Why we can only observe chromosome loss - not increase in chromosome numbers?


(Tomi Aalto) #1

We can pick and study any evolutionary tree of any diploid organism and make an obvious observation: Chromosomes are typically lost when so-called speciation occurs. Lets’s have an example, the Fox lineage:

Bat-eared fox 72 chromosomes
Gray Fox 66 chromosomes
Fennec Fox 64 chromosomes
Bengal Fox 60 chromosomes
Kit Fox 50 chromosomes
Tibetan sand fox 36 chromosomes
Red Fox 34 chromosomes

And here’s the phylogenetic tree of the Foxes and their assumed ‘evolution’:

Have you ever asked the most important question:
Why we can only observe chromosome loss but not increase in chromosome numbers?

The reason for chromosome loss can be found in epigenetic factors. Here’s a brief summary.

  1. Poor diet, stress and other environmental factors alter the epigenetic layers. Aberrant methylation patterns trigger sequence changes. You can read about the connection between oxidative stress and deamination from several sources, for example from here:
  1. Sequence changes typically cause SNPs, single nucleotide polymorphism. For example, there are about a million SNPs, useless genetic errors in the human DNA. These alterations are genetic errors but due to other mechanisms, like overriding microRNAs, all of them are not crucial or harmful errors. When there are a lot of faulty genes, the cellular mechanisms start to hide and suppress these erroneous genes by methylating histones. This can be observed as chromatin remodeling and packaging.
  1. Strongly packaged (silenced) regions of chromatin are called heterochromatin. Regions at open state are not having faulty genes and these areas are called euchromatin.

  2. During meiosis, the clever cellular mechanisms try to make new chromosomal recombinations using euchromatins, because these regions have no errors. Heterochromatins are dropped out. The final result is loss of genetic information and loss of chromosomes.

Keywords: heterochromatin chromosome loss

For the theory of evolution this phenomenon is a very inconvenient fact. That’s why they have invented another term: a chromosome fusion. But that is false science. The correct and approvable term is chromosomal recombination due to loss of biological information.

These mechanisms explain the following observations:

  • Speciation is not evolution. It happens after significant loss of biological information that causes barriers for reproductive mechanisms.
  • Some people have already lost a pair of chromosomes.
    Keywords: chinese man 44 chromosomes
  • Increase of biological information has never been observed.

There are no mechanisms for evolution. Conclusions are obvious:

Organisms are designed and created by God. Don’t get lost.


(Christy Hemphill) #2

That’s certainly debateable. We’ve published a whole series on that. http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/biological-information-and-intelligent-design-evolving-new-information


(Curtis Henderson) #3

This is an interesting observation and a good question. It is notable that the fox family is a bit of an outlier for having an unusually large number of chromosomes. Do you have any other examples of similar reduction in chromosome numbers in other families? Also noteworthy is that the loss of chromosomes is not as severe of a problem as we might first guess. Robertsonian translocations and fusions often lead to reduced chromosome numbers without significant loss in actual coding information. This even still happens in humans (as you alluded to late in the post), but often without a significant impact on the individual. There are mechanisms that can result in increased chromosome numbers, as well.

I can do some more research to try to answer your question in more detail, but I’d like to hear your response to a question of mine first. Are you genuinely interested in scientific discussion, and willing to accept scientific correction, if need be?


(George Brooks) #4

@Tomi_Aalto

So then, what you are saying, is that God needed more Chromosomes for foxes than for humans?

Are you suggesting that the human chromosome count of 46 indicates a loss of information compared to virtually all foxes?

Have you considered that information is reflected in utilized locations, regardless of how many chromosomes there are to “package” these genetic locations?

Everything points to God-Guided Evolution. Don’t be misled by untrained amateur scientists!


(Tomi Aalto) #5

Unfortunately gene sequences don’t determine traits.


(Tomi Aalto) #6

Chromosome loss is a fact within all mammals. And it occurs rapidly. For example a Madeira mouse lost half of its chromosomes just in 500 years due to intensive adaptation. The best example is Muntjacs:

Rapid ‘speciation’ and chromosome loss don’t support the theory of evolution

Excerpt: “The Red Muntjac has the lowest diploid chromosomal number in mammals (2n = 6 for females and 7 for males) whereas Reeves’ Muntjac has 2n = 46 in both sexes (remarkably, these two species can produce viable F1 hybrids in captivity).”

My comment: Despite the huge difference in chromosome count (2n=6 and 2n=46), those two breeds of Muntjac are able to get viable offspring. Such interesting cases of hybridization can be observed in captivity, for example in zoos.


