary for removal of introns (e.g., exonic splice enhancers) affects both amino acid usage and rates of protein evolution. We find that the majority of amino acids show skewed usage near intron - exon boundaries, and that differences in the trends for the 2-fold and 4-fold blocks of both arginine and leucine show this to be owing to effects mediated at the nucleotide level. More specifically, there is a robust relationship between the extent to which an amino acid is preferred/avoided near boundaries and its enrichment/paucity in splice enhancers. As might then be expected, the rate of evolution is lowest near intron - exon boundaries, at least in part owing to splice enhancers, such that domains flanking intron - exon junctions evolve on average at under half the rate of exon centres from the same gene. In contrast, the rate of evolution of intronless retrogenes is highest near the domains where intron - exon junctions previously resided. The proportion of sequence near intron - exon boundaries is one of the stronger predictors of a protein's rate of evolution in mammals yet described. We conclude that after intron insertion selection favours modification of amino acid content near intron - exon junctions, so as to enable efficient intron removal, these changes then being subject to strong purifying selection even if nonoptimal for protein function. Thus there exists a strong force operating on protein evolution in mammals that is not explained directly in terms of the biology of the protein.

Introduction

Why do some parts of proteins evolve more slowly than others? Why, in turn, do some proteins evolve more slowly than others? Intragenic conserved regions are typically considered to reflect domains of functional importance to the protein [1]. Similarly, proteins with a high density of important functional sites should evolve slowly. There are, however, potentially multiple other correlates to rates of protein evolution [1]. The expression parameters of a gene (rate of expression, protein abundance, and number of tissues in which a gene is expressed) are consistently reported to be important predictors [2 - 5]. This may in part reflect selection to resist mistranslation [6]. Other possible covariates include essentiality and the number of protein interactions, but the issues here are more contentious, not least because of covariance with expression parameters [7 - 17]. Here we test the hypothesis that selection acting to ensure that introns are correctly removed skews amino acid content in predictable ways and imposes constraints on rates of protein evolution.

In mammalian genes, which are rich in introns [18], correct removal of introns often requires the presence, in the flanking exons, of splice-enhancer domains, these being short (six nucleotide) blocks required for binding of serine/arginine-rich proteins [19]. The need for splice enhancers can impact the use of synonymous codons in the domains flanking intron - exon junctions, such that when a synonymous codon is used commonly in splice enhancers it is preferred over its less commonly used synonym [20,21]. Moreover, selection to preserve splice enhancers affects both the synonymous single nucleotide polymorphism profile [22,23] and the rate of evolution at synonymous sites of splice-enhancer-associated domains [24].

Might the same forces also act to cause skews in amino acid usage in the vicinity of intron - exon junctions? In a preliminary analysis, we showed that there is a tendency for enrichment near boundaries of an amino acid whose codons are common in splice enhancers: lysine is coded by AAA and AAG, both of which are common in splice enhancers, and at both 5' and 3' ends of exons, lysine's proportional usage increases [24]. Is it more generally the case that an amino acid's usage increases near intron - exon junctions if it commonly features in splice enhancers? Conversely, are some amino acids avoided near such boundaries if they are rare in splice-enhancer domains? To address these issues, we derive patterns of amino acid preference in the vicinity of intron - exon boundaries and compare these patterns with a metric of enrichment of amino acids in splice enhancers relative to rates of usage in the genome. In turn, we ask whether selective constraints are stronger near intron - exon boundaries, and whether such constraints explain much of the variation between proteins in their rate of evolution.

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Tuesday, February 06, 2007

Ken Ham's 'The Lie: Evolution' - Online Book (+ Video)

The Education Resources page of Answers in Genesis currently lists (and links to) Ken Ham's "The Lie: Evolution" as a 'Featured Online Book'. No doubt it will eventually also be linked to from their Online resources page

Table of Contents

Foreword

By Luther D. Sunderland, author of Darwin's Enigma - Ebbing the Tide of Naturalism [1]:

..Mr. Ham shows that Genesis, in particular, is a dependable account of actual events that are supported by solid scientific evidence. Furthermore, he shows how the questioning of this foundational book of the Bible, even by many Christians, has led to the degeneration of society so that the only moral codes it accepts are based upon "survival of the fittest," "do your own thing," and "if it feels good, do it." There are no moral absolutes.

Introduction

..My parents knew that evolution was wrong because it was obvious from Genesis that God had given us the details of the creation of the world. These details were important foundational truths for the rest of Christianity. At that time, the current wealth of materials on the creation/evolution issue produced, for instance, by the Institute for Creation Research, were not available. I recall going to my local minister and asking him what to do about the problem. He told me to accept evolution but then add it to the Bible so that God used evolution to bring all forms of life into being. This was an unsatisfactory solution to the problem. If God did not mean what He said in Genesis, then how could one trust Him in the rest of the Scriptures?

Chapter 1: Christianity Is Under Attack

Chapter 2: Evolution Is Religion

..The term "evolutionist" is used extensively throughout the following chapters. In other parts of this book, we will discuss the ideas of Christians who try to marry the concepts of evolution and the Bible. However, because the majority of evolutionists are not Christians, I wish the reader to understand that the term "evolutionist" is used to mean those who believe that evolution - in the sense of time, chance, and struggle for survival - rather than the God of the Bible, is responsible for life.

