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Challenges to Endosymbiotic Theory

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1 Challenges to Endosymbiotic Theory on Sat Nov 16, 2013 10:04 am

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On the Origin of Mitochondria: Reasons for Skepticism on the Endosymbiotic Story 4

http://reasonandscience.heavenforum.org/t1303-challenges-to-endosymbiotic-theory

http://www.molevol.de/gallery/The_symbiotic_origin_of_eukaryotes_high.mp4

Most biology textbooks now tell us that organelles such as chloroplasts and mitochondria, both of which have circular DNA, evolved through endosymbiosis – an hypothesis promoted by LynMargulis (Margulis, 1991). However, the evidence for this is weak, and a much more likely origin of organelles such as the ER, mitochondria, lysosomes, peroxisomes, secretory vesicles, chloroplasts and the tonoplast in plants is invagination of membranes. Comparisons of mitochondrial DNA throughout animals, plants and eukaryotic microbes supports the hypothesis that mitochondria arose only once in evolution, and were from a proto-bacterial cell (Lang et al., 1999). But, the genomes of mitochondria and chloroplasts are too small to code for the genes necessary for a complete organism. 6

Human mitochondrial DNA has just 16 569 base pairs, coding for only 37 genes, which are all essential for mitochondrial function, but far too little for a cell to survive. Thirteen of these genes produce proteins essential for ATP synthesis by oxidative phosphorylation, the other 25 coding for tRNA and rRNA, necessary for mitochondrial protein synthesis. Mitochondrial ribosomes are like bacterial ribosomes. None are involved in Ca2+ signalling. Yet, E. coli has some 300 essential genes which cannot be knocked-out without killing the cell, yet there are some 1500 proteins found inside a mitochondrion, several of which are involved in transporting Ca2+ in and out, or responding to a rise in intra-mitochondrial free Ca2+. Mitochondrial divide, make proteins, make ATP, and carry out several other biochemical pathways, such as fatty acid oxidation. So if mitochondria originated from an endosymbiont such as Rickettsia there are three problems:

1. How did the endocytosed bacterium survive and multiply if its internal environment was oxidising? The cytosol of all cells is reducing, preventing the formation of S–S bonds and damaging oxidative reactions involving reactive oxygen species. But, remember the first eukaryotes formed before there was significant oxygen in the atmosphere. So oxidative phosphorylation in mitochondria must have evolved after photosynthesis, some 2000 million years ago.
2. Since cells need at least several 100 proteins to survive and replicate, what happened to the proteins essential for nucleotide and nucleic acid, and protein synthesis, and the reactions necessary for ATP synthesis, e.g. glycolysis?
3. How did the 1500 or so mitochondrial proteins in the main genome become targeted to the mitochondria, if they were lost by the initial endosymbiont?

For the endosymbiotic hypothesis to work, the primitive bacterium engulfed by the eukaryote precursor must have lost over 90% of its genes, these being taken up by the nuclear genome. Furthermore, most of the proteins involved in Ca2+ signalling must have come from another source.

Plastid DNA contains just 60–100 genes, whereas a typical cyanobacterium DNA codes for 1500. The rest of the chloroplast proteins, like mitochondria, are coded for by the nuclear genome. A chloroplast genome of around 140 kb is comparable to a large bacteriophage, such as T4 whose genome is about 65 kb.

The start of the sequence for the origin of a mitochondrion or chloroplast would have to be a bacterium or cyanobacterium being taken up by the eukaryotic precursor. Then this has to lose genes, which are captured by the main genome. Then some of these genes have to have targeting sequences added them and they have to change several codons so that their genetic code matches the main genome, and not the proteins that remain in the mitochondrial or chloroplast genome, since there are differences in the genetic code between non-plant mitochondria and nuclear DNA, and losses of antocodons in chloroplasts. This is too many ‘ifs’ and ‘buts’ to be credible!

