It is NOT uncommon for organisms to have duplicate copies of some genes. Duplicate genes enhance existing traits as well as add to the genomic stability of an organism, but duplicate genes have also been linked to disease. While there is no lack of theories attempting to explain these phenomena, there are no definitive answers:
- “Human beings can run long distances because we carry multiple copies of a gene that helps supply our cells with energy, a new study suggests. That supports the idea that endurance running gave our human ancestors an evolutionary edge...
Humans are believed to possess anywhere from 20,000 to 25,000 different genes. But in some cases, we carry multiple copies of the same gene. And the more duplicates of a gene that exist within a cell, the more protein from the gene that gets produced, according to James Sikela at the University of Colorado Health Sciences Center in Aurora, Colorado, US.
In some cases, though, having an extra copy of a gene can translate into a serious health problem.”
“Duplicate genes help humans go the extra mile,” July 30, 2007, Genome Research 10.1101/GR.6557307.
- “Knocking out a gene from a genome often causes no phenotypic effect. This phenomenon has been explained in part by the existence of duplicate genes. However, it was found that in mouse knockout data duplicate genes are as essential as singleton genes …
From single-gene knockout data in A. thaliana obtained in our study and from the literature, we found that duplicate genes play a significant role in functional compensation.”
RIKEN Plant Science Center and by National Institutes of Health, “Evolutionary Persistence of Functional Compensation by Duplicate Genes in Arabidopsis,” October 29, 2009, Oxford Journals Genome Biol Evol 1 409-414.
- “Scientists have discovered that a familial form of a rare bone cancer called chordoma is explained not by typical types of changes or mutations in the sequence of DNA in a gene, but rather by the presence of a second copy of an entire gene.”
National Cancer Institute, “Gene Duplication Identified in an Uncommon Form of Bone Cancer,” October 4, 2009.
- “Phenotypic variation and disease phenotypes induced by duplications are more diverse and widespread than previously anticipated, and duplications are a major class of disease-related genomic variation.”
“Gene Duplication: A Drive for Phenotypic Diversity and Cause of Human Disease,” Annual Review of Genomics and Human Genetics, March 26, 2007.
The record holder for duplicate genes is the bacterium Epulopiscium fishelsoni, which can have up to 85,000 duplicates of its entire genome:
“A new study carried out at Cornell and published in the Proceedings of the National Academy of Sciences journal has unveiled the secret of this gigantism: it consists in the ability of the bacterium to copy its DNA up to 85,000 times. This bacterium has a DNA amount 25 times higher than the one found in a human cell.”
Cornell University, “The Secret of the World's Largest Bacterium Revealed,” May 8, 2008, Softpedia.com.
Darwinists believe that evolution is driven by the accidental creation of duplicate genes when random mutations disrupt partial or full chromosomal duplication. When a duplicate gene 'slips through' the duplication process, they believe that it is free from selective pressure, which means that it can supposedly mutate without causing damage to the organism.
It is claimed that repeated genetic rearrangements caused by insertions, deletions, inversions, and translocations in a duplicate gene can eventually assemble new sequences with the necessary instructions to build new functional features.
A star is born and gene duplication is now the mechanism of choice for Darwinism!
What is the evidence for this occurring? Notice that the following 'scientific' article makes the claim that the “primary evidence” for this kind of gene duplication is nothing more than the “widespread existence” of duplicate genes:
”The primary evidence that duplication has played a vital role in the evolution of new gene functions is the widespread existence of gene families …
Duplicate gene evolution has most likely played a substantial role in both the rapid changes in organismal complexity apparent in deep evolutionary splits and the diversification of more closely related species. The rapid growth in the number of available genome sequences presents diverse opportunities to address important outstanding questions in duplicate gene evolution.”
Public Library of Science, “Gene Duplication: The Genomic Trade in Spare Parts,” doi:10.1371/journal.pbio.0020206, July 13, 2004.
The next research paper claims that gene duplication created a new antifreeze gene from a duplicate copy of another gene that had a similar small section of its sequence:
“We report here clear experimental evidence for EAC-driven evolution of type III antifreeze protein gene from an old sialic acid synthase (SAS) gene in an Antarctic zoarcid fish.”
