Jump to content
Islamic Forum
Sign in to follow this  
Absolute truth

Dna & Chromosomes, Proof Of Evolution ?

Recommended Posts

A) Karyotype


According to darwinism, human has a microbe-like grandfather, It kept reproducing till we found an imaginary common ancestor for human and chimp.


This tale was confronted by the fact that human has 46 chromosomes while apes have 48 !

Looks more or less similar ?!


Let's have a look at creatures that have the same number of chromosomes-just like human !


- Black rat (Rattus rattus) , but not all of them have 46


- Merriam’s ground squirrel (Spermophilus canus)


- Southern short-tailed shrew (Blarina carolinensis)

- Grevy’s zebra (Equus grevyi)
- Mountain beaver (Aplodontia rufa)

- Muntjacs (Muntiacus reevesi)


- Beach vole (Microtus breweri)
- Nilgai (Boselaphus tragocamelus)
- Kirk’s dik-dik (Rhynchotragus/Madoqua kirkii )

- Grey/common vole (Microtus arvalis)


- Large bentwing bat (miniopterus schreibersi)
- Bolivian Tuco-tuco (Ctenomys boliviensis)

- Crowned Lemur (Lemur mongoz coronatus)
- Red Titi (Callicebus cupreus)

Sable antelope  (Kafue, Zambia)





On the other hand these species also have 48 chromosomes, just like chimpanzee.


- European hare/jackrabbit (Lepus europeus)










It's obvious that none is a supposed relative neither for human nor chimpanzee !

In fact, the number of chromosomes doesn't hold much importance. What really counts is the genetic information itself.

Share this post

Link to post
Share on other sites

chromosome 2 fusion model

To solve the problem of different number of chromosomes between apes and humans, Darwinists suggested the ‘chromosome 2 fusion model’. This scenario involves the claim that the fusion of two small chimpanzee-like chromosomes (2A and 2B) formed one chromosome in humans, leading to the difference in diploid chromosome numbers between humans and great apes. While the chromosome 2 fusion model is routinely touted as dogma, very little new genomic data, although readily available for analysis, has been presented as evidence.


Wikipedia said that the model is "widely accepted":

But, What you need to know is:
1- A majority of the data for the fusion model is based on DNA hybridization and chromosomal staining experiments conducted prior to the sequencing of the human and chimpanzee genomes.
2- Synteny (shared ordering of genes between organisms) of the chromosomes is not a surprise. We already knew there was a vast amount of similarity between humans and primates both in terms of physical characteristics and genetic material and structure. It is a mistake to assume that observing similarities necessarily brings you to the conclusion of common descent. Taxonomy based on physical characteristics was already a very well established science when the idea of common descent came on the scene.

3- The telomere region involves a complex and dynamic framework of DNA motif repeats 5’ to 3’ (TTAGGG)n , structural loops, structural and a wide variety of proteins. and it confer stability and preventing fusion or shortening of the chromosomes. It's in perfect tandem of DNA from about 10 to 15 kb (10,000 to 15,000 bases) and contains 1,667 to 2,500 telomere repeats at each chromosome end.

4- In a head-to-head fusion of two chromosomes, we would expect at least 5,000 bases of (TTAGGG)n repeats in tandem, we would also expect the orientation of the plus-strand repeat to change to the reverse complement (CCCTAA)n, which should also occur in near-perfect tandem for approximately 5,000 or more bases. The area containing the suspected ‘fusion region’ is often called 2qfus or 2chr2fus and occupies the genomic area between 2q13 and 2q14.1.

5- Within the 10 to 30 kb window of DNA sequence surrounding the hypothetical fusion site,a glaring paucity of telomeric repeats exist that appear mostly as independent monomers, not tandem repeats. The TTAGGG repeat to the left of the fusion site, less than 35 motifs exist. For the CCCTAA reverse complement sequence, to the right of the fusion site, less than 150 telomere motifs can be found.

6- The only research group to seriously analyze the actual fusion site DNA sequence data in detail were confounded by the results which showed a lack of evidence for fusion—a genomic condition for this region which they termed ‘degenerate’.(Fan, Y. et al., Genomic structure and evolution of the ancestral chromosome fusion site in 2q13-2q14.1 and paralogous regions on other human chromosomes, Genome Research 12:1651–1662, 2002. )

7- Fairbanks said that 44 out of 158 repeats match (28%) and that the rest of the sequences are ‘close’. The problem is, to obtain even this low match level, the consensus reading frame is entirely ignored and ambiguous matches are contrived by assuming many insertion and deletion mutations of varying sizes.