Functional Anatomy Of Prokaryotic And Eukaryotic Cells


With regret, ENV recently noted the passing of biologist Lynn Margulis. Margulis, a scientist whom I admired greatly, was never a stranger to controversy, going so far as to call neo-Darwinism "a complete funk" and asserting that "The critics, including the creationist critics, are right about their criticism. It's just that they've got nothing to offer by intelligent design or 'God did it.' They have no alternatives that are scientific." She was a scientist who wasn't afraid to think creatively, disregarding the scorn of her colleagues. According to the Telegraph, a response to one grant application she made said: "Your research is crap. Don't ever bother to apply again."
Lynn Margulis took a controversial view on how evolution works, stressing the importance of symbiotic and co-operative relationships over competition. This concept of evolution inspired what is now recognized as her most notable idea, the notion that the eukaryotic mitochondrion -- the power plant of the cell -- was acquired by virtue of an endosymbiotic event. Endosymbiotic theory essentially maintains that mitochondria arose by virtue of a symbiotic union of prokaryote cells. The nearest living relative to the mitochondrion is thought to be the alpha-proteobacteria Rickettsia (Emelyanov, 2000Andersson et al., 1998). Chloroplasts are also thought to have arisen in a similar manner from the photosynthetic cyanobacteria.
In November 2010, I drew attention to a paper in Nature by Nick Lane and Bill Martin, who showed that the prokaryote-to-eukaryote transition was effectively impossible without the energy demands, pertinent to the biggest event of gene manufacture in the history of life on earth, being met by the mitochondrial processes of oxidative phosphorylation and the electron transport chain. The bacterial cell alone could not meet these energy demands. The evidence that is typically offered for endosymbiotic theory includes the following:

Mitochondria possess a circular genome (lacking in introns and independent from the nuclear DNA) in which transcription is coupled to translation, characteristic of bacterial DNA. There are also some other notable similarities. For example, in both mitochondria and Mycoplasma, the codon UGA specifies the amino acid Tryptophan , whereas in the conventional code it serves as a stop codon. Mitochondria divide and replicate independently of host cell division and do so in a manner akin to binary fission, possessing homologues of the bacterial division protein FtsZ .They are enclosed by a double-membrane.Mitochondria and bacteria are of a similar size and shape.Circular Mitochondrial Genome. As noted, one of the core arguments for endosymbiosis points to its circular genome. What is often not noted, however, are the cases where eukaryotic mitochondria have linear genomes with eukaryotic telomeres. Indeed, two strains of the same species of yeast differ with respect to the linearity or circularity of their mitochondrial genome .In the case of linear chromosomes, the DNA polymerase enzymes are unable to replicate right to the end of the chromosome. This is because the enzymes are unable to replace the lagging strand's terminal RNA primer. Unless there is a mechanism for circumventing this, it will result in the chromosomes shortening after each round of replication (in eukaryotes, the enzyme telomerase attaches extra DNA to the chromosomal ends).

 This means that the transition from genome circularity to linearity -- a fete in itself given the changes that have to be made to the mode of replication -- must happen in concert with the evolution of a mechanism to prevent progressive chromosomal shortening. 

In order to have a transition from prokaryotic to eukaryotic dna replication, telomerase enzymes must arise simultaniously, to prevent the shortening of the telomere region after every replication. 

Telomerase, also called telomere terminal transferase,[1] is a ribonucleoprotein that adds the polynucleotide "TTAGGG" to the 3' end of telomeres, which are found at the ends of eukaryotic chromosomes. A telomere is a region of repetitive sequences at each end of a chromatid, which protects the end of the chromosome from deterioration or from fusion with neighbouring chromosomes. 5

Such an evolutionary transition is far from trivial. Biologist Albert de Roos writes,n linear mitochondrial chromosomes various different mechanisms to "prevent" shortening exist, ranging from hairpin loops and self-priming to protein-assisted primer synthesis (see here). The telomeric regions of mitochondrial chromosomes do not seem to have a direct phylogenetic relation since they use other proteins and mechanisms than nuclear telomeres. Thus, it is difficult to deduce evolutionary pathways purely based on phylogenetic data on telomeres and mechanisms for end replication.Furthermore, mitochondrial genes often do possess introns . These are particularly prevalent in the mtDNA of fungi and plants. The mitochondrial genetic code may also be slightly different from that of bacteria .Mitochondrial DNA Replication: 

The claim one often hears is that circular mitochondrial DNA replication resembles bacterial binary fission. While this is true, in at least some respects, there are also important differences. For example, many of the key components are of eukaryotic origin and replication beginning at the Displacement (D-) loop (Fish et al., 2004Clayton, 1996) is not the same as bacterial DNA replication.
Double Membrane
It is frequently asserted that the double membrane of mitochondria provides evidence for its endosymbiotic origin. There are, however, important differences between bacterial and mitochondrial membranes. Albert de Roos observes,


