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

http://www.nature.com/nature/journal/v463/n7280/full/nature08700.html

“Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content.”

Thanks for the question. Traits are determined by epigenetic information layers.

Human traits are determined by epigenetic control of gene expression

  1. Height

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208652/

Excerpt: “Genome‐wide SNP analyses have identified genomic variants associated with adult human height. However, these only explain a fraction of human height variation, suggesting that significant information might have been systematically missed by SNP sequencing analysis. A candidate for such non‐SNP‐linked information is DNA methylation. Regulation by DNA methylation requires the presence of CpG islands in the promoter region of candidate genes. Seventy two of 87 (82.8%), height‐associated genes were indeed found to contain CpG islands upstream of the transcription start site (USC CpG island searcher; validation: UCSC Genome Browser), which were shown to correlate with gene regulation. Consistent with this, DNA hypermethylation modules were detected in 42 height‐associated genes, versus 1.5% of control genes (P = 8.0199e−17), as were dynamic methylation changes and gene imprinting. Epigenetic heredity thus appears to be a determinant of adult human height. Major findings in mouse models and in human genetic diseases support this model. Modulation of DNA methylation are candidate to mediate environmental influence on epigenetic traits. This may help to explain progressive height changes over multiple generations, through trans‐generational heredity of progressive DNA methylation patterns.”

  1. Facial features

Excerpt: “Visel’s team was particularly interested in the portion of the genome that does not encode for proteins – until recently nicknamed “junk” DNA – but which comprises around 98% of our genomes. In experiments using embryonic tissue from mice, where the structures that make up the face are in active development, Visel’s team identified more than 4,300 regions of the genome that regulate the behaviour of the specific genes that code for facial features. These “transcriptional enhancers” tweak the function of hundreds of genes involved in building a face. Some of them switch genes on or off in different parts of the face, others work together to create, for example, the different proportions of a skull, the length of the nose or how much bone there is around the eyes.”

  1. Skull morphogenesis

Excerpt: “Histone deacetylases (Hdacs) are transcriptional repressors with crucial roles in mammalian development. Here we provide evidence that Hdac8 specifically controls patterning of the skull by repressing a subset of transcription factors in cranial neural crest cells. Global deletion of Hdac8 in mice leads to perinatal lethality due to skull instability, and this is phenocopied by conditional deletion of Hdac8 in cranial neural crest cells. Hdac8 specifically represses the aberrant expression of homeobox transcription factors such as Otx2 and Lhx1. These findings reveal how the identity and patterning of vertebrate-specific portions of the skull are epigenetically controlled by a histone deacetylase.”

  1. Hair color
  1. Skin and eye color

My comment: Traits are not determined by gene sequences. There are no mechanisms for evolution. Everything points to Design and Creation. Don’t get misled.

So epigenetics (and not genetics) determines traits? What would be a good definition for epigenetics? How does epigenetics work? You say that epigenetics controls gene expression, does that suggest that gene expression might be involved in traits?

Anyone else amused by the irony of this sentence used with a quote from dailymail?

Sources matter.

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What I see here in general is:

  1. One interesting set of observations related to the number of fox chromosomes decreasing at various speciation events.
  2. The assumption that losing chromosomes represents a loss in functionality or decrease in certain abilities.
  3. The grand conclusion, i.e. ‘aha’ moment where one interesting observation that isn’t immediately obvious which proves God supernaturally did it all (perhaps some 6,000 years ago).

I would challenge each of these three points and conclusions without even getting into the specifics of losing but not gaining chromosomes.

  1. To come into any well established theory of science and point out some irregularity (at least as you understand it which likely is different from how expert geneticists understand it) as proof that the entire theory is bad is a ridiculous argument to make. You still must account for as young earth creationist Todd Wood put it:

Evolution is not a theory in crisis. It is not teetering on the verge of collapse. It has not failed as a scientific explanation. There is evidence for evolution, gobs and gobs of it. It is not just speculation or a faith choice or an assumption or a religion. It is a productive framework for lots of biological research, and it has amazing explanatory power. There is no conspiracy to hide the truth about the failure of evolution. There has really been no failure of evolution as a scientific theory. It works, and it works well.

  1. An obvious example would be human losing a chromosome from other primates. While we are remarkably similar in our abilities (different only in degree not kind of abilities), one could safely argue that the merging of our chromosome #2 did not lead to an overall ‘loss’ of functionality for us human beings.
  2. Gaps in a scientific theory (or alleged gaps) does not mean or prove that God supernatually did it. This is a dangerous place to argue from as science relentlessly moves forward and closes the gaps that only God could previously fill. A great example of this was outlined recently by Dr. Venema in this post as he outlined some ‘science’ apologetics of the late 1600s that were doomed to fail.