8- There are genes throughout the alleged fusion region. In an analysis of a 614 kb area encompassing the postulated chromosome fusion site, Fan et al. found evidence of “at least 24 potentially functional genes and 16 pseudogenes”.(Fan, Y. et al., Gene content and function of the ancestral chromosome fusion site in human chromosome 2q13-2q14.1 and paralogous regions, Genome Research 12:1663–1672, 2002.). In the 30-kb region directly encompassing the fusion site, which should definitely be devoid of any genes, there exists two actively transcribed genes, each in a flanking position in regard to the fusion site (one on each side). There are also at least two other genes in the immediate vicinity of the fusion site thought to be inactive due to frame shift mutations. However, research related to the human ENCODE (Encyclopedia of DNA Elements) project has shown that many genes thought to be inactive (pseudogenes) are actually functional due to a variety of newly discovered regulatory mechanisms.(Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project, Nature 447:799–816, 2007)

9- If the telomere motifs that populate internal areas of chromosomes serve some important, yet unknown function, the chromosome fusion model actually impedes research aimed at determining possible function in these regions.

10- telomeres are designed to prevent fusion. Broken chromosomes at any location immediately invoke the cell’s double-stranded DNA repair machinery where the aberrant fusion of fragments actually triggers cell fault tolerance mechanisms.6 In the case of an aberrant fusion, a senescence response or programmed cell death (apoptosis) cascade is normally triggered, effectively eliminating the damaged cell from the system.

A cell with telomeres that have progressively shortened over time and reached a threshold length will also activate the double-stranded DNA repair machinery; inducing cell senescence and/or death. When in certain types of germline cells, telomerase adds telomere repeats to shortened telomeres, chromosomes are ‘healed’ and can again become stable. The telomeres cap the ends of linear chromosomes and effectively prevent fusion or trigger cell elimination if the telomere is shortened to a certain point, damaged, or aberrantly fused.6 According to the fusion model, this protective process was somehow bypassed in early humans.

11- Telomere sequence is not unique to the telomere. the existence of telomeric repeats in internal sites is not unusual or unexpected. We know that ITS (interstitial telomeric sequences) present in Chromosomes 1,4,5,9,12,16, and 17 (http://www.ncbi.nlm.nih.gov/pubmed/19420924?dopt=Abstract)

12- The evidence for a second remnant centromere at any stage of sequence degeneracy is negligible.The supposed evidence includes the finding that “every human and great-ape chromosome centromere contains a highly variable DNA sequence that is repeated over and over, a 171 base-pair sequence called the Alphoid sequence.”3 Fairbanks adds that scientists have “searched for Alphoid sequences in human chromosomes and found them at every centromere, as expected. They also found Alphoid sequences at the site in human chromosome 2 where the remnants of this second centromere should be. These remnants are evidence of a now-defunct centromere.” problem is that, although research has been done on some primates, no systematic study of centromeres exists to determine how common alphoid DNA is in mammals.(Baldini, A. et al., An alphoid DNA sequence conserved in all human and great ape chromosomes: evidence for ancient centromeric sequences at human chromosomal regions 2q21 and 9q13, Human Genetics 90:577–583, 1993) Baldini et al. found that the “highest sequence similarity between human and great ape alphoid sequences is 91%, much lower than the expected similarity for selectively neutral sequences.”

13- Alpha-satellite DNA or alphoid DNA, although found in centromeric areas, is not unique to centromeres and is also highly variable. Because highly variable alphoid DNA is also commonly found in non-centromeric regions of human chromosomes, their presence does not indicate the remnants of a degenerate centromere. Based on the reasoning of Fairbanks and others promoting the human chromosome 2 fusion model, one could conclude that human chromosomes contain literally hundreds of degenerate centromeres.


Share this post

Link to post
Share on other sites

Pseudogenes & Junk DNA

Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes. Pseudogenes have long been labeled by Darwinists as “junk” DNA, failed copies of genes that arise during the evolution of genomes.
But, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene expression, gene regulation, generation of genetic (antibody, antigenic, and other) diversity. Pseudogenes are involved in gene conversion or recombination with functional genes.









Share this post

Link to post
Share on other sites

Human-chimp DNA similarities

Claim: Human DNA is 99 percent similar to chimpanzee DNA, so, they have common ancestor.

What you need to know:

1- The claim itself is a logical fallacy (Jumping to conclusion) (Fallacy of Reification) as well as being inaccurate, read below.