The bacterial membrane is one of the basic characteristics that distinguish bacteria from eukaryotes, see some examples here. In order for mitochondria to resemble bacterial membranes, they should share characteristics such as a cell wall with peptidoglycan and lipopolysaccharides, gram-staining and antibiotic sensitivity. Some effects of antibiotics have been seen with both bacteria and mitochondria, but the effect is minor while the use of antibiotics is based on the principle that they distinguish between bacteria and eukarytes, including the mitochondrion (here). Until then, the selection of a few apparent similarities while ignoring the many differences does not indicate a bacterial origin for mitochondria. On the contrary, the fact that their membranes are so different as well as the fact that nearly all genes are encoded by the nucleus is primarily evidence against a bacterial origin.
Even though some shared characteristics may be found, we have to realize that bacterial and eukaryotic membranes are fundamentally different. It seems virtually impossible to change all fundamental bacterial membrane characteristics and replace them with a eukaryotic counterpart without loosing membrane integrity. The differences between the membranes of mitochondria and the cell walls of bacteria make the endosymbiotic theory mechanistically difficult. It seems quite clear that bacterial membranes do not change easily into other membranes, and frankly I don't see any scenarios in which to change all these membrane components without drastically affecting fitness.

The Size and Shape of Mitochondria
The argument based on the size and shape of mitochondria is one that has been turned on its head in recent years, being transformed from an argument forendosymbiosis to one against it. These organelles are now acknowledged in the literature to be better understood as dynamic reticular structures (see this linkfor references).
Electron micrographs displaying cross-sections of mitochondria portrayed the mitochondrion as a sphere. However, when one looks at 3D models of the organelle, the reality is somewhat different. You can take a look at some of these images by going hereherehere, or here.
The Lack of a Mechanism
By far the most potent challenge to the endosymbiotic origin of eukaryotic mitochondria is the lack of a viable mechanism, perhaps most particularly with respect to the transfer of genes from the mitochondrion to the nucleus.
For one thing, there are the variants on the conventional genetic code. This means that, over the course of their transfer to the nucleus, the genes would need to be "recoded" so as to comply with the conventional genetic code. For example, recognizing UGA as a stop codon instead of the codon for Tryptophan(or vice versa) would cause cellular mayhem.
Secondly, mitochondrial proteins made at the ribosomes in the eukaryote cytoplasm need to be identified as such to ensure that they are properly dispatched (this is normally done by attaching a "label" in the form of an extra length of polypeptide to the protein). This would require a coincidental modification of the correct structural gene (which seems unlikely). Biologist Timothy G. Standish [url=http://www.google.co.uk/url?sa=t&rct=j&q=if genes were to move from the mitochondria to the nucleus they would have to somehow pick up the leader sequences necessary to signal for transport before they could be]notes[/url],



  • If genes were to move from the mitochondria to the nucleus they would have to somehow pick up the leader sequences necessary to signal for transport before they could be functional.


  • While leader sequences seem to have meaningful portions on them, according to Lewin (1997, p251) sequence homology between different sequences is not evident, thus there could be no standard sequence that was tacked on as genes were moved from mitochondria to nucleus.


  • Alternatively, if genes for mitochondrial proteins existed in the nucleus prior to loss of genes in the mitochondria, the problem remains, where did the signal sequences come from? And where did the mechanism to move proteins with signal sequences on them come from?



Albert de Roos explains,


All evolutionary theories must offer an explanation in mechanistic terms of how it should or could have happened in order to be tested. The difficult thing with the endosymbiotic theory is that it proposes no real mechanism and most textbooks show the simplistic picture of a cell that swallows another cell that becomes a mitochondrion. Unfortunately, it is not so simple as that. There is a difference between the process of endosymbiosis and its incorporation in the germline, necessitating genetic changes. What were those changes? What was the host? Was it a fusion, was it engulfment, how did the mitochondrion get its second membrane, how did two genomes in one cell integrate and coordinate? The theory is also strongly teleological, illustrated by the widely used term 'enslavement'. But how do you enslave another cell, how do you replace its proteins and genes without affecting existing functions? The existence of obligate bacterial endosymbionts in some present eukaryotes is often presented as a substitute for a mechanism, but they remain bacteria and give not rise to new organelles. So, before we can speak of the endosymbiotic as a testable scientific theory, we need a mechanistic scenario which is lacking at the moment.
When we do try to envision a mechanistic scenario based on the endosymbiotic theory, we quickly run into problems. Genetic mutations that allow bacteria to thrive in the cytoplasm would not be strategic for survival. Anaerobic cells normally do not survive in environment that contains oxygen, while the endosymbiont would need oxygen in order to present fitness advantage. The two organisms would initially compete for energy sources since bacteria are users of ATP and do not export it. The extensive gene transfer that is needed in the endosymbiotic theory would wreak havoc in a complex genome since frequent insertion of random pieces of mitochondrial DNA would disrupt existing functions. Furthermore, gene transfer is a multi-step process were genes need to be moved to the nucleus, the different genetic code of mitochondria needs to be circumvented, the genes need to be expressed correctly, as well as imported back into the mitochondria in order to be functional. All in all, mechanistic scenarios for the endosymbiotic theory imply many non-functional intermediates or would just be plain harmful to an organism. Therefore, the endosymbiotic theory is in contrast with the concept of gradualism that forms the basis of modern evolutionary theory.


