The fingerprints of a mighty creator in Proteomics, impact factor >5

wardahanCreationism/intelligent design is not really an issue for me as I am a biologist working with mitochondria and stem cells, also a life extension supporter, whose angle on things and projections are based on the recent advancements in science and technology. As far as I know, creationism/ID neither suggests any new experiments or heuristic solutions in my research field, nor does it help to plan&build new technologies to extend healthy lifespan. From my point of view, thinking about creationism is a waste of valuable scientific/technological processor time.

But I am not used to encounter with explicit creationism and the fingerprints of a mighty creator as an explanatory force behind a natural phenomenon in scientific peer-review journals. That’s exactly what happened to me in a recent review published online by the Wiley journal, Proteomics (ISI Impact Factor 2006: 5.735) by Mohamad Warda and Jin Han, entitled Mitochondria, the missing link between body and soul: Proteomic prospective evidence.

Last week when I wrote the post Can you tell a good article from a bad based on the abstract and the title alone? on the review I had only 10 minutes for figuring out the post between 2 experiments in the lab during lunchtime. The only thing that came into my mind reading the abstract – popped out of PubMed feeds – was that something stinks here. Now it’s Mardi Gras day and I have a couple of minutes more to address this issue and hopefully no more.

Myrmecologist and blogger Alex Wild picked one sentence from the paper in a comment, and here is the complete paragraph:

Alternatively, instead of sinking in a swamp of endless debates about the evolution of mitochondria, it is better to come up with a unified assumption that all living cells undergo a certain degree of convergence or divergence to or from each other to meet their survival in specific habitats. Proteomics data greatly assist this realistic assumption that connects all kinds of life. More logically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life.

This is the closing paragraph of the section Mitochondrial integrated function disproves endosymbiotic hypothesis of mitochondrial evolution. The mitochondrial part of the well established evolutionary endosymbiotic theory claims that ATP-producing mitochondria were ancient prokariotic invaders of host prokariotic cells eventually turned out to be the common ancestors of eukaryotic cells. I always found this hypothesis one of the most fruitful scientific concepts as it constantly suggest new ideas and warns that current eukaryotic cells are the products of an evolutionary, accidental and instable alliance between the mitos and their hosts. As the endosymbiotic theory is the mainstream academic theory of mitochondrial evolution it is a challenge for scientists to attack it with counterarguments and that’s what Warda and Han are aiming for in that section. What they are doing seems like a legitimate discussion of a scientific theory but ends with the logically unacceptable jump to the fingerprints of a mighty creator as an alternative explanation.

Before I cite the section in question in full length and recommend to my readers to analyze it, I also like to suggest the detailed comment of D. Spencer saying amongst others:

If Wiley and the journal Proteomics allow this into print (it is currently only “published” online) they can kiss goodbye to any hope that Proteomics will ever again be regarded as a serious scientific publication.

Here is the complete section by Warda and Han without references that could be found in the full text:

Mitochondrial integrated function disproves endosymbiotic hypothesis of mitochondrial evolution.

Many debates concern the still-accepted endosymbiotic hypothesis of mitochondrial evolution [96–99]. The endo-
symbiont hypothesis can be traced back more than 100 years [100]. The hypothesis was then resurrected and modernized into serial endosymbiosis theory (SET) [101].