University of Illinois at Urbana-Champaign, “Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict,” 10.1073/pnas.1007883107 PNAS December 14, 2010, PNAS.
What is the “experimental evidence” that supports this conclusion? Refer to S01-S08 images:
All that is apparently required now to qualify as “experimental evidence” is this:
1.Examine the genetic sequences of gene #1;
2.find a similar sequence in gene #2;
3.incrementally add, change, and delete the genetic material enough times in #2 to make it identical to gene #1;
4.claim that it all evolved through unguided naturalistic forces.
Except for the fact that it also required human intelligence, DNA sequencing knowledge and techniques, and some cleverly made images!
Also refer to “How to Play the Gene Evolution Game” :
Notice that genetic material magically reassembles exactly where needed, and each incremental step was presumed as having been 'fixed' within that population for some period of time before going on to the next rearrangement. The arbitrarily switching from being 'free from selective pressure' to suddenly being under 'positive selection' displays the standard schizophrenic response to evolutionary-based hypothetical scenarios. Too bad that there is NO evidence to back it up, but the standard come-back is, “It doesn't mean it couldn't happen!”
- “A duplicated gene newly arisen in a single genome must overcome substantial hurdles before it can be observed in evolutionary comparisons. First, it must become fixed in the population, and second, it must be preserved over time. Population genetics tells us that for new alleles, fixation is a rare event, even for new mutations that confer an immediate selective advantage. Nevertheless, it has been estimated that one in a hundred genes is duplicated and fixed every million years (Lynch and Conery 2000), although it should be clear from the duplication mechanisms described above that it is highly unlikely that duplication rates are constant over time.”
Public Library of Science, “Gene Duplication: The Genomic Trade in Spare Parts,” doi:10.1371/journal.pbio.0020206, July 13, 2004.
- “A major hindrance to progress has been confusion regarding the role of positive (Darwinian) selection, i.e., natural selection favoring adaptive mutations. In particular, problems have arisen from the widespread use of certain poorly conceived statistical methods to test for positive selection (1, 2). Thousands of papers are published every year claiming evidence of adaptive evolution on the basis of computational analyses alone, with no evidence whatsoever regarding the phenotypic effects of allegedly adaptive mutations.”
Austin L. Hughes, "The origin of adaptive phenotypes,” Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193-13194, Sept. 9, 2008 (internal citations removed).
They tried this ruse in 2004 with yeast (where they used the same hypothetical sequence rearrangements-see figures in article), and it was used again in 2009 with zebrafish:
- “Here, we show that the yeast Saccharomyces cerevisiae arose from ancient whole-genome duplication, by sequencing and analysing Kluyveromyces waltii, a related yeast species that diverged before the duplication.”
“Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae”:
The Broad Institute, Massachusetts Institute of Technology and Harvard University, “Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae,” April 8, 2004, Nature Publishing Group.
- “Scientists have suspected that spare parts in the genome—extra copies of functional genes that arise when genes or whole genomes get duplicated—might sometimes provide the raw materials for the evolution of new traits. Now, researchers report in a study published online on September 3rd in Current Biology, that they have discovered a prime example of this in fish. The researchers show that a duplicate copy of a gene involved in embryonic development has taken up a newer and decidedly less essential role in the development of fish scales …
"By 'tweaking' the use of one of the two copies of the fish fgfr1, the teleost order that contains zebrafish and carp have a specialized 'toolbox' gene that now controls adult-specific variation in form," added Nicolas Rohner, also of the Max Planck Institute.”
Cell Press, “Spare Gene Is Fodder For Fishes' Evolution,” September 8, 2009, ScienceDaily.
The funny thing is that they must not have been confident in either scenario because this newer antifreeze gene duplication ruse was presented as “the first clear demonstration”:
"'This is the first clear demonstration – with strong supporting molecular and functional evidence – of escape from adaptive conflict as the underlying process of gene duplication and the creation of a completely new function in one of the daughter copies,' Cheng said. 'This has not been documented before in the field of molecular evolution.'”
University of Illinois at Urbana-Champaign, “Researchers show how 1 gene becomes 2 (with different functions)”, January 12, 2011, Physorg.