Furthermore, this gene transfer must have taken place at a time extremely early in the history of eukaryotes, substantially reducing the window of time in which gene transfer could have occurred.
Summary and Conclusion
While we find examples of similarity between eukaryotic mitochondria and bacterial cells, other cases also reveal stark differences. In addition, the sheer lack of a mechanistic basis for mitochondrial endosymbiotic assimilation ought to -- at the very least -- give us reason for caution and the expectation of some fairly spectacular evidence for the claim being made. At present, however, such evidence does not exist -- and justifiably gives one cause for skepticism.

Graham JonesSaturday:
I read Nick Lanes's The Vital Question, and there's something that puzzles me, which relates to this article: The energetics of genome complexity, Nick Lane & William Martin, 2010. (http://www.nature.com/nature/journal/v467/n7318/abs/nature09486.html)

They do a back-of-the-envelope calculation. Prokaryotes metabolise about 3x faster than eukaryotes in terms of watts/g, but eukaryotic cells are 15,000x bigger, so eukaryotic cells have 5000x times as much power in terms of watts/cell. Eukaryotes have 4x as many genes as prokaryotes, so they have 1200x as much power per gene.

About 80% of a cell's power is used for making proteins, so it seems eukaryotes make about 1200x as much protein per gene. I started wondering about the mechanics of that. Transcription rates and translation rates per nucleotide are at least as fast in prokaryotes, and there's no introns to transcribe or splice out, so you'd think prokaryotes would make more protein per gene, not 1200x less.

Eukaryotic cells cells live longer of course, and most are diploid, so have two copies of each gene. Some are polyploid or multinucleated - and I think Lane and Martin's "15,000x bigger" includes some eukaryotic cells with lots of nuclei. A fair comparison would be of (rate of protein synthesis)/(gene copy).

So I got some numbers, from the book Cell Biology by the Numbers, and the biomumbers site (http://bionumbers.hms.harvard.edu/). I found it easiest to get figures for cell volumes. I assume (protein weight)/volume is similar for these cells. They are for organisms when they are growing fast (but not as fast as possible). V = volume in um^3 per gene copy per hour.

E Coli: volume 0.7 um^3, #gene copies 4400, doubling time 1h. V = 1.6e-4
Budding yeast: volume 37 um^3, #gene copies 6000, doubling time 3h. V = 20e-4
C Elegans: volume 1800 um^3, #gene copies 40000, doubling time 10h. V = 45e-4
Euglena gracilis: volume 3700 um^3, #gene copies 60000, doubling time 12h. V = 50e-4

It seems that these eukaryotic cells make protein 10-30x faster than E Coli, per gene copy. Looks very odd to me. Presumably the limiting factor for prokaryotes is power, as Lane and Martin suggest. Apparently prokaryotes have the molecular machinery to make protien faster than eukaryotes, but they hardly ever have enough energy to run the machinery anywhere near full speed.


1) https://en.wikipedia.org/wiki/Pre-replication_complex
2) http://nar.oxfordjournals.org/content/27/17/3389.full
3) http://www.answersingenesis.org/articles/2006/10/11/endosymbiotic-theory
4) http://www.evolutionnews.org/2012/01/on_the_origin_o054891.html
5) https://en.wikipedia.org/wiki/Telomerase
6) Intracellular Calcium, page 578



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PROTEIN IMPORT INTO CHLOROPLASTS



Endosymbiosis was accompanied by massive gene transfer from the endosymbiont to the host nucleus.

Begging the question at its best........