(Christy Hemphill) #7

Um, that’s changing the subject. You said “increase in biological information has never been observed.” I pointed you to an in depth discussion of exactly those kind of observations. You couldn’t possibly have looked at a thirteen article series in ten minutes. I might conclude you aren’t that interested in actually discussing your own claims.


(George Brooks) #8

@Tomi_Aalto

I can only assume that by your use of “gene sequences” … you actually mean the order in which genes are found on a chromosome.

Nobody here has ever proposed that a chromosome with A > B > C sequence of genes will operate differently than a chromosome with a C > A > B sequence.

So why don’t you read a little slower and come up with a better answer?


(George Brooks) #9

@Tomi_Aalto

I think it is safe to say that the pattern you see in Mammals is not universal across all life forms … from plants, to bacteria, to insects.

Every group of life forms has evolved it’s own way of quickly adapting to changes in environment. For some life forms, dramatic increases in chromosome count are their ticket to species survival.

Some group somewhere had to eventually stumble on chromosome reduction as a helpful trend; mammals won that trophy.

But chromosome loss is not the same as information loss. Otherwise, you would be tempted to conclude that Humans are a “degraded form of fox!”


(Lynn Munter) #10

I recommend reading this entire article, but particularly the bit about whole genome duplication:

"Whole genome duplication, or polyploidy, is a product of nondisjunction during meiosis which results in additional copies of the entire genome. Polyploidy is common in plants, but historically has also occurred in animals, with two rounds of whole genome duplication in the vertebrate lineage leading to humans.[3] After whole genome duplications many sets of additional genes are eventually lost, returning to singleton state. However, retention of many genes, most notably Hox genes, has led to adaptive innovation.

Polyploidy is also a well known source of speciation, as offspring, which have different numbers of chromosomes compared to parent species, are often unable to interbreed with non-polyploid organisms. Whole genome duplications are thought to be less detrimental than aneuploidy as the relative dosage of individual genes should be the same."


(Tomi Aalto) #11

I think the number of chromosomes has been much higher let’s say 2000 years ago. We know that especially Y chromosome is rapidly decreasing. This can be observed within older men and the phenomenon is spreading into germ line.

Today we can observe rapid loss of genes. This a scientific fact for example in Iceland and certain areas of Pakistan, where close relatives are married.

There are 200,000 disease-causing mutations in the human genome. Over 10,000,000 SNPs point out that so called natural selection is not able to filter those mutations out.

There are no beneficial random mutations. Gene sequences don’t determine traits.


(Tomi Aalto) #12

No it’s not. If you think information is gained by gene duplications, then you have to think that gene sequences determine traits.


(Steve Schaffner) #13

I haven’t asked that question because the premise isn’t true. We observe both chromosome loss and chromosome gain. For example, human (and ape) chromosomes 14 and 15 represent a ancestral fission of a single chromosome, which is still seen in monkeys.

A more important question: do you care about the actual biology?


(Tomi Aalto) #14

Chromosome fission has been observed in lab petri dishes only. Let’s talk about actual, observed biology.


(George Brooks) #15

@Tomi_Aalto

Well, since you think the earth is less than 6000 years old, you would have to, yes?

But samples of old cadaver animals from all over Life’s family tree probably wouldn’t support that conclusion at all… unless you want to argue that a body tested to be 3000 years old is really only 300 by your reckoning.


(George Brooks) #16

@Tomi_Aalto

I think @glipsnort’s observation of seeing the architecture of one human chromosome actually at work as two chromosomes in other primtaes is observed biology!

Everything points to God-Guided Evolution. Don’t be misled by untrained amateur scientists!


(Lynn Munter) #17

My head is spinning—something that happens in a petri dish isn’t “actual, observed biology?” What would be? Sticking your microscope into the sex organs of a wild tiger at the exact moment that a chromosomal fission event happened?


(Steve Schaffner) #18

Monkeys and apes don’t live in Petri dishes. (Here is a paper on this chromosome fission, by the way.)

I’m afraid your response is suggesting an answer to the question I asked.


(Curtis Henderson) #19

I’m afraid in @Tomi_Aalto’s case, the answer is a resounding “no”.


(Curtis Henderson) #20

Despite my disinclination to participate in what appears to be a fruitless discussion, I am highly intrigued! If gene sequences (I must guess you mean the nucleotide sequence of genes) don’t determine traits, then what does determine traits?