2- Genetic information in all living creatures is encoded as a sequence of only 4 nucleotides (guanine, adenine, thymine, and cytosine) recorded using the letters G, A, T, and C. It is surely natural for the human body to bear some molecular similarities to other living beings, because they all are made up of the same molecules, they all use the same water and atmosphere, and they all consume foods consisting of the same molecules. Certainly, their metabolisms and therefore genetic make-ups would resemble one another. This, however, is not evidence that they evolved from a common ancestor. It is possible to explain this matter with an example; all construction in the world is done with similar materials (brick, iron, cement, etc.). They are constructed separately by using common materials. The same holds for living beings as well.

3- We know that DNA in cells contains much of the information necessary for the development of an organism. In other words, if two organisms look similar, we would expect there to be some similarity also in their DNA. The DNA of a cow and a whale, two mammals, should be more alike than the DNA of a cow and a bacterium. If it were not so, then the whole idea of DNA being the information carrier in living things would have to be questioned. Likewise, humans and apes have a lot of morphological similarities, so we would expect there would be similarities in their DNA. Of all the animals, chimps are most like humans,1 so we would expect that their DNA would be most like human DNA.

4- Similarity (‘homology’) is not evidence for common ancestry (evolution) as against a common creator. Why ?
Whether similarity is morphological (appearance), or biochemical, is of no consequence to the lack of logic in this argument.

5- Humans and chimps share about 96 percent of their sequence.1 so the difference is about 120,000,000 base pairs , The similarity isn't something unexpected. We already knew there was a vast amount of similarity between humans and primates both in terms of physical characteristics and structure. It is a mistake to assume that observing similarities necessarily brings you to the conclusion of common descent. Taxonomy based on physical characteristics was already a very well established science when the idea of common descent came on the scene.Would it mean that humans could have ‘evolved’ from a common ancestor with chimps? Not at all! The amount of information in the 3 billion base pairs in the DNA in every human cell has been estimated to be equivalent to that in 1,000 books of encyclopaedia size.2

6- About 35 million DNA base pairs differ between the shared portions of the two genomes, each of which, like most mammalian genomes, contains about 3 billion base pairs. In addition, there are another 5 million sites that differ along with a much smaller number of different chromosomal arrangements.1

7- As many as 3 million of the differences lie in crucial protein-coding genes or other functional areas of the genome.1

8- Moreover, the basic proteins are common vital molecules present in various other living things. The structure of the same kinds of proteins present not only in chimpanzee, but also in completely different living creatures, is very similar to that in humans.
For example:

  • Cats have 90% of homologous genes with humans, 82% with dogs, 80% with cows, 79% with chimpanzees, 69% with rats and 67% with mice. 3
  • Cows (Bos taurus) are 80% genetically similar to humans4
  • 99% of mouse genes turn out to have analogues in humans 5-75% of mouse genes have equivalents in humans6 , 90% of the mouse genome could be lined up with a region on the human genome 7
  • The fruit fly (Drosophila) shares about 60% of its DNA with humans 8
  • About 60% of chicken genes correspond to a similar human gene.9

9 - Telomeres in Chimpanzees and other apes have about 23 kilobases (a kilobase is 1,000 base pairs of DNA) of repeats. Humans are unique among primates with much shorter telomeres only 10 kilobases long.10

10 - The Y chromosome in particular is of a different size and has many markers that do not line up between the human and chimpanzee. Page's team found that the chimp Y chromosome has only two-thirds as many distinct genes or gene families as the human Y chromosome and only 47% as many protein-coding elements as humans. The remainder of the chimp and human genomes are thought to differ in gene number by less than 1%. More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa, whereas this is true for less than 2% of the remainder of the genome.
11- If humans were entirely different from all other living things, or indeed if every living thing was entirely different, would this reveal the Creator to us? No! We would logically think that there must be many creators rather than one. The unity of the creation is testimony to the One True God who made it all.

- Biochemist Prof. Michael Denton made the following comments;

Each class at molecular level is unique, isolated and unlinked by intermediates. Thus, molecules, like fossils, have failed to provide the elusive intermediates so long sought by evolutionary biology… At a molecular level, no organism is "ancestral" or "primitive" or "advanced" compared with its relatives… There is little doubt that if this molecular evidence had been available a century ago… the idea of organic evolution might never have been accepted (Michael Denton, Evolution: A Theory in Crisis. London: Burnett Books, 1985, p. 290-291)


Share this post

Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

Sign in to follow this  

  • Similar Content

    • By Absolute truth
      This topic is for miscellaneous darwinism-related information in sha Allah..
      Don't you understand how microbes turned to humans ???!!!!
      You need to educate yourself on biology...

