Subfunctionalisation, Neofunctionalisation, and ...

[Timothy Chase]

Subfunctionalisation may occur when a gene is duplicated, then both genes diverge and perform more specialised tasks, splitting up the task which the original gene performed. Neofunctionalisation is where a gene becomes duplicated, then the duplicate becomes co-opted for an entirely different purpose. However, evolution seems to have other uses for duplicate genes...

GENE CLASSES FOLLOW DIFFERENT FATES AFTER PLANT GENOME DUPLICATION
By Heather Ramsey
The Science Creative Quarterly
Issue 2, Sep - Nov 2006
http://www.scq.ubc.ca/?p=596

Multiple copies of a mystery gene may make us human
From mice to monkeys to chimps to people, a brain-protein gene pumps up.
Bio Ed Online, August 31, 2006
http://www.bioedonline.org/news/news.cfm?art=2760

A gene that makes us human?
Saturday, September 02, 2006
http://pharyngula.org/index/weblog/comm ... _us_human/

Identification by full-coverage array CGH of human DNA copy number increases relative to chimpanzee and gorilla
Gary M. Wilson, Stephane Flibotte, Perseus I. Missirlis, Marco A. Marra, Steven Jones1, Kevin Thornton, Andrew G. Clark and Robert A. Holt
Genome Research 16:173-181, 2006
http://www.genome.org/cgi/content/full/16/2/173

Punctuated duplication seeding events during the evolution of human chromosome 2p11
Julie E. Horvath, Cassandra L. Gulden, Rhea U. Vallente, Marla Y. Eichler, Mario Ventura, John D. McPherson, Tina A. Graves, Richard K. Wilson, Stuart Schwartz, Mariano Rocchi and Evan E. Eichler
Genome Research 15:914-927, 2005
http://www.genome.org/cgi/content/full/15/7/914

[Anonymous]

Two newly posted articles you would like the look of, Timothy:


-----------------

[received via automated e-mail]

Here is a reply to Carl Wieland of Answers in Genesis. He wrote a
critique of my 'Mitochondrial Eve article and I show why his critique is
fundamentally flawed:

http://www.evolutionpages.com/Mteve_not ... al_eve.htm
And here is an article on a new kind of transitional:

http://www.evolutionpages.com/Organelle ... tional.htm

[Timothy Chase]

Two newly posted articles you would like the look of, Timothy:


Here is a reply to Carl Wieland of Answers in Genesis. He wrote a
critique of my 'Mitochondrial Eve article and I show why his critique is
fundamentally flawed:

http://www.evolutionpages.com/Mteve_not ... al_eve.htm

I have run across information to the effect we can't trace matrilineal lines the same way that we can patrilineal lines, something quite recent, but I haven't been able to follow it up as of yet. I remember that one of the potential problems with tracing the matrilineal lie in the possibility that our mitochondia might reproduce sexually - some yeasts have this sort of thing going on. However, I will have to check to see whether this is the actual problem.

And here is an article on a new kind of transitional:

http://www.evolutionpages.com/Organelle ... tional.htm

Those are perhaps my most favourite kinds of transitionals. 1966 is an important year for me personally, in a manner of speaking, and it was that year that the first accidental case of symbiosis was observed occuring in the lab between a species of bacteria and a species of amoeba. It started out as an infection which nearly wiped out the biologists amoebas, but then the survivors were permanently infected - and removing the bacteria would kill both the hosts and the bacteria. They had become interdependent. Initially the infection climbed to I believe 120,000 bacteria per host, but symbiosis resulted in it ultimately stabilising around 30,000. They are refered to as the x-amoeba and the x-bacteria.

The other big event of that year was Sol Spiegelman's experiments with what became known as Spiegelman's monster. A phage was allowed to reproduce in nutrients where it no longer had to infect bacteria, and it evolved from over 10,000 bases to 220. It multiplied like gangbusters - sliming down permitted it to replicate much more quickly than the original, hence the name. In 1974 Manfred Eigen repeated the experiment, but gradually reduced the amount of the phage he began with until there was no phage at all - and it still multiplied like gangbusters. A single enzyme was all it took. A protein - giving rise to an RNA virus, in this case 120 bases long. (I have the original articles for anyone who is interested - or I will just post the Spiegelman and Eigen papers a little later.)