This is a fun question though for us to explore and I greatly appreciate you pointing this out!

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Sources, you say? Seems Mr. Aalto “borrowed” a lot of his material from James V. Kohl, an actual scientist who went off the deep end and came up with his own theory that explains evolution and proves everyone else wrong. Kohl’s main page is RNA-mediated.com, where he has an archive dedicated to what he claims is plagiarism by Aalto.

Mr. Aalto also can be found on the Creationministry.org website, where he and our old friend Otangelo Grasso hang out and provide Creation News and Views, although they seem to have much more to say here than on their own dedicated forum.

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So the fact that I have green eyes, my younger brother has blue eyes, and my sisters have brown eyes is not related to DNA sequences in our genes?

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I’ve learned from experience that if someone swoops into a discussion and confidently dismisses hundreds of years of science with an attitude of “I’m the only one who knows real science,” we’re in for a rough ride.

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@Jpm,

They certainly do! Some are really hard to get … some not so hard.

But what I don’t understand about this convulsion of “handouts” from T. Alto is why he thinks some of this has any bearing on the issue of speciation and common ancestry.

And then I saw this post - - which is a re-do of one earlier:

@Christy, I apologize … I really did think he was merely talking about “sequence” … I didn’t realize he really was intent on maintain that genes don’t determine traits! Awesome, huh?

I’m not sure how he gets out of the Evolutionary logic by pointing to Epigenetics ? Even if we discovered there were “ghost” DNA strands … that can only be seen from Heaven … something is still driving changes in phenotype and - - most importantly - - the reproductive compatibility between populations.

But I guess we’ll save that conversation with someone who cares more about the connections than T.A.

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

So I came back to this thread when asked a wonderful question about chromosome number and common descent in a class I was teaching. The whole thread was essential created and then subsequently disrailed by the OP but I did want to put this here. To begin, it is important to understand how the actual graph mentioned was created:

“The phylogenetic tree is based on ∼15 kb of exon and intron sequence (see text). Branch colours identify the red-fox-like clade (red), the South American clade (green), the wolf-like clade (blue) and the grey and island fox clade (orange). The tree shown was constructed using maximum parsimony as the optimality criterion and is the single most parsimonious tree. Bootstrap values and bayesian posterior probability values are listed above and below the internodes, respectively; dashes indicate bootstrap values below 50% or bayesian posterior probability values below 95%. Horizontal bars indicate indels, with the number of indels shown in parentheses if greater than one. Underlined species names are represented with corresponding illustrations.”

It is extremely wrong when the OP writes that such phylogenies are ‘assumed.’ They outline how they calculate it and he simply writes its assumed. Very dishonest. But I did want to put the chromosome numbers that he mentioned on the actual phylogeny. And the list of chromosomes:

When you put them on the phylogeny do not support what he said at all. While he arranged a list of fox chromosomes in a decreasing order the actual relationship between foxes has no support for his claim at all! This is important that even if one disagrees with an idea, at least get your facts straight!

Ya think? 

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Hey… I just re-discovered one of my short-lived mottoes ! Hmmm… I wonder if I should start using it again?

@Tomi_Aalto, I don’t think that anyone has mentioned this but a decrease in number of chromosomes does not mean an equivalent decrease in number of genes. A Robertsonian fusion combines the long arms of two telocentric chromosomes: the tiny short arms are lost, and the result is a reduced number of chromosomes. Ref.

It would be interesting if you could find for those foxes not only the number of chromosomes but also the total genome size for comparison.

Note that different numbers of chromosomes need not prevent cross breeding. The domestic horse and Przewalski’s horse have different numbers of chromosomes but can still interbreed.

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Plants can evolve by doubling their chromosomes… and thus they can speciate in literally a single generation!

Of course since it’s duplication of the genome it does not in itself increase genetic information, any more than my having two copies of “Origin of Species” increases my information on the subject.

But by having two copies the plant can do something that the plant with one copy can not. While it might not be an increase in information in a strict sense it is an increase in function.

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As you said, the duplication in itself wouldn’t add much but it provides a lot of new material to play around with at no detriment to the organism. Here’s a nice example from drosophila where duplication events led to novel expressions through exon shuffling (@aarceng) :

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@asrceng

So we can speciate and have no loss of info, right?

And by having a spare … changes can be made in one set without risking the ooerational version… whuch makes it easy to develop new working tools without dying in the orocess.

That’s a great example from tandem duplications, which are very common in animal genomes. Here’s an example from whole-genome duplication, which shows how changes in ploidy (which was the question a few entries above in the thread) create numerous changes in “information.” Note that such things are not surprising in the least. But they’re interesting.

https://genome.cshlp.org/content/24/8/1348

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