      Wait !


      Philip Ball’s opinion piece in this week’s Nature, the most popular science magazine in the world, is news not because he stated that we don’t fully understand how evolution works at the molecular level, but because he urged his fellow evolutionists to admit it. On this 60th anniversary of the discovery of the DNA double helix, Ball reviews a few of the recent findings that have rebuked the evolution narrative that random mutations created the biological world.
      But it’s a Fact Anyway ?!
    • By Saracen21stC
      By Tia Ghose, LiveScience Staff Writer | LiveScience.com

      Neanderthals Doomed by Vision-Centered Brains
      Neanderthals' keen vision may explain why they couldn't cope with environmental change and died out, despite having the same sized brains as modern humans, new research suggests.
      The findings, published today (March 12) in the journal Proceedings of the Royal Society B, suggest that Neanderthals developed massive visual regions in their brains to compensate for Europe's low light levels. That, however, reduced the brain space available for social cognition.
      "We have a social brain, whereas Neanderthals appear to have a visual brain," said Clive Gamble, an archaeologist at the University of Southampton, who was not involved in the study.
      As a result, the extinct hominids had smaller social and trading networks to rely on when conditions got tough. That may have caused Neanderthals to die off around 35,000 years ago.
      Brain size riddle
      Just how smart Neanderthals were has been a long-standing debate.
      "Either they get regarded as lumbering brutes, or the other side says, 'No, they weren't that stupid. They had enormous brains, so they must have been as smart as we are,'" said study co-author Robin Dunbar, an evolutionary psychologist at the University of Oxford.
      To help solve the riddle, Dunbar and his colleagues looked at 13 Neanderthal skull fossils dating from 25,000 to 75,000 years ago and compared them with 32 anatomically modern human skeletons. The researchers noticed that some of the Neanderthal fossils had much larger eye sockets, and thus eyes, than do modern humans. [10 Odd Facts About the Brain]
      Low lighting
      The team concluded that Neanderthals used their oversized eyes to survive in the lower-light levels in Europe, where the northern latitude means fewer of the sun's rays hit the Earth. (Modern humans also tend to have slightly bigger eyes and visual systems at higher latitudes than those living in lower latitudes, where light levels are higher.) The researchers hypothesized that Neanderthals must, therefore, also have had large brain regions devoted to visual processing.
      And in fact, Neanderthal skulls suggest that the extinct hominids had elongated regions in the back of their brains, called the "Neanderthal bun," where the visual cortex lies.
      "It looks like a Victorian lady's head," Dunbar told LiveScience.
      Anatomically modern humans, meanwhile, evolved in Africa, where the bright light required no extra visual processing, leaving humans free to evolve larger frontal lobes.
      By calculating how much brain space was needed for other tasks, the team concluded that Neanderthals had relatively less space for the frontal lobe, a brain region that controls social thinkingand cultural transmission.
      Isolated and dying
      The findings explain why Neanderthals didn't ornament themselves or make art, Gamble told LiveScience.
      These results may also help explain the Neanderthals' extinction, Dunbar said.
      Smaller social brain regions meant smaller social networks. In fact, artifacts from Neanderthal sites suggest they had just a 30-mile (48.3 kilometers) trading radius, while human trade networks at the time could span 200 miles (321.9 km), Dunbar said.
      With competition from humans, a bitter ice age and tiny trading networks, the Neanderthals probably couldn't access resources from better climates, which they needed in order survive, he said.
    • By Absolute truth
      "... the evidence supporting descent with modification ... is both overwhelming and compelling."
      Many Darwinists wonder how we could possibly deny the 'fact of evolution'. After all, we can actually observe changes in nature, such as bacteria 'evolving' to become resistant to antibiotics. How can the history-denying people possibly not see this? The only explanation, Darwinists say, is that we are willingly ignorant of the truth.

      However, we do not deny variation. Not even the most fundamental die-hard scientist would ever deny that change occurs! Presenting variations, such as bacterial resistance, with the view that we deny them is a misrepresentation of our position.

      A net gain of new genetic information cannot arise by recombination of genes in the same way that rearranging a small book will not result in the British library. Theoretically, another small book with new information may arise, but there is no net gain.

      Define evolution !

