It must be awful being a creationist pseudo-scientist having to keep finding ways to ignore the latest piece of scientific research which shoots creationism down in flames.
Here we see yet another example of just this sort of recent discovery.
One of the mysteries in the biology of complex multicellular organism is how cells fuse together to form some of the organs like muscle and skin. The cells don't just stick together but actually unite rather like sperm and eggs unite to form a single cell. This produces large, multinucleated cells. In muscle, for example, a single muscle fibre can consist of a single, very long cell. This makes propagation of a wave of contraction almost instantaneous, instead of needing a chain reaction to stimulate a sequence of small cells.
For cells to unite in this way, they need to be able to break down their cell walls at the point of contact and that requires an enzyme. The problem was that these protein enzymes were hard to find so we weren't really sure what they were and how they worked.
Then in 2000 Sha Mi, Xinhua Lee and colleagues of the Genetics Institute, Cambridge, Massachusetts, USA, found the protein involved in producing this cell fusion to form the cyncytia in mammalian placentae. This layer forms an effective barrier between the mother and the developing foetus which prevents material passing across which would be recognised as foreign by the mother, who would then form antibodies against the foetus, so killing it, just as we would do with any other foreign tissue invading our body.
Not only did they discover the protein but they found that the gene for producing it had come from a virus.
Many mammalian viruses have acquired genes from their hosts during their evolution. The rationale for these acquisitions is usually quite clear: the captured genes are subverted to provide a selective advantage to the virus. Here we describe the opposite situation, where a viral gene has been sequestered to serve an important function in the physiology of a mammalian host. This gene, encoding a protein that we have called syncytin, is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W. We find that the major sites of syncytin expression are placental syncytiotrophoblasts, multinucleated cells that originate from fetal trophoblasts. We show that expression of recombinant syncytin in a wide variety of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell line expressing endogenous syncytin can be inhibited by an anti-syncytin antiserum. Our data indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be important in human placental morphogenesis.
Sha Mi, Xinhua Lee, et al, Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis;
Nature 403, 785-789 (17 February 2000) doi:10.1038/35001608;
So here we had evidence that infection by a retrovirus had resulted in one of its genes being captured by the genome of one of our remote, pre-placental ancestors. This gene was the gene it had used to break down the cell wall and inject itself into the cell - exactly what happens when cells fuse to form the structure we are discussing.
And without that infection, placental mammals, including us, could not have evolved.
In 2002 a team led by William A. Mohler of the Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA, found a protein called EFF-1 in the roundworm Caenorhabditis elegans which it uses to make its skin.
Multinucleate cells are widespread in nature, yet the mechanism by which cells fuse their plasma membranes is poorly understood. To identify animal fusogens, we performed new screens for mutations that abolish cell fusion within tissues of C. elegans throughout development. We identified the gene eff-1, which is expressed as cells acquire fusion competence and encodes a novel integral membrane protein. EFF-1 sequence motifs suggest physicochemical actions that could cause adjacent bilayers to fuse. Mutations in the extracellular domain of EFF-1 completely block epithelial cell membrane fusion without affecting other prefusion events such as cell generation, patterning, differentiation, and adhesion. Thus, EFF-1 is a key component in the mechanism of cell fusion, a process essential to normal animal development.
William A. Mohler, Gidi Shemer, et al; The Type I Membrane Protein EFF-1 Is Essential for Developmental Cell Fusion;
Developmental Cell, Volume 2, Issue 3, 355-362, (1 March 2002) doi:10.1016/S1534-5807(02)00129-6
By 2007, after another similar protein, AFF-1, had been found it was clear that there was a family of very similar proteins called FF proteins which all have similar rolls and without which we would not be able to make many of our organs. Some have gone so far as to suggest multicellularity and even sexual reproduction might not have been possible without them.
It is plausible that all cell fusion stems from viral genes slipping into our genome, but the jury is still out.Now Felix Rey of the Pasteur Institute, Paris, France, has found that the gene for the EFF-1 protein also comes from viruses. Using crystallography and X-ray diffraction to work out the 3D structure Rey's team has shown that it is very similar to virus proteins and that the active part is virtually identical. It looks almost certainly as though C. elegans got its ability to make skin by being infected with a retrovirus in its early evolutionary history.
Johns Hopkins University, Baltimore, Maryland, USA
Johns Hopkins University, Baltimore, Maryland, USA
There is still a lot of work to be done and other teams are looking for the protein responsible for muscle formation, for example, but with the first two such proteins to be found both coming from viruses, its likely that more, if not most of them will be found to have too.
Before cells can make something like skin or a digestive tract – as soon as you are thinking tissue and organs – usually you need some kind of fusion. If it's proved, it could be a Nobel prize.Why is this a problem for creationists?
Fasseli Coulibaly, Monash University, Melbourne, Australia.
Well, notice that the proteins found have been nearly identical, but not exactly so, to those of viruses even though the active parts are almost identical. It is possible to argue, of course, that this is simply the 'Intelligent Designer' reusing the same genes he invented for viruses to do a similar job, but why not make them exactly identical in that case? On the other hand, if the genes were acquired from viruses, and only the active part is essential, then the rest is free to mutate and change in any way, so long as the active region remains active. So, the most vicarious explanation - the one which doesn't require us to account for the origins of an 'Intelligent Designer' and to incorporate magic into the explanation, in other words the one which has an entirely natural explanation, is that these organisms have evolved in the presence of viruses which 'gifted' them these proteins and so greatly expanded their 'fitness landscape' into which they were now free to evolve.
This makes me think that viruses have contributed enormously to the communication between cells, and to the appearance of multicellular organisms on Earth.It is even possible that this interaction with viruses allowed disorganised clumps of single-celled organisms to evolve sexual reproduction and to become organised into the colonies of coordinated cells we call multi-cellular organisms. We already know that it allowed placental mammals to evolve, probably from pre-placental mammals such as the monotremes or marsupials only now found in Australia and a few other places. The findings of course fit entirely comfortably within the model of animals evolving by unguided, unplanned and unintelligent Darwinian Evolution and genetic drift which does not require magic or supernatural beings.
Felix Rey, The Pasteur Institute, Paris, France
Imagine being a professional liar for the Institute for Creation Research or the Discovery Institute and having to think up ways to mislead people over the significance of these findings, and to have to do that day after day after day as the evidence mounts up against you. It must feel at times like King Cnut trying to order the tide to turn, only faced with a tsunami.
They must consider themselves fortunate to be parasitising a bunch of people who are the least likely to be aware of this research if for no other reason than it tends to be published in science journals and pop-science magazines where the cognitive dissonance produced by reading them is far too uncomfortable, so they will be avoided like the plague.
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