It looks like you're using an Ad Blocker.

Please white-list or disable AboveTopSecret.com in your ad-blocking tool.

Thank you.

 

Some features of ATS will be disabled while you continue to use an ad-blocker.

 

Abiogenesis - The Impossible Theoretical Miracle

page: 14
30
<< 11  12  13    15  16  17 >>

log in

join
share:

posted on Oct, 15 2018 @ 09:21 PM
link   
a reply to: cooperton

Burden of proof has been demonstrated, you choose to ignore it. Business as usual.




posted on Oct, 15 2018 @ 09:42 PM
link   
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.




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).


www.ncbi.nlm.nih.gov...

I don't know if this occurs in the lactase gene, but there's more than a few papers in the literature which describe this duplication process with the new gene assuming a new functionality.



posted on Oct, 15 2018 @ 09:57 PM
link   
a reply to: cooperton

Duplication is not to be confused with alleles. Alleles are variants that occur at the same locus on the chromosome. Duplicates are in different positions on the chromosome and are independent of the original gene.





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
.

www.sciencedirect.com...



posted on Oct, 16 2018 @ 02:04 AM
link   
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.



posted on Oct, 16 2018 @ 02:34 AM
link   
a reply to: cooperton

Yes, I did. Is it wrong? No, so your point is mute, yet again. Please address my statements from before.

bscb.org...

This includes a very good explanation on epigenetics. You're confusing gene mutability with epigenetics, but ultimately they are part of the same grand mechanisms that constitute the explanation for evolution.

I would also like to add that while my genetics knowledge is kinda of rusty, you do see to have done your research, allowing you to actually pretend to have somewhat of an understanding, but then you misinterpret every piece of information to form a narrative that shows an actual lack of understanding (and this is an understatement).

Let me give you a novel piece of information about genetics: Gene X may stay unchanged but the phenotype corresponding to said gene may change because Gene Y mutated. Genes don't generally "code" one characteristic and stay there, they often contain the information that allow for the codification of other genes. There's a high degree of interdependability between them.

Something that may also come as a surprise, because you simply lack the ability to think in large time frames, is thinking that we don't change because you haven't seen us change is not lack of proof for evolution, it's actually not having the slightest gasp on how small changes contribute to a bigger change down the road. I've previously mentioned that we are genetically different from a 20000 year old homo sapiens and that we do have a different phenotype and genotype, even if you decide to ignore lactose tolerance, something you like to think disproves evolution (it doesn't).

I'm missing both my lower wisdom teeth and my first lower right pre-molar due to agenesis, and this is simply part of the evolutionary process. My chin was receeding before I actually wore braces to partially correct the issue, and this is due to the evolutionary process. Our chins are indeed receeding, our aforementioned teeth are indeed disappearing, our brains are getting smaller and we are getting less hairier. This is all due to the evolutionary process.

Here is another article that actually provides examples of real time evolution for macro species: discovermagazine.com...

Good day.
edit on 16-10-2018 by JameSimon because: Added info



posted on Oct, 16 2018 @ 02:49 AM
link   
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
edit on 16-10-2018 by 5StarOracle because: Word



posted on Oct, 16 2018 @ 07:17 AM
link   

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.


We've gotten cordial and are discussing the necessary mechanics that would be involved in the generation of new genes. You should join the discussion


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.



Good find. That would be the first piece of the puzzle. I tried looking for evidence of these gene duplicates being able to amalgamate large sequences of additional base pairs. Scientists have tried and they don't seem to be able to get past a couple base pairs (i.e. red and green opsin which are only 2 base pairs different). They all seem to be dealing with SNPs.

The main proof remaining is the ability for a duplicate gene to forego many mutations and remain viable. Take for example the leap necessary to mutate a gene to create the titin protein which has over 35,000 amino acids in it's largest isoform. This means it has over 100,000 base pairs in its sequence, so to make a leap from a duplicate gene, to a gene that codes for such a large gene sequence is the dilemma at hand. Not to mention how meticulous the sequence is, and how precise these mutations would have to be along the way, althewhile avoiding a point inviability due to a destruction genetic sequence.
edit on 16-10-2018 by cooperton because: (no reason given)



posted on Oct, 16 2018 @ 09:05 AM
link   
a reply to: cooperton

One of the ways de novo genes can occur is from non-coding sequences. This was thought to be impossible until recently when it was discovered that proto-genes arise frequently from non-coding sequences which are then thrown into the natural selection process. The article below describes how protein-coding genes of increasing complexity are created through this process. From the article: "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."




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.



The many ways genetic novelty can occur:



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.



Unanswered questions still to be elucidated: How did the organism survive without this gene?



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.



Functional contribution of de novo genes:



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.



Nature continues to experiment:



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.


www.ncbi.nlm.nih.gov...

I like this article for its detail and references. Several papers describe the viability of these de novo genes, which was one of your questions. As the article states, there's no particular time frame or sequence of events leading to these new genes. New gene development can be rapid or slow depending on mutational events. Natural selection continues the process by weeding out whatever the gene doesn't need (both good and bad).



posted on Oct, 16 2018 @ 02:38 PM
link   
And yet again he ignores the posts. Beautiful. You really don't like people that call you on your bull, right cooperation?



posted on Oct, 16 2018 @ 03:31 PM
link   

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...