However, before genes could be eliminated from the endosymbiont genome, a system to import the now nuclear-encoded gene products into the new organelle had to be established. Although the endosymbiotic bacterium had several systems to export (or secrete) proteins across the membranes, the organelle now had to import proteins (see figure above).

Most striking is the homology of the translocon of the outer-chloroplast-envelope subunit TOC75 to bacterial outer-membrane proteins that are involved in the transport
of polypeptides across the outer membrane of Gram-negative bacteria95,96.This conserved β-barrel, bacterial-type channel now forms the outer-chloroplast-envelope import channel. The TOC75 homologue in cyanobacteria, SynToc75 seems to be indispensable for growth67,68. A β-barrel ion channel has, in most cases, no strong preference for the direction of ion permeation and therefore represents an ideal starting point to build a translocon.

Subunits that convey the specificity and directionality of transport are eukaryotic additions, for example, the TOC34 receptor and the TOC159 motor.

But, what formed the translocon of the inner chloroplast envelope (TIC)? There is no detectable homologue for the putative TIC110 channel, and the putative second channel
subunit TIC20 shows only a low homology to bacterial proteins.


The homology is most striking, except when it isnt..... and when it isnt, its time to make things up, and just assert that the subunits were  " eukaryotic additions ". Homology can well be explained through common design. Thats common practice. Examples which seem to fit evolutionary assumptions are  cited, while the  examples that do not fit are ignored, or baseless assertions are made, as above shows.

The many similarities that exist among members of the animal kingdom is the result of the fact that a single designer created the basic kinds of living 'systems', then specially modified each type of life to enable it to survive in its unique environmental niche.

Structural similarities among automobiles, however, even similarities between older and newer models  are due to construction according to pre-existing patterns, i.e., to design. Ironically, even striking similarities are not sufficient to exclude design-based explanations. In order to demonstrate naturalistic evolution, it is necessary to show that the mechanism by which organisms are constructed (unlike the mechanism by which automobiles are constructed) does not involve design.


Maybe the early endosymbiont continued to use bacterial export systems in reverse, such as the secretory pathway (SEC), the twin-arginine translocon (TAT) system or the albino3 (ALB3) homologue YIDC8,10.Therefore, the TIC translocon — including the adaptation of chaperones in the stroma to provide the driving force for import — could have been an invention of the endosymbiont

Its remarkable how proponents of evolution frequently borrow a vocabulary from where they are not aloud to. Evolution has no intelligence to invent things.....

Molecular Cell biology, Lodish, 5th edition, pg. 691

At least three chloroplast outer-membrane proteins, including a receptor that binds the stromal-import sequence and a translocation channel protein, and five inner-membrane proteins are known to be essential for directing proteins to the stroma. Although these proteins are functionally analogous to the receptor and channel proteins in the mitochondrial membrane, they are not structurally homologous.The lack of homology between these chloroplast and mitochondrial proteins suggests that they may have arisen independently


Or they were designed.......

1) file:///E:/Desktop/apdf%20files/protein%20import%20of%20chloroplasts.pdf



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3 At the Dawn of Life, a Mystery on Thu Oct 01, 2015 4:37 pm

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Did DNA replication evolve twice independently? 1

DNA replication is central to all extant cellular organisms. There are substantial functional similarities between the bacterial and the archaeal/eukaryotic replication machineries, including but not limited to defined origins, replication bidirectionality, RNA primers and leading and lagging strand synthesis. However, several core components of the bacterial replication machinery are unrelated or only distantly related to the functionally equivalent components of the archaeal/eukaryotic replication apparatus.
Consequently, the modern-type system for double-stranded DNA replication likely evolved independently in the bacterial and archaeal/eukaryotic lineages.

This should be one more reason to doubt of the endosymbiotic theory

At the Dawn of Life, a Mystery 2

Stories exist for how mitochondria and chloroplasts came to be present in eukaryotic cells -- they mainly involve the incorporation of ancient bacteria into the incipient eukaryotic cell. The proposed process has been given the name endosymbiosis. There is no single proposed mechanism for the evolution of the nucleus or the other structures I have named. I deliberately call such evolutionary accounts "stories." To become a eukaryote like C. reinhardtii involves enormous changes in cell organization that affect every aspect of cellular life. Most of these structures are common to eukaryotic cells, and most are membrane-bound. Membranes mean there must be transport mechanisms in or out of each compartment. DNA replication and division becomes more complicated because the nuclear membrane must break down and reform at each division. Nuclear genes have somehow come to specify proteins necessary for mitochondrial function; they must be transcribed, the RNA exported to the cytoplasm, made into protein, and then the proteins must be transported into the mitochondrion. Specific problems associated with the replication of chromosomes versus circular DNA as in bacteria have to solved. There are more differences to be dealt with than I can cover -- exons and introns, and the separation of mRNA production in the nucleus from protein synthesis in the cytoplasm, just to name two. All of these problems must be solved somehow if the story of undirected evolution is true.