What is truly alarming about these made-up scenarios is that these people still believe in the outdated gene-centered philosophy and have yet to address how the necessary and complex regulatory genetic elements evolved in unison so that the new gene would be precisely regulated.
For decades, Darwinists have dismissed regulatory elements as “junk DNA” that they believed was just useless genetic remnants left over from evolutionary predecessors. It is now known that “junk DNA” makes up approximately 98.5% of DNA and it is the key to cell health and development, and primary link to disease when not functioning properly. For more information, go to:
Is it that most evolutionary-based researchers are truly ignorant of the truth, or is it that they have chosen to ignore it hoping that it will just go away?:
- “For me, the most important outcome of the human genome project has been to expose the fallacy that most genetic information is expressed as proteins … In contrast to protein-coding genes, the extent of noncoding intronic and intergenic sequences increases markedly with complexity; only 1.5% of the human genome encodes proteins ...
These observations suggest that we need to reassess the underlying genetic orthodoxy, which is deeply ingrained and has been given superficial reprieve by uncritically accepted assumptions about the nature and power of combinatorial control.”
John Mattick, University of Queensland, “The genomic Foundation Is Shifting,” February 18, 2011, Science Magazine Vol. 331 no. 6019 p. 874.
- “Gene regulation has turned out to be a surprisingly complex process governed by various types of regulatory DNA, which may lie deep in the wilderness of so-called junk DNA that lies between genes. Far from being humble messengers, RNAs of all shapes and sizes are actually powerful players in how genomes operate. Finally, there's been increasing recognition of the widespread role of chemical alterations called epigenetic factors that can influence the genome across generations without changing the DNA sequence itself. The scope of this 'dark genome' became apparent in 2001, when the human genome sequence was first published.”
Elizabeth Pennisi, “Shining a Light on the Genomen's 'Dar Matter',” Science, Vol. 330 (6011):1614, December 17, 2010.
- “In order to understand gene regulation, accurate and comprehensive knowledge of transcriptional regulatory elements is essential.”
Michael Zhang Lab, Cold Spring Harbor Laboratory.
- “The commercial media is both ignorant of and blocks coverage of stories about non-centrality of the gene because its science advertising dollars come from the gene-centered Darwin industry …
Thus, the public is unaware that its dollars are being squandered on funding of mediocre, middle-brow science or that its children are being intellectually starved as a result of outdated texts and unenlightened teachers.”
Suzan Mazur, "Altenberg 16: An Exposé Of The Evolution Industry” an E-Book in 8 Parts - Part 1, July 6, 2008.
Examples of regulatory mechanisms are specialized molecular switches that turn genes 'on' and 'off' at specific intervals so that genes are expressed properly. If gene duplication is a random event, it's absurd to even suggest that these complex “highly complex, sophisticated regulatory mechanisms” evolved at the same time in order to regulate the new gene's function:
- “The cell uses highly complex, sophisticated regulatory mechanisms to make sure that not all genes are read at the same time. Particular gene switches need to be activated and, in addition, there are particular chemical labels in the DNA determining which genes are transcribed into RNA and which others will be inaccessible, i.e. where the book literally remains closed. The biological term for this is epigenetic gene regulation...
More than half of our genetic material is transcribed into noncoding RNA. This prompts Ingrid Grummt to speculate: 'It is very well possible that there are exactly matching noncoding RNA molecules for all genes that are temporarily silenced. This would explain how such a large number of genes can be selectively turned on and off.'”
Helmholtz Association of German Research Centres, “A mystery solved: How genes are selectively silenced,” October 18, 2010, Physorg.
- “The ability of cells to work together in a co-ordinated fashion is paramount for a multicellular organism to function. The multitude of cell types each have specialised roles to play, yet remain dependent upon the products of other cells for survival. Even the needs of individual cells can change according to their stage of development and environmental conditions. Multicellular organisms had to develop complex systems of control in order to regulate the different processes going on in different cells at different times. For such a system to work, there must be a sophisticated means of communication between cells. GPCRs (G protein-coupled receptor) and their G proteins (guanine nucleotide-binding proteins) form one of the most prevalent signalling systems in mammalian cells, being involved in the control of nearly every aspect of physiology and behaviour.”
Jennifer McDowall, “G Proteins,” InterPro database, European Bioinformatics Institute.