One Species' Genome Discovered Inside Another Species' Genome

[doG]

A team of researchers has discovered that a bacterial parasite (called Wolbachia) can insert almost its entire genome into the genomes of members of one host species (a fly called Drosophila ananassae), and can insert parts of its genome into the genomes of members of several other host species.

 

"We've found at least one species where the parasite's entire or nearly entire genome has been absorbed and integrated into the host's," says Jack Werren of the University of Rochester, principle investigator of the study and a world-leading authority on the Wolbachia parasite. "The host's genes actually hold the coding information for a completely separate species."

 

This research, which has important implications for evolution, is reported in the August 30 issue of Science. It was funded by the National Science Foundation's (NSF) Frontiers in Integrative Biological Research program, which supports large, integrative projects addressing major questions in biology.

 

More at the National Science Foundation...

 

I wonder how many other species do this and to what extent this effects evolution. How much mutation is effectivelt steered instead of random?

 

 

 

P.S.

You need a news forum here for stuff like this...

[pioneer]

When you think about what viri can do, and in this case what a bacteria can do, i.e., insert genes, while also taking into consideration how efficient cells are at duplicating the DNA, it is a wonder the random mutation theory lasted as long as it did. Maybe it was due to some type of legal contract. Most chemical things that affect the DNA usually do more harm than they do good. This should have raised at least a yellow flag with respect to the very slow progression theory of genetic mutations.

 

Part of the problem may have been due to the need to fill in time. A theory using viral or bacterial genetic insertions for mutations would mean fast genetic changes and could theoretically outpace the slow progress of the evolutionary data, which appears to be better supported by the slower selective advantage/mutation theory.

 

One way to explain how fast genetic progression can be slowed down to fit the data, can be explained by the environment setting the standard for change. For example, if you look back at the age of dinosaurs, things were supersized. In modern times, animals have shunk in relative size. The advantage of a smaller size is a much lower food/water requirement, while also allowing a better brain/body ratio. A smaller size has a greater range of adaptation, if the food supply varies.

 

If in the age of the dinosaurs, one of the dinos mutated into a smaller size, with a more modern brain to body ratio, even though this will be the direction of the future, in a stable dinosaur environment, this would be more of a selective disadvantage than selective advantage. In other words, from a genetic point of view, this little body is the future, but from an environmental point of view, it makes this future animal a lightweight in the land of heavy weight champions. That environment could give selective advantage to the less evolved genetics of larger dinosaurs.

 

In terms of a real example, mammals were around during the latter stages of the dinosaurs. In terms of genetics, they were far more advanced. But this advanced genetics did not give them a selective advantage in an environment that was dominated by the less genetically evolved dinosaurs. The dinosaurs were still the top of the food chain. It took some drastic climate change to alter the environment so the advanced genetics of the mammals, gave them a selective advantage. As such, even if viri and bacteria advanced the DNA quickly, often a stable environment based on less advanced genetics, may still have the selective advantage, such that a genetic advance may not establish itself.

 

If the little dino had mutated to only 90% size, this may have made it more agile and quicker, while still allowing it to be a heavy weight. It is not as advanced, genetically, as the little dino with his modern brain to body ratio, but it may have more advantage in the environment. The result may be that stable eco-systems will favor only smaller advances.

[CharonY]

Bacteria do not that commonly insert pieces of DNA (either accidentally or with purpose, so to speak) in eukaroytes. At least, to date relatively few examples are known.

The majority of these are parasites, of which Agrobacterium is probably the best known one. It injects genes controlling growth and opine production into its host plants. The plants is induced to produce tumour-like cells that overproduce opines which is then used by the bacterium.

This process is also exploited for biotechnological purposes for the creation of transgenic plants.

This is an example for natural directed mutagenesis. The large scale DNA exchange as described in the article is of course less common (hence the high-profile publication in Science). For example, mitochondria formation occurred only once until today. Viruses on the other hand are nothing more than DNA/RNA injectors, however their entire genome consist only of a couple of genes. Their contribution to evolution of e.g. the human species is well recognized, though.

Most genomes, even those that have a selection on genome size, like for instance prokaryotes, are abundant with phage sequences (often inactive) or other mobile genetic elements (e.g. transposons, IS-elements and so forth).

 

In evolutionary terms these additions of external DNA basically enhance the overall variety of the gene pool. They can be essentially regarded as a kind of mutagen.

[lucaspa]

I wonder how many other species do this and to what extent this effects evolution. How much mutation is effectivelt steered instead of random?

 

P.S.

You need a news forum here for stuff like this...

 

1. With your question, this probably should have gone in the Evolution forum.

 

2. How many of the bacterial genes are expressed? Having the genome present in Drosophila does not mean the Drosophila cells are making the proteins from the bacterial genome.

 

3. This is not "steering" in terms of evolution. When evolutionists speak of "random", they mean "random with respect to the needs of the individual or population". Mutations are NOT "random" with respect to areas of the DNA they appear in or some of the substitutions. For instance, when you have substitution mutation for A, it will almost always be T, not G or C.

 

This insertion of the bacterial genome is still "random" in terms of the Drosophila. After all, what were the needs of the Drosophila as an individual or population? Did the bacteria genes fill that need or not?

 

What this discovery does do is tell us another way that huge amounts of DNA can be "created". That is, how new pages of "information" can be added. Since the Drosophila operated just fine without the bacterial genes, this means that those genes (if expressed) can now be mutated without taking anything away from the Drosophila. Instead, those changes can ADD to the repertoire of