The PsbO protein is common among all oxygenic photosynthetic organisms, but the number of copies associated with each PSII complex differs between plants and cyanobacteria. The PsbR protein is unique to plants. Both plants and cyanobacteria contain the PsbP and PsbQ proteins, but their roles and modes of association with PSII complexes differ significantly between the two systems.

Co-evolution of primordial membranes and membrane proteins

The chemical compositions and biogenesis pathways of archaeal and bacterial membranes are fundamentally different [4,5,12].The glycerol moieties of the membrane phospholipids in all archaea and bacteria are of the opposite chiralities. With a few exceptions, the hydrophobic chains differ as well, being based on fatty acids in bacteria and on isoprenoids in archaea; furthermore, in bacterial lipids, the hydrophobic tails are usually linked to the glycerol moiety by ester bonds whereas archaeal lipids contain ether bonds [4,5,12]. The difference extends beyond the chemical structures of the phospholipids, to the evolutionary provenance of the enzymes involved in membrane biogenesis that are either non-homologous or distantly related but not orthologous in bacteria and archaea [4,5,12,13]. 



1) http://nar.oxfordjournals.org/content/27/17/3389.full
2) http://www.evolutionnews.org/2015/05/at_the_dawn_of095801.html
3) http://newunderthesunblog.wordpress.com/my-research/
4) Co-evolution of primordial membranes and membrane proteins



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4 Re: Challenges to Endosymbiotic Theory on Sun Feb 07, 2016 1:18 pm

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http://reasonandscience.heavenforum.org/t2277-the-different-genetic-codes

if the mitochondria in invertebrates use a different genetic code from the mitochondria in vertebrates, and both of those codes are different from the “universal” genetic code, what does that tell us? It means that the eukaryotic cells that eventually evolved into invertebrates must have formed when a cell that used the “universal” code engulfed a cell that used a different code. However, the eukaryotic cells that eventually evolved into vertebrates must have formed when a cell that used the “universal” code engulfed a cell that used yet another different code. As a result, invertebrates must have evolved from one line of eukaryotic cells, while vertebrates must have evolved from a completely separate line of eukaryotic cells. But this isn’t possible, since evolution depends on vertebrates evolving from invertebrates.
Now, of course, this serious problem can be solved by assuming that while invertebrates evolved into vertebrates, their mitochondria also evolved to use a different genetic code. However, I am not really sure how that would be possible. After all, the invertebrates spent millions of years evolving, and through all those years, their mitochondrial DNA was set up based on one code. How could the code change without destroying the function of the mitochondria? At minimum, this adds another task to the long, long list of unfinished tasks necessary to explain how evolution could possibly work. Along with explaining how nuclear DNA can evolve to produce the new structures needed to change invertebrates into vertebrates, proponents of evolution must also explain how, at the same time, mitochondria can evolve to use a different genetic code!


  In Current Biology,5 Paul Jarvis wrote about the “backchat” that goes on between chloroplasts and the nucleus in plant cells.  He assumed that chloroplasts evolved as once free-living cells that were engulfed by an ancestral prokaryote, and that their separate genomes were partitioned, most of the DNA going to the nucleus of the host.  Still, a remarkable degree of communication is required to ensure the proper amounts of chloroplast proteins are produced in the nucleus: “To ensure the correct, stoichiometric assembly of these complexes, and to enable their rapid reorganization in response to developmental or environmental cues, the activities of the nuclear and chloroplast genomes must be synchronized through intracellular signalling,” he said.  Each protein must then traverse the inner and outer membranes of the chloroplast, assisted by complexes of molecular machines.  Jarvis presented one example of the complexity involved in signalling:


A particularly nice example is provided by the plastid protein import 1 (ppi1) mutant, which lacks the chloroplast protein import receptor atToc33.  This is actually one of two similar receptors in Arabidopsis, the other being atToc34, which are thought to have distinct substrate preferences: atToc33 mediating the import of the highly abundant precursors of the photosynthetic apparatus, and atToc34 the import of‘housekeeping’ proteins (for example, components of the plastid’s genetic system, or enzymes of non-photosynthetic metabolism).  Remarkably, the ppi1 mutation triggers the specific down-regulation of photosynthesis-related genes (Figure 2), suggesting that retrograde signalling mechanisms exist to prevent the futile expression of proteins not able to reach their final, organellar destination.  Clearly, such exquisite regulation specificity could not be achieved were all plastid signalling pathways to converge and control gene expression through a common process.