Then prove it. Show me anything in the history of science that has been PROVED to be irreducibly complex. You people simply can't do it, yet you continue to talk trash about it while offering no substance at all.

Maybe you don't know what the word "impossible" means. It means that it absolutely can't happen no matter what. It doesn't mean that we don't know how it happened or that something is unlikely. This is why this thread is completely wrong and dishonest. Nobody has shown abiogenesis to be impossible. Not even 1 point made by you or the OP has demonstrated that. Epigenetics has zero to do with abiogenesis, it would be nice if you guys actually presented a valid argument but that never happens.


edit on 10 16 18 by Barcs because: (no reason given)



posted on Oct, 16 2018 @ 03:49 PM
link   
a reply to: cooperton

Neighbour I AM involved in the discussion. You should address the burden of proof.



posted on Oct, 18 2018 @ 08:35 AM
link   
a reply to: cooperton

Coop, where are you? We're supposed to be having a civil conversation as you requested. I think that's a very interesting article that I posted. Please engage. Thanks.



posted on Oct, 18 2018 @ 12:54 PM
link   

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


why is it that people always forget about mendel.



posted on Oct, 18 2018 @ 08:58 PM
link   

originally posted by: Barcs

Show me anything in the history of science that has been PROVED to be irreducibly complex.



Some examples of irreducible complexity in humans:

Show me a heart working without lungs/gills. Show me a stomach without an acid-resistant stomach lining. Show me bones without tendons. Testes without vas deferens. Actin without myosin. spindle fibers without a kinetochore. A Retina without an optic nerve. A Spinal cord without vertebrate. A blood cell without hemoglobin. Mammary glands without a child with lactase. Adrenal glands without adrenoreceptors. etc, etc


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.


Very relevant info you found. I am glad they admit the difficulty of the genesis of even one de novo gene. To return to the OP regarding abiogenesis, If one de novo protein is very rare, how could many have formed to generate the first viable life form? Especially since the mechanisms required for genetic mutation wouldn't even be in place yet. We're not talking about 5 or 6 genes spawning from primordial goo, but the smallest viable microbial genome has 473 genes.

can you admit that 473 genes spawning from randomness is outright implausible by ordinary natural processes?



posted on Oct, 18 2018 @ 09:32 PM
link   
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.

If you read the references, you would see that de novo gene genesis is, in fact, common. The point of the article is that de novo genes are relevant to an organism and to the evolution of that organism. There's a large variability among organisms as to how these new genes actually function. And that makes sense since every organism will have a unique evolutionary trail. As speciation occurs, genetic drift increases and the "likeness" between organisms decreases. The dinosaur and the bird are ancestrally related. The probability that de novo genes played a role in the divergence between dinosaur and bird is probably very high. Evolution is a sequence of events where nature and natural selection make the call as to the outcome.

You need to focus on the content of the article - the purpose, the methods, the discussion and the conclusions. There's a lot more there that you're not seeing.

If you can find fault with that paper, please discuss. As I see it, the paper clearly outlines the current knowledge regarding the genesis of new genes.
edit on 18-10-2018 by Phantom423 because: (no reason given)

edit on 18-10-2018 by Phantom423 because: (no reason given)

edit on 18-10-2018 by Phantom423 because: (no reason given)

edit on 18-10-2018 by Phantom423 because: (no reason given)

edit on 18-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 18 2018 @ 11:37 PM
link   
a reply to: Barcs

3.5 billion years old with flagellum do you suppose the first cells were immobile?
Prove they were...
The op gives you a nice little picture to look at...
Since evolution takes an impossibly long time the age of the earth says you are full of yourself and some smelly brown substance...



posted on Oct, 19 2018 @ 06:40 AM
link   

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.
edit on 19-10-2018 by cooperton because: (no reason given)



posted on Oct, 19 2018 @ 09:47 AM
link   
a reply to: cooperton




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.


It's been demonstrated many times in the lab that nucleic acids can self assemble into amino acids. The self assembly process is driven by thermodynamics and kinetics. There are many research papers discussing the dynamics. Self assembly is a well known phenomenon.

In your original post, you start at a place which bypasses a very long history of events. To really understand abiogenesis you would have to go back to the first reproducing molecule. Since life as we know it is defined as anything that can reproduce, that would be the starting point. Then to study that molecule, you would have to go back to self assembling atoms that form a particular molecule like a nucleic acid. And to study that, you would have go way, way back to study the origin of atoms. 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.

This is an interesting video on the origin of genes.


edit on 19-10-2018 by Phantom423 because: (no reason given)

edit on 19-10-2018 by Phantom423 because: (no reason given)



posted on Oct, 19 2018 @ 03:41 PM
link   
a reply to: Phantom423


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.


That is the summation of what you guys have been arguing with... God did it...

Which I have no problem with, but it wasn't in the way these people are implying

(It all started with Adam in the garden)




posted on Oct, 20 2018 @ 07:51 AM
link   
a reply to: Akragon

Not really. I was referring to macro molecules - they don't pop out of nowhere. Quantum mechanics allows for virtual particles which go in and out of existence, albeit very complex. There's no evidence for or against an intelligent being behind the whole mess. There's a lot more to learn about this universe (and possibly others) before we can even ask that question.




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.


www.scientificamerican.com...




top topics



 
30
<< 11  12  13    15  16  17 >>

log in

join