      Evolutionists usually define their theory as 'change over time', 'descent with modification', or 'the change of allele frequencies of a population over time'. But these definitions are oversimplified.
      The theory of Evolution (the idea that all life has descended from a common ancestor) requires a net gain in new genetic information for it to occur. E.g., for a Lego house to change into a skyscraper, we must add the instructions for making steel, bricks, foundations etc. to the manual of the Lego house. These instructions do not already exist in the manual and cannot come about by rearranging the information already inside the manual.

      In much the same way, we must add the 'instructions' which make blood, limbs, organs etc. to the genome of our supposed microbe-like common ancestor. These instructions must be
      entirely new — they cannot come about by a rearrangement of pre-existing DNA, since the 500,000 DNA 'letters' of our common ancestor must change to the three billion 'letters' of humans.

      The Real Definition according to neo-darwinism:

      'the idea that all life has descended from a single common ancestor over millions of years via a net gain in new genetic information'.

      'Change over time', 'descent with modification', and 'a change in the allele frequencies of a population over time' are too ambiguous and do not actually explain how all life may have evolved from a common ancestor.

      So why does this matter?

      Fallacy of equivocation:

      Evolutionists use undeniable examples of 'change over time' (variation) to prove 'the idea that all life has descended from a single common ancestor over millions of years via a net gain in new genetic information' (microbe-like-to-man evolution).

      This inexcusable logic is called equivocation or the bait-and-switch fallacy, and occurs when someone changes the definition of a word halfway through an argument.
      The supposed Evidence for Evolution is full of examples of 'change over time' as evidence for microbes-to-man evolution.

      When an evolutionist claims that evolution is a fact, as almost all do, ask him what he means by the word 'evolution' and what facts he has to support this. No doubt 'evolution' will mean 'change over time' and the facts supporting it are simply examples of change over time, such as bacterial resistance (an example which everyone entirely agree with).

      To sum it all up, evolutionists provide examples of simple variation (where no new genetic information is added) to prove microbes-to-man evolution (where a net gain in new genetic information is required).
      This is illogical to say the least.
      One of two or more genes that may occur alternatively at a given site (locus) on a chromosome (gene version).
    • By Absolute truth
      One of the most popular alleged evidences for evolution on the internet is Endogenous RetroViral sequences (ERVs). Evolutionists think that a type of virus called a 'retrovirus', once inserted genetic information into one of our ape ancestors' genome. So how is this evidence for evolution?
      Scientists have noticed that chimps and humans have ERV genetic sequences at very similar points in our DNA. And so the story goes: our common ancestor acquired these ERVs and since humans and chimps are closely related, we should have them in similar spots in our genomes. We do. If we and chimps didn't evolve from a common ancestor (which first acquired the ERVs), how is it possible that we and chimps have ERVs in almost precisely the same locations? The only plausible explanation, evolutionists say, is evolution.
      But this is far from the truth. If we can show that ERVs are not the product of retroviruses, this evidence for evolution would fall flat.
      ERVS are simply more or less similar to retrovirus genome:
      The first problem with this argument is that it’s hard to tell what an ERV is when you meet one. It doesn’t come with a tag attached saying: ” This is an ERV “. It could be that these genes something completely different. That is because if a virus is embedded in it’s complete form, its almost impossible to pass it down to further generations.
      ERVS are Functional
      If ERVs are found to have function, it would be highly likely that they didn't originate from retroviruses. It would be inconceivable that viral non-functional ERVs somehow became functional. Evidence has surfaced that they do have function.
      "We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs)."(Conley, A.B., Piriyapongsa, J. and Jordan, I.K., "Retroviral promoters in the human genome," Bioinformatics 24(14):1563, 2008)
      The previous quote is very telling. There are many thousands of ERV sequences in our genome and in that of chimps. Does this mean that all are beneficial?
      "Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence ... and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome."("Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates," ScienceDaily, University of California - Santa Cruz, Nov. 15, 2007.)

      As we can see, it has been discovered that ERVs aid transcription in one fifth of the human genome!
      "We report that human ERVs actively shape the p53 transcriptional network in a species-specific manner ... At least one ERV insertion likely reshaped the transcriptional landscape of its surrounding genomic area and was instrumental in creating a new gene that became part of the human-specific p53 regulatory network ... We discovered a unique distribution pattern of p53 sites within repetitive sequences of the human genome, and several ERV families emerged as being substantially enriched for p53 sites in their LTRs."("Retroviral promoters in the human genome,2008"