He did not elaborate on how all this “organellar repartee” could have evolved, though.  He just ended on the note, “Observations such as these suggest that a great deal remains to be learnt concerning plastid-to-nucleus signalling.”


http://creationsafaris.com/crev200707.htm

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5 Re: Challenges to Endosymbiotic Theory on Sun Dec 18, 2016 3:50 am

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The origin of mitochondria in light of a fluid prokaryotic chromosome model

http://rsbl.royalsocietypublishing.org/content/3/2/180

On the basis of sequence similarity to α-proteobacterial homologues, it has been estimated that 630 eukaryotic genes trace to α-proteobacteria (Gabaldon & Huynen 2003). But there are thousands of eukaryotic nuclear genes that are clearly eubacterial, but not specifically α-proteobacterial, in terms of their patterns of sequence similarity (Esser et al. 2004Rivera & Lake 2004Embley & Martin 2006). Finding a eukaryotic gene that branches with a group other than α-proteobacteria is often taken as evidence for an origin from that group (for example, Baughn & Malamy 2002), the methodological problems of deep phylogenetic trees notwithstanding (Susko et al. 2006). But if we let go of the static prokaryotic chromosome model and assume a fluid chromosome model for prokaryotes, then the expected phylogeny for a gene acquired from the mitochondrion would be common ancestry for all eukaryotes, but not necessarily tracing to α-proteobacteria, because the ancestor of mitochondria possessed an as yet unknown collection of genes. A previous investigation of genome evolution in α-proteobacteria considered the genome size and functional classes (Boussau et al. 2004), but not sequence similarities. Hence, we wished to know how many of the α-proteobacterial genes pass the test of being α-proteobacterial by the nearest-neighbour criterion.
The answer, based upon the current sample, ranges from approximately 97% for Sinorhizobium to approximately 33% for Magnetococcus sp. The mitochondrial genomes studied (figure 1d) did not differ in terms of the nearest-neighbour composition from α-proteobacterial genomes.


An Overview of Endosymbiotic Models for the Origins of Eukaryotes, Their ATP-Producing Organelles (Mitochondria and Hydrogenosomes), and Their Heterotrophic Lifestyle

http://www.molevol.de/molevol2/publications/98.pdf

The evolutionary processes underlying the differentness of prokaryotic and eukaryotic cells and the origin of the latter’s organelles are still poorly understood. For about 100 years, the principle of endosymbiosis has figured into thoughts as to how these processes might have occurred. A number of models that have been discussed in the literature and that are designed to explain this difference are summarized. The evolutionary histories of the enzymes of anaerobic energy metabolism (oxygen-independent ATP synthesis) in
the three basic types of heterotrophic eukaryotes – those that lack organelles of ATP synthesis, those that possess mitochondria and those that possess hydrogenosomes
– play an important role in this issue. Traditional endosymbiotic models generally do not address the origin of the heterotrophic lifestyle and anaerobic energy metabolism in eukaryotes. Rather they take it as a given, a direct inheritance from the host that acquired mitochondria. Traditional models are contrasted to an alternative endosymbiotic model (the hydrogen hypothesis), which addresses the origin of heterotrophy and the origin of compartmentalized energy metabolism in eukaryotes

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6 Re: Challenges to Endosymbiotic Theory on Sun Feb 19, 2017 6:08 pm

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The evolution of cardiolipin biosynthesis and maturation pathways and its implications for the evolution of eukaryotes
Cardiolipin (CL) is an important component in mitochondrial inner and bacterial membranes. Its appearance in these two biomembranes has been considered as evidence of the endosymbiotic origin of mitochondria. But CL was reported to be synthesized through two distinct enzymes--CLS_cap and CLS_pld in eukaryotes and bacteria. Therefore, how the CL biosynthesis pathway evolved is an interesting question.



Its not just an interesting question. Its evidence against the endosymbiotic theory. 

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