Endosymbiont theory wrong?

This paper really doesn't challenge endosybiosis at all it says that these parasites did't diverge from other eukaryotes before the gain of mitochondria. In fact it makes sense that a parasite that gets all of its energy from its host would have smaller or vestigial mitochondria. There is alot of evidence in favour of the bacterial origin of chloroplasts and mitochondria such as their own circular DNA, bacterial ribosomes, the phylogenetic analysis of many proteins and the recent discovery of bacteria living inside other bacteria.here is the full reference and abstract:Nature 2002 Aug 22;418(6900):865-9
A mitochondrial remnant in the microsporidian Trachipleistophora hominis.
Williams BA, Hirt RP, Lucocq JM, Embley TM.Microsporidia are obligate intracellular parasites of several eukaryotes. They have a highly complex and unique infection apparatus but otherwise appear structurally simple. Microsporidia are thought to lack typical eukaryotic organelles, such as mitochondria and peroxisomes. This has been interpreted as support for the hypothesis that these peculiar eukaryotes diverged before the mitochondrial endosymbiosis, which would make them one of the earliest offshoots in eukaryotic evolution. But microsporidial nuclear genes that encode orthologues of typical mitochondrial heatshock Hsp70 proteins have been detected, which provides evidence for secondary loss of the organelle or endosymbiont. In addition, gene trees and more sophisticated phylogenetic analyses have recovered microsporidia as the relatives of fungi, rather than as basal eukaryotes. Here we show that a highly specific antibody raised against a Trachipleistophora hominis Hsp70 protein detects the presence, under light and electron microscopy, of numerous tiny ( approximately 50 x 90 nm) organelles with double membranes in this human microsporidial parasite. The finding of relictual mitochondria in microsporidia provides further evidence of the reluctance of eukaryotes to lose the mitochondrial organelle, even when its canonical function of aerobic respiration has been apparently lost.

Evolution is falsifiable, for example if new species couldn't form or new genes hadn't been seen to be created by natural processes it would be impossible for evolution to occur. Ayway i thought we were talking about endosymbiosis."If it demonstrates anything it is de-evolution.
By the way, there are no such thing as vestiges. That is 19th century blahblah."evolution is not necessarily an increase in complexity, greater efficiency is also important and this includes the loss of unecessary parts and even evolving towards inevitable extinction (for example adapting to a short lived ecological niche). How would you describe the smaller remains of an organelle that has lost most of its original function apart from relics or vestiges. Degeneration of genes and structures in parasites and symbionts has been demonstrated many times.The research is nothing new it just confirms earlier work (Hirt RP, Healy B, Vossbrinck CR, Canning EU, Embley TM. A mitochondrial Hsp70 orthologue in Vairimorpha necatrix: molecular evidence that microsporidia once contained mitochondria. Curr Biol. 1997 Dec 1;7(12):995-8.PMID: 9382838)ok lets discuss all the evidence in favour of this 'fairytale'.
Here is just some of it:Both mitochondria and chloroplasts have their own genome and it resembles that of prokaryotes not that of the nuclear genome.Both genomes consist of a single circular molecule of DNA.
There are no histones associated with the DNA.The mitochondrial genome contains type II introns which have similarities to those found in bacterial but not eukaryotic genomes. This was used by answers in genesis as evidence against the bacterial origin of mitochondria!
( http://www.answersingenesis.org/docs2/4341_endosymbiont.asp ).Both mitochondria and chloroplasts have their own protein-synthesizing machinery, and it resembles that of prokaryotes not that found in the cytoplasm of eukaryotes.
Their ribosomal RNA (rRNA) and the structure of their ribosomes resemble those of prokaryotes, not eukaryotes.The first amino acid of their transcripts is always fMet as it is in bacteria (not methionine [Met] that is the first amino acid in eukaryotic proteins).A number of antibiotics (e.g., streptomycin) that act by blocking protein synthesis in bacteria also block protein synthesis within mitochondria and chloroplasts. They do not interfere with protein synthesis in the cytoplasm of the eukaryotes.
Conversely, inhibitors (e.g., diphtheria toxin) of protein synthesis by eukaryotic ribosomes do not - sensibly enough - have any effect on bacterial protein synthesis nor on protein synthesis within mitochondria and chloroplasts.The antibiotic rifampicin, which inhibits the RNA polymerase of bacteria, also inhibits the RNA polymerase within mitochondria. It has no such effect on the RNA polymerase within the eukaryotic nucleus.it is even possible to identify the type of bacteria that was the likely ancestor of mitochondria, the most similar today being the alpha-probacteria Rickettsia. This is due to the similarities of the genes for proteins such as cytochrome b and cytochrome c oxidase and ATP production in Rickettsia is the same as that in mitochondria. Hsp60 homologues from alpha-purple bacteria (such as Rickettsia) and mitochondria contain unique sequences that are not found in other prokaryotes. Rickettsia also have a carrier-mediated transport system which allows specific transport of ADP and ATP. The ATP/ADP translocases are homologous between mitochondria and Rickettsia. Its clear from many differnt pieces of evidence that mitochondria and Rickettsia have a commmon ancestor.The fact that no bacteria were thought to live inside other bacteria was interpreted as evidence against endosymbiosis, but the discovery of secondary endosybitic bacteria within bacteria found inside mealybugs (Pseudococcidae) proves this not to be the case. These endosybionts were found to have a double membrane surrounding them like mitochondria do.There is dispute about the details and timing of the various events of endosymbiosis but the theory has been proved to be correct even though most biologists were sceptical at first when it was proposed in its modern form by Dr Lynn Margulis.from this and other evidence i believe the endosybiosis to be a fact. as Stephen Jay Gould put it "In science "fact" can only mean "confirmed to such a degree that it would be perverse to withhold provisional consent.""shortened reference list:The ncbi human mitochondria page:
http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/framik?db=Geno...type II introns:
http://www.fp.ucalgary.ca/group2introns/wherefound.htmMealybug [beta]-proteobacterial endosymbionts contain [gamma]-proteobacterial
symbionts. von Dohlen, Carol D.; Kohler, Shawn*; Alsop, Skylar T.; McManus, William R.
Nature Volume 412(6845) 26 July 2001 pp 433-436.Evolutionary relationship of Rickettsiae and mitochondria
Victor V. Emelyanov. FEBS Letters 501 (2001) 11-18.Degenerative Minimalism in the Genome of a Psyllid Endosymbiont
MARTA A. CLARK,1 LINDA BAUMANN,1 MYLO LY THAO,1 NANCY A. MORAN,2
AND PAUL BAUMANN. JOURNAL OF BACTERIOLOGY, Mar. 2001, p. 1853—1861.Origin and Evolution of the Mitochondrial Proteome. C. G. KURLAND1,2* AND S. G. E. ANDERSSON. MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS,Dec. 2000, p. 786—820 Vol. 64, No. 4The genome sequence of Rickettsia prowazekii and the origin of mitochondria
Siv G. E. Andersson*, Alireza Zomorodipour*, Jan O. Andersson*, Thomas Sicheritz-Ponte n*, U. Cecilia M. Alsmark*, Raf M. Podowski*, A. Kristina Na slund*, Ann-Soe Eriksson*, Herbert H. Winkler & Charles G. Kurland. NATURE |VOL 396 | 12 NOVEMBER 1998 .