By favoring the origin of mitochondria to be direct descendants of a bacterial endosymbiont, the classical SET proposes that an amitochondriate but otherwise eukaryotic host cell acquired an endosymbiotic bacterium that was subsequently converted into the mitochondrion [102–105]. The proof of SET was based on the parallel connection between plant mitochondrial and phage T4 genome replication [107, 108], together with other phylogenic and evolutionary data pointing to an ancient alpha-proteobacterium, most likely an ancestor of the Rickettsiales, and had established a symbiotic relationship inside a primitive eukaryotic cell circa two billion years ago [102, 109, 110]. Surprisingly, to date there is no supportive evidence demonstrating the presence of the proposed intermediate model that links mitochondria and their alpha-proteobacteria ancestors in the frame of a basic concept of natural variation and selection with dynamic evolutionary ability toward possible future transformation [111]. Additionally, current evidence of the presence of relicts of mitochondria within certain organisms that lack these organelles reflects the elastic adaptive ability of mitochondria to cope with microaerophilic or anaerobic environments among the species, rather than imposing their origination from bacterial descent as suggested by others [112]. Furthermore, recent advances in the fields of proteomics and comparative genomics give us a clear picture of the processes that shape the mitochondrial proteome among different species, ranging from the lower species to eukaryotic mitochondria with diverse environments and cellular functions. The SET, however, is currently unable to afford reasonable interpretation for such data. Since mitochondria are highly specialized organelles that adaptively respond to metabolic and homeostatic roles at different organization levels among species, a desired adaptation should consequently meet with dramatic changes on the genetic level, which would obviously end up with major proteome remodeling towards eukaryotes [113]. In fact, with the exception of the evolutionary source of the mitochondrial genome itself, the credibility of SET, as an explanation of how the mitochondrion originated, is today considerably less certain than it appeared to be a decade ago. Therefore, the debates concerning the mitochondrial endosymbiotic hypothesis recently terminated with many questions still left unanswered [111].
It is worthy to address here many recent affirmative genomics and proteomics data less appreciate the SET theory of mitochondrial evolution. The vast majority of mitochondrial imported proteins (about 900 vs. only 37 genes of the mtDNA genome) are fairly encoded by the nuclear genome [105] and more importantly, over 90% of the initial bacterial gene complement does not match with that of mtDNA. Almost 15% of nuclear-encoded mitochondrial proteins are synthesized in the cytoplasm and subsequently imported into the organelle. On the transcription level, yeast Rpo41 has a coordinated control of nuclear and mitochondrial transcription and there is a direct correlation between in vivo changes in mitochondrial transcript abundance and in vitro sensitivity of mitochondrial promoters to ATP concentration [114]. Concerning the mitochondrial synthesis machinery, all mitoribosomal proteins, aminoacyl-tRNA ligases, translation factors, and chaperones are nuclear encoded [115]. The process of protein importation to mitochondria is another challenge carried out by a complex N-terminal signal-directed machinery of proteins located in the inner and outer membranes of the mitochondria [116]. With the aid of ATP and the membrane potential energizing facilities, the synthesized proteins were recognized by mitochondrial surface receptors, where the outer and inner membrane translocases mediate the import and intramitochondrial sorting. The TOM protein complex transfers the proteins across the outer membrane, the TIM23 protein complex imports them into the matrix, the TIM22 complex integrates proteins destined for the inner membrane, and the two complexes TIM9/10 and TIM8/13 guide the precursor proteins from TOM to TIM22 [117]. None of these complexes has any recognizable bacterial homologue [118]. Most of the mitochondrial proteins, therefore, are encoded by nuclear genes, synthesized in the cytoplasm and subsequently imported into the organelles via complex machinery. This is not the case with ancient endosymbiont that was autonomous in protein synthesis, with no sophisticated system for the import of proteins synthesized in the cytosol. According to SET, such a system is a prerequisite not only for the escape from mitochondria to the nuclear genes, whose products should be targeted back, but also for the recruitment of proteins of different origin to the organelle. This is another crucial point of critique against the credibility of the SET theory of evolution. Beyond this hypothesis, the relationship between mitochondria and the cell, however, is more likely as a built-in integrated circuit demonstrated by cytochrome c as double agent being a partner of respiratory machinery during life and the initiator of apoptotic cascades at the end. This is more conclusive evidence of the indispensable role of mitochondria from the start to the end.
Alternatively, instead of sinking in a swamp of endless debates about the evolution of mitochondria, it is better to come up with a unified assumption that all living cells undergo a certain degree of convergence or divergence to or from each other to meet their survival in specific habitats. Proteomics data greatly assist this realistic assumption that connects all kinds of life. More logically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life.