Chapter 3: Creation Is Religion

..However, we no longer live in the world God originally created. Because our first parents placed human opinion above God's Word (as we continue to do), struggle and death entered the world, and God cursed the creation. Charles Darwin called this struggle to the death "natural selection" and offered his theory as a substitute for the Creator. Evolutionists later added accidental changes in heredity (mutations) to their theory. But death and accident do not create: instead they bring disease, defects, and decay into the world God created.

Chapter 4: The Root of the Problem

..Why do evolutionists not want to admit that evolution is really a religion?

It is related to the fact that whatever you believe about your origins does affect your whole world view, the meaning of life, etc. If there is no God and we are the result of chance random processes, it means there is no absolute authority. And if there is no one who sets the rules, then everyone can do whatever he likes or hopes he can get away with. Evolution is a religion which enables people to justify writing their own rules.

Chapter 5: Crumbling Foundations

..Students in most of our schools are given a totally anti-biblical foundation: the foundation of evolution. This foundation, of course, will not allow the Christian structure to stand. A structure of a different type - humanism - is the one built on this foreign foundation.

Chapter 6: Genesis Does Matter

..Atheistic evolutionary philosophy says: "There is no God. All is the result of chance and randomness. Death and struggle are the order of the day, not only now, but indefinitely into the past and future." If this is true, there is no basis for right and wrong. The more people believe in evolution, the more they are going to say, "There is no God. Why should I obey authority? Why should there be rules against aberrant sexual behavior? Why should there be rules concerning abortion? After all, evolution tells us we are all animals. So, killing babies by abortion is no worse than chopping the head off a fish or a chicken." It does matter whether you believe in evolution or creation! It affects every area of your life.

Chapter 7: Death: A Curse and a Blessing

..Each Lord's Day we rejoice in Christ's resurrection, and thus the conquering of sin and death.

But evolution destroys the very basis of this message of love. The evolutionary process is supposed to be one of death and struggle, cruelty, brutality, and ruthlessness. It is a ghastly fight for survival, elimination of the weak and deformed. This is what underlies evolution - death, bloodshed, and struggle bringing man into existence.

Chapter 8: The Evils of Evolution

..Particularly in the Western nations, where Christian ethics were once very prevalent, Darwinian evolution provided a justification for people not to believe in God and, therefore, to do those things which Christians would deem as wrong. As one non-Christian scientist said in a TV interview, "Darwinian evolution helped make atheism respectable."

Chapter 9: Evangelism in a Pagan World

..There is a war going on in society - a very real battle. The war is Christianity versus humanism, but we must wake up to the fact that, at the foundational level, it's really creation versus evolution.

Having agreed on all this, however, we must remember that our enemies are not the humanists and evolutionists themselves, but the powers of darkness that have deceived them.

Chapter 10: Wake Up, Shepherds!

..At one seminar, a lady told me that evolutionism had destroyed her faith in the Scriptures. She had such an emptiness in her life that she cried to the Lord and prayed for a solution to this problem. She was finding it impossible to trust the Scriptures. She was led to a library and happened to find a book on the Gap Theory. (The Gap Theory basically allows for billions of years between Genesis 1:1 and Genesis 1:2.) She was thrilled at this explanation and set about rebuilding her Christian life. At the end of the seminar, she came to me and exclaimed what a thrill it was to know she did not have to believe the Gap Theory.

Chapter 11: Creation, Flood, and Coming Fire

..There is a prophecy in 2 Peter 3 concerning the last days of this earth's history, and it very much relates to the whole creation/evolution issue:

Knowing this first, that there shall come in the last days scoffers, walking after their own lusts, and saying, Where is the promise of his coming? for since the fathers fell asleep, all things continue as they were from the beginning of the creation. For this they willingly are ignorant of, that by the word of God the heavens were of old, and the earth standing out of the water and in the water: Whereby the world that then was, being overflowed with water, perished: But the heavens and the earth, which are now, by the same word are kept in store, reserved unto fire against the day of judgment and perdition of ungodly men (2 Pet. 3:3–7).

Appendix 1: Twenty Reasons Why Genesis and Evolution Don't Mix

..For those who try to harmonize evolution with Genesis, the order of evolution must compare with the order of events in Genesis. There are a number of problems here. The basic tenets of evolution totally conflict with the order in Genesis. For instance, Genesis teaches that God created fruit trees before fish - plants on day three, fish on day five. Evolution teaches that fish came before fruit trees. Evolution teaches that first life began in the sea, and after millions of years life was established on the land. The Bible teaches that the earth was first created covered with water: evolutionary teaching is that the earth first began as a hot molten blob. There is no way that the order of events according to evolution and Genesis can be reconciled.

Appendix 2: Why Did God Take Six Days?

..Probably one of the major reasons people tend not to take the days of Genesis as ordinary days is because they believe that scientists have proved the earth to be billions of years old. But this is not true. There is no absolute age-dating method to determine how old the earth is. Besides this, there is much evidence consistent with a belief in a young age for the earth, perhaps only thousands of years.

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The Ken Ham video "Do Animals Evolve?":

Evolution Research - General Evolution News

Saturday, February 10, 2007

Which Genome Variants Matter?

Friday, February 09, 2007

Professor Contends Biological Underpinnings Of Darwinian Evolution Not Valid

Wednesday, February 07, 2007

Human proteins evolving slowly thanks to multi-tasking genes

Tuesday, February 06, 2007

Ken Ham's 'The Lie: Evolution' - Online Book (+ Video)

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