mark24
feel free to plagiarise me although you should probably also credit: http://users.rcn.com/...et/BiologyPages/E/Endosymbiosis.html who i forgot to mention in my original post.This page is critical of endosymbiosis although not from a creationist perspective: http://www.gwu.edu/...win/BiSc151/Eukaryotes/Eukaryotes.html
if anyone knows any other sites or articles that have criticisms of endosymbiosis i would be interested in reading them.

Hi Peter B,Your objection is interesting but i have already answered it in a previous post:"The fact that no bacteria were thought to live inside other bacteria was interpreted as evidence against endosymbiosis, but the discovery of secondary endosybitic bacteria within bacteria found inside mealybugs (Pseudococcidae) proves this not to be the case. These endosybionts were found to have a double membrane surrounding them like mitochondria do."Bacteria live inside other bacteria, fact. So endocytosis must have happened, therefore your idea that microtublules are necessary for endocytosis just plain isn't true.Reference:
Mealybug [beta]-proteobacterial endosymbionts contain [gamma]-proteobacterial
symbionts. von Dohlen, Carol D.; Kohler, Shawn*; Alsop, Skylar T.; McManus, William R.
Nature Volume 412(6845) 26 July 2001 pp 433-436.

I did a bit of reading on the bacterial cytoskeleton and ended up finding out more interesting things about mitochondria. Bacteria do have a gene (FtsZ) that is similar to tubulin (the monomer that makes up microtubes) and so there was presumably a form of it in the universal common ancestor. This indicates that the eukaryotic ancestor could have had microtubules before endosymbiosis occured. The difference in much of the cellular machinery of mitochondria/bacteria and eukaryotes indicates they diverged substantially before endosymbiosis. Although this is just speculations since microtubules are irrelevant to endosymbiosis it doesn't really matter in this context.The interesting thing about some mitochondria and all chloroplasts is that they use the products of bacterial FtsZ genes (most closely related to alpha-proteobacterial genes yet again) to divide. FtsZ has been lost in fungi animal and plant mitochondria in which division is mediated by dynamin a protein of eukaryotic origin but if FtsZ genes from mitochondria are put into organisms from which it has been lost the product interacts usefully with the mitochondria. Dynamin does seem to play a part in the division of intracellular parasitic bacteria such as Chlamydia that lack FtsZ.Thanks peter B. without your post i wouldn't have looked into this area and found yet more compelling evidence in favour of endosymbiosis.

Ok i am prepared to conceed that it might be impossible for a bacteria to be engulfed by another one outside of a eukaryotic host but until all the questions about the mechanisms of secondary endosymbiosis have been answered and hopefully more examples discovered will be found the possiblilty remains that i am wrong. But at the moment even though we don't know everything i would say it's evidence that is in favour of my point of view rather than your's peter B.The point that the organism that evolutionists think engulfed the pre-mitochondrial bacteria was not a modern bacterium and therfore almost certainly had at least a proto cytoskeleton (the fact it is present in a similar form in all eukaryotes suggests this is true) is still valid. If Peter B. can provide evidence in favour of the hypothesis that ancient eukaryotic cells did not have a microtubule cytoskeleton then wheather or not bacteria can engulf on another IS irrelevant. If the ancestor of eukayotes at the proposed time of endosymbiosis had a rigid membrane like modern bacteria then the issue of bacterial endosybiosis would without question be relevant.Although the gene complement of mitochondria is very similar amoungst metazoans its not necessarily a result of a non random mechanism. There are examples of genes such as FtsZ that have been lost in some lineages but retained in others (the fact that FtsZ product interacts with mitochondria that have lost it is highly suggestive that they once had it). To determine if the process of gene transfer is random or not it would be best to look at plastids where several different endosymbiotic events are thought to have taken place and see if the process has transfer has proceeded along different lines. Also the genes contained within mitochondria are the most essential for respiration and maintainance of the mitochondria so those are the genes you would expect to find due to natural selection. There are probably a limited number of solutions to the problem 'what is the minimal mitochondrial genome ?', therefore a limited number of possible outcomes. The hypothesis advanced by evolutionists is that the major genetic changes happened very rapidly and early in eukaryotic evolution and once a small and fairly stable genome had been formed there was no reason for it to change alot. Also research on Buchnera aphidicola, the obligate endosymbionts of aphids has revealed that once an organism has lost phages repeated elements and the RecA systems the genome becomes extremely stable at least with respect to rearrangements (not gene inactivation, loss and sequence evolution though). Even if it could be demonstrated that the genome of mitochondria is the result of directed non random change, how they got there in the first place would still be a mystery and enosymbiosis the most likely explanation.Peter B. you say: "Loss of genes sounds familiar."i am not sure what point you making but yes loss of genes has been demonstrated many times in intracellular, endosymbiotic and parasitic organisms, organisms in a similar situation to the ancestor of mitochondria. But it doesn't challenge the main point of the paragraph that mitochondrial FtsZ proteins are very similar to alpha-probacterial bacteria believed to be closely related to the ancestors of mitochondria and therefore common ancestory is the most likely explanation.There are still many questions that havn't been answered by the critics of endosymbiosis which basically can be summarised as 'if mitochondria were not bacteria why are there so many similarities'. Also no theory (as far as i am aware) about the origins of mitochondria has been advanced by the critics of endosymbiosis to account for the features of miotchondria. If there is a choice between two clear theories the evidence can be used to distinguish between the two not liking a theory means its possible to criticise a theory without having to face the same critical examination.

Hi peter B.Although your objection does provide an interesting theoretical block to endosymbiosis there are many observations that suggest that in practice there is not a problem. The previously mentioned secondary endosymbiotic bacteria have not been killed by low PH. A better model for mitochondrial and plastid endosymbiosis, rather than two prokaryotes is a eukaryote and a prokaryote especially intracellular parasites such as Rickettsia prowazekii which are thought to be the closest living relatives of mitochondria. These Rickettsia bacteria have also not been killed by low PH. In amoeba an endosymbiotic bacterium that can be a pathon has been found to have adapted perfectly happily to an intracellular lifestyle in some strains. In algae there are also examples of tertiary endosybiosis, that is they engulfed an organism that already contained mitochondria and plastids and made use of them. Also the relationship was not necessarily beneficial at first and could have been a form of parasitism in which case mechanisms to evade host toxicity would have evolved. So real life observations of intracellular bacteria and secondary endosymbiotic bacteria show no toxicity or immediated death.As entertaining as defending the endosymbiosis theory is it would provide some variation if you could provide an explanation as to the origin of mitochondria and/or plastids and the evidence for it. I would also be curious as to the theoretical/philosophical basis of your objections to endosymbiosis.