References:

[96] Esser, C., Ahmadinejad, N., Wiegand, C., Rotte, C. et al., A genome phylogeny for mitochondria among alpha-proteobacteria and a predominantly eubacterial ancestry of yeast nuclear genes. Mol. Biol. Evol. 2004, 21, 1643–1660.
[97] Burger, G., Gray, M. W., Lang, B. F., Mitochondrial genomes: anything goes. Trends Genet. 2003, 19, 709–716.
[98] Timmis, J. N., Ayliffe, M.A., Huang, C. Y., Martin, W., Endosymbiotic gene transfer: organelle genomes forge eukaryotic chromosomes. Nat. Rev. Genet. 2004, 5, 123–135.
[99] Nosek, J., Tomaska, L., Mitochondrial genome diversity: evolution of the molecular architecture and replication strategy. Curr. Genet. 2003, 44, 73–84.
[100] Schimper, A. F. W., Uber die Entwicklung der Chlorophyllkorner und Farbkorner. Bot. Z. 1883, 41, 105–114.
[101] Taylor, F. J. R., Implications and extensions of the Serial Endosymbiosis Theory of the origin of eukaryotes. Taxon 1974, 23, 229–258.
[102] Gray, M. W., Burger, G., Lang, B. F., Mitochondrial evolution. Science 1999, 283, 1476–1481.
[103] Gray, H. L., Sorensen, E. L., Hunt, J. S., Ober, C., The origin and early evolution of mitochondria. Genes Immun. 2001, 2, 469–470.
[104] Gabaldon, T., Huynen, M. A., Shaping the mitochondrial proteome. Biochim. Biophys. Acta. 2004, 1659, 212–220.
[105] Wallace, D. C., A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine. Annu. Rev. Genet. 2005, 39, 359–407.
[107] Oldenburg, D.J., Bendich, A.J., Mitochondrial DNA from the liverwort Marchantia polymorpha: circularly permuted linear molecules, head-to-tail concatemers, and a 50 protein. J. Mol. Biol. 2001, 310, 549–562.
[108] Oldenburg, D. J., Bendich, A. J., Changes in the structure of DNA molecules and the amount of DNA per plastid during chloroplast development in maize. J. Mol. Biol. 2004, 344, 1311–1330.
[109] Hedges, S. B., Blair, J.E., Venturi, M. L., Shoe, J. L., A molecular time scale of eukaryote evolution and the rise of complex multicellular life BMC. Evol. Biol. 2004, 4, 2.
[110] Yang, D., Oyaizu, Y., Oyaizu, H., Olsen, G.J. et al., Mitochondrial origins. Proc. Natl. Acad. Sci. USA 1985, 82,
4443–4447.
[111] Gray, P. M., Parks, G. D., Alexander-Miller, M. A., Modulation of CD81 T cell avidity by increasing the turnover of viral antigen during infection. Cell. Immunol. 2004, 231, 14–19.
[112] Voncken, F., Boxma, B., Tjaden, J., Akhmanova, A. et al.,Multiple origins of hydrogenosomes: functional and phylogenetic evidence from the ADP/ATP carrier of the anaerobic chytrid. Mol. Microbiol. 2002, 44, 1441–1454.
[113] Gabaldo’n, T., Huynen, M. A., Reconstruction of the protomitochondrial metabolism. Science 2003, 301, 609.
[114] Amiott, E. A., Jaehning, J. A., Mitochondrial transcription is regulated via an ATP ‘sensing’ mechanism that couples RNA abundance to respiration. Mol. Cell 2006, 22, 329–338. 279, 14473–14476.
[117] Koehler, C., Protein translocation pathways of the mitochondrion. FEBS Lett. 2000, 476, 27–31.
[118] Karlberg, O., Canbaeck, B., Kurland, C. G., Andersson, S. G. E., The dual origin of the yeast mitochondrial proteome. Yeast Comp. Funct. Genom. 2000, 17, 170–187.

Update: PZ Myers’ post A baffling failure of peer review asks the real question: What happened in the peer review of this paper?

I’ve also sent emails with links to Michael Dunn, Editor-in-Chief of Proteomics and to the co-authors of the paper (Mohamad Warda and Jin Han).

3 thoughts on “The fingerprints of a mighty creator in Proteomics, impact factor >5

  1. Attila,

    You are entirely correct: thinking about creationism is a waste of valuable scientific/technological processor time.

    Now get your butt off the computer, put the cells back in the incubator and go Mardi Gras! It may be your last chance in a long time! It is not worth it!

  2. Attila,

    you are entirely wrong: thinking about creationism is a waste of valuable scientific/technological processor time.

    Now, stop looking at “evidence” and go find some FACT. You can disprove evolutionary thinking, but you can’t disprove the bible, too much FACT.

    Evolutionists can only make hypotheses.

    Creationists can make conclusions, because we are based on FACT.

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