Not quite the origin of life, but very close.

[molecanthro]

There are a few possible problems with using mtDNA in phylogenetics. It has been shown that, in a number of species, mitochondrial recombination occurs. There are a number of articles on scholar.google.com. A few of which are
http://www.broad.mit.edu/personal/arokas/pdfs/2003_Rokas_etal_mtDNA_TREE.pdf

http://mbe.oxfordjournals.org/cgi/content/abstract/22/4/925

Some other possible confounding factors include heteroplasmy, which is the situation where two or more types of mitochondrial DNA molecules occur within the same individual. While originally thought to be rare, heteroplasmy has recently been shown to be common. Much of the research on this topic has been on humans, and some researchers have strongly proposed the idea that heteroplasmy is not merely an exception to the rule, but rather it is a principle. http://www3.interscience.wiley.com/cgi-bin/abstract/70000788/ABSTRACT?CRETRY=1&SRETRY=0

Another potential problem associated with the amplification and analyses of mitochondrial DNA is the translocation of mitochondrial genome segments into the nuclear genome. These nuclear integrations of mitochondrial DNA are called Numts. According to a review article of these mitochondrial pseudogenes, Numts have been found in over 82 different eukaryotic species, with over 26 of those being mammals. Because Numts mutate at a slower rate than the authentic mitochondrial sequences, if they are unknowingly amplified, they can mislead researchers into thinking that there is less genetic variation than actually exists. However, they can be useful as well.
I have loads of references if anyone is interested in Numts.

[Timothy Chase]

There are a few possible problems with using mtDNA in phylogenetics. It has been shown that, in a number of species, mitochondrial recombination occurs. There are a number of articles on scholar.google.com. A few of which are
http://www.broad.mit.edu/personal/arokas/pdfs/2003_Rokas_etal_mtDNA_TREE.pdf

http://mbe.oxfordjournals.org/cgi/content/abstract/22/4/925

I will be adding that to my collection. I am guessing that much of the recombination occurs due to plasmids rather than phages or sexual recombination, but I am guessing the literature will give me a better idea.

Some other possible confounding factors include heteroplasmy, which is the situation where two or more types of mitochondrial DNA molecules occur within the same individual. While originally thought to be rare, heteroplasmy has recently been shown to be common. Much of the research on this topic has been on humans, and some researchers have strongly proposed the idea that heteroplasmy is not merely an exception to the rule, but rather it is a principle. http://www3.interscience.wiley.com/cgi-bin/abstract/70000788/ABSTRACT?CRETRY=1&SRETRY=0

I had heard that this happens, but even if what one had were strictly clonal at one point, recombination would undoubtedly occur.

Another potential problem associated with the amplification and analyses of mitochondrial DNA is the translocation of mitochondrial genome segments into the nuclear genome. These nuclear integrations of mitochondrial DNA are called Numts. According to a review article of these mitochondrial pseudogenes, Numts have been found in over 82 different eukaryotic species, with over 26 of those being mammals. Because Numts mutate at a slower rate than the authentic mitochondrial sequences, if they are unknowingly amplified, they can mislead researchers into thinking that there is less genetic variation than actually exists. However, they can be useful as well.
I have loads of references if anyone is interested in Numts.

I would certainly be interested. At the same time, in the age of the internet, if you know the name of a thing, you can find out about it. You have already given me a great deal. Not that suprising, given your background, but it is appreciated.

I understand though that most of the traffic goes the other way. Not that it has much of an effect - most of the lateral gene transfer the metazoans (multicellulars) experience is due to viruses - with 49% of our genome consisting of relics from exogenous retroviral infections.

However, the good majority of this is due to relatively few events - with a great deal of the replication taking place soon after the retroviruses have been endogenised. Then of course there is the turnover - something which is currently finishing-up with respect to the retrovirus now responsible for the barrier to the mother's immune system in sheep.