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Gene duplication—raw material for the emergence of new genes Gene duplication is a very common phenomenon in all eukaryotic organisms (but also in prokaryotes; for review, see Romero and Palacios 1997) that may occur in several different ways (Lynch 2007). Traditionally, DNA-mediated duplication mechanisms have been considered and widely studied in this context, although peculiar intronless duplicate gene copies may also arise from RNA sources (see further below). DNA duplication mechanisms include small-scale events, such as the duplication of chromosomal segments containing whole genes or gene fragments (termed segmental duplication), which are essentially outcomes of misguided recombination processes during meiosis (Fig. 1A). However, they also include duplication of whole genomes through various polyploidization mechanisms (Lynch 2007; Conant and Wolfe 2008; Van de Peer et al. 2009). Thus, duplicate gene copies can arise in many different ways. But what is their functional fate and evolutionary relevance?
Gene duplication and new gene functions At least since a famous monograph, authored by Susumu Ohno, was published over 40 yr ago (Ohno 1970), the word has spread that gene duplication may underlie the origin of many or even most novel genes and hence represents an important process for functional innovation during evolution. Essentially and consistent with earlier ideas (Haldane 1933; Muller 1935), Ohno emphasized that the presence of a second copy of a gene would open up unique new opportunities in evolution by allowing one of the two duplicate gene copies to evolve new functional properties, whereas the other copy is preserved to take care of the ancestral (usually important) function (the concept of neofunctionalization). Ohno also reviewed that duplicate genes can be preserved by natural selection for gene dosage, thus allowing an increased production of the ancestral gene product (Ohno 1970). Finally, it should be emphasized that it has been widely agreed for a long time that the most probable fate of a duplicate gene copy is pseudogenization (Ohno 1972) and that hence the majority of duplicate gene copies are eventually lost from the genome. While these fundamental hypotheses have been confirmed by a large body of data, they have since also been significantly extended and refined. In particular, in addition to the process of neofunctionalization (i.e., the emergence of new functions from one copy—Ohno's basic concept), it was proposed that the potentially multiple functions of an ancestral gene may be partitioned between the two daughter copies. This process was dubbed “subfunctionalization” and may be shaped by natural selection or involve purely neutral processes (Force et al. 1999; Conant and Wolfe 2008; Innan and Kondrashov 2010).
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Gene Duplication D. Carroll, in Encyclopedia of Genetics, 2001
In the genomes of higher organisms, there are many examples of gene families that have arisen by gene duplication. For instance, the five human genes for the various β chains of hemoglobin that are expressed at different times during development are located in a cluster on chromosome 11 (Figure 2). There is also one pseudogene in this cluster. The four genes for the chains of hemoglobin reside in a separate cluster on chromosome 16, where there are also three pseudogenes. Examining the sequence relationships among these genes, we can deduce that an ancient duplication event created separate α and β genes, and they were subsequently dispersed. Then, each of these was amplified by several tandem duplication events. Accumulated mutations created the current distinctions among the family members
originally posted by: Noinden
a reply to: cooperton
I am not convinced you actually know what you are arguing. To be honest all you are doing is waving around the phrase epigenetics, as if that is proof. As opposed to a term, you have yet to show you have even a vague understanding of. Honestly if this was physics you would be using it, like someone who says "quantum physics" yet does not know what that is.
originally posted by: peter vlar
a reply to: cooperton
Burden of proof has been demonstrated, you choose to ignore it. Business as usual.
originally posted by: Phantom423
a reply to: cooperton
It looks like gene duplication uses the original gene as a template several ways. According to this article (and some of the references), the new gene can take its own evolutionary course through various mutations. The new gene is independent of the original gene. Assuming that mutations take place in the new gene, its functionality can be similar or totally different than the original gene.
New genes from non-coding sequence: the role of de novo protein-coding genes in eukaryotic evolutionary innovation Aoife McLysaght and Daniele Guerzoni
ABSTRACT The origin of novel protein-coding genes de novo was once considered so improbable as to be impossible. In less than a decade, and especially in the last five years, this view has been overturned by extensive evidence from diverse eukaryotic lineages. There is now evidence that this mechanism has contributed a significant number of genes to genomes of organisms as diverse as Saccharomyces, Drosophila, Plasmodium, Arabidopisis and human. From simple beginnings, these genes have in some instances acquired complex structure, regulated expression and important functional roles. New genes are often thought of as dispensable late additions; however, some recent de novo genes in human can play a role in disease. Rather than an extremely rare occurrence, it is now evident that there is a relatively constant trickle of proto-genes released into the testing ground of natural selection. It is currently unknown whether de novo genes arise primarily through an ‘RNA-first’ or ‘ORF-first’ pathway. Either way, evolutionary tinkering with this pool of genetic potential may have been a significant player in the origins of lineage-specific traits and adaptations.
A persistent and fundamental question in evolutionary genetics concerns the origin of genetic novelty [1–3]. Although it is possible for novel functions to arise within an existing gene [4], it is likely that there will be some degree of antagonism or adaptive conflict between the new and the old functions (e.g. [3,5]). By contrast, new loci are free of such constraints and constitute genetic novelty that may form the basis for lineage-specific adaptations and diversification [6–8]. The most radical form of genetic novelty comes from genes that originate de novo from non-genic DNA in that they are not similar to any pre-existing genes. Both protein-coding and RNA genes are important, but for the purposes of this perspective we will only consider the former. Clearly, protein-coding genes must have arisen de novo from non-coding sequence in very early life evolution. However, it is likely that the processes of evolution once life was established were very different from those processes that established life [9]. Consequently, de novo origin was usually considered so improbable as to be impossible for more recent evolution [2,8]. Instead, gene duplication, fusion and fission of genes, exon shuffling and other ‘bricolage’ events were considered to be the only viable sources of novel protein-coding genes—all variations on a genetic theme [9]. Proteins were thought to be made from a small and finite ‘universe of exons' [10]. François Jacob articulated this best when he said ‘To create is to recombine’ [9]. However, in recent years, there has been a growing appreciation for the role of de novo gene origination.
One important question concerns how a newly evolved gene can become essential. It is an apparent paradox because clearly the organism previously survived in the absence of that gene. It could be that coevolution of a de novo gene with an older gene interaction partner could lead to such essentiality [21]. It is also possible that the new gene might have provided an alternative function in the cell that resulted in relaxed constraint on some functions of other genes or pathways which were subsequently lost. Whereas duplicated genes may become essential by passive processes such as subfunctionalization, de novo genes can only become essential through neofunctionalization [21], a process which is expected to involve positive selection.
In the Descent of Man, Darwin draws a distinction between a difference of ‘degree’ and a difference of ‘kind’. In the same way, we can consider whether apparently lineage-specific traits are the result of genes that are different by degrees (diverged form of a gene present in the common ancestor) or of a different kind (de novo genes). Phylostratigraphic studies of eukaryotic genomes have pointed to several evolutionary periods that have disproportionately experienced a high rate of emergence of new genes [7]. These periods are associated with major species radiations and thus support the notion that new genes are integral to evolutionary innovation. A large part of the interest in de novo genes is to do with understanding their potential to evolve novel functions in a relatively short time-frame. There are a few examples of de novo genes with well-characterized functionality. The human-specific de novo gene FLJ33706 was discovered to be most highly expressed in brain tissue and was furthermore found to have elevated levels in Alzheimer's disease brain tissue, and a single-nucleotide polymorphism within the gene has been linked to addiction disorders [27]. Knockdown experiments demonstrated that the novel, human-specific gene ESRG is required for the maintenance of pluripotency in human naive stem cells [30]. It is difficult to definitively show that it is the peptide rather than the RNA that is functional, but these experimental results are encouraging.
The discovery of de novo genes is more than simply a discovery of a set of genes in eukaryotic genomes, it is the discovery of the viability of this process that can release genomic variation for testing through the filter of natural selection. Given the large number of ORFs in eukaryotic genomes and the growing understanding of the importance of short peptides, it will be interesting to discover whether the underlying dynamics enable this pool of cryptic ORFs to have a significant evolutionary impact. De novo genes are not only important for their functional and biological contribution to the lineages in which they originate; they are also very informative in terms of our growing understanding of the evolution the genome and of new gene functions. Evolution continues to tinker.
originally posted by: 5StarOracle
a reply to: cooperton
The irreducible complexity inherent in the miracle event as you call it,according to the great monkey king Darwin himself...
Is proof positive his theory is invalid false an outright lie even...
originally posted by: 5StarOracle
a reply to: cooperton
The irreducible complexity inherent in the miracle event as you call it,according to the great monkey king Darwin himself...
Is proof positive his theory is invalid false an outright lie even...
Not that any reasonable individual couldn’t figure that out for themselves though...
And I myself look forward to my future with my sky daddy...
That poor little fellow always spouting sky daddy like he’s above it all...
Hahaha
originally posted by: Barcs
Show me anything in the history of science that has been PROVED to be irreducibly complex.
originally posted by: Phantom423
a reply to: cooperton
The origin of novel protein-coding genes de novo was once considered so improbable as to be impossible. In less than a decade, and especially in the last five years, this view has been overturned by extensive evidence from diverse eukaryotic lineages. There is now evidence that this mechanism has contributed a significant number of genes to genomes of organisms as diverse as Saccharomyces, Drosophila, Plasmodium, Arabidopisis and human.
originally posted by: Phantom423
a reply to: cooperton
I think you're somewhat confused on the sequence of events. Mutations can be related or unrelated to de novo genes. The size of the resultant protein is dependent on its functionality.
The topic was new genes independent of any other genes in the organism. That's what the paper is about. You're digressing into other areas which are far removed from the topic. I understand that the title of this thread is about abiogenesis. However, the conversation developed into very specific areas of research and development. I addressed your recent queries about new genes. Nothing else.
It ties back to the original post though. The integral question in the original post is where do these protein-coding genes come from if there are no mechanisms in play to even create de novo genes (because there are no introns or other genetic fragments yet)? Especially since you need hundreds of genes to allow the most basic form of life. It's an insurmountable leap.
This process goes to the physics of atomic structure. The notion that anything - living or inert - popped out of nowhere is ridiculous. Our universe and everything in it is formed through process. Life is no different.
Are virtual particles really constantly popping in and out of existence? Or are they merely a mathematical bookkeeping device for quantum mechanics?
Gordon Kane, director of the Michigan Center for Theoretical Physics at the University of Michigan at Ann Arbor, provides this answer. Virtual particles are indeed real particles. Quantum theory predicts that every particle spends some time as a combination of other particles in all possible ways. These predictions are very well understood and tested.
Quantum mechanics allows, and indeed requires, temporary violations of conservation of energy, so one particle can become a pair of heavier particles (the so-called virtual particles), which quickly rejoin into the original particle as if they had never been there. If that were all that occurred we would still be confident that it was a real effect because it is an intrinsic part of quantum mechanics, which is extremely well tested, and is a complete and tightly woven theory--if any part of it were wrong the whole structure would collapse.
But while the virtual particles are briefly part of our world they can interact with other particles, and that leads to a number of tests of the quantum-mechanical predictions about virtual particles. The first test was understood in the late 1940s. In a hydrogen atom an electron and a proton are bound together by photons (the quanta of the electromagnetic field). Every photon will spend some time as a virtual electron plus its antiparticle, the virtual positron, since this is allowed by quantum mechanics as described above. The hydrogen atom has two energy levels that coincidentally seem to have the same energy. But when the atom is in one of those levels it interacts differently with the virtual electron and positron than when it is in the other, so their energies are shifted a tiny bit because of those interactions. That shift was measured by Willis Lamb and the Lamb shift was born, for which a Nobel Prize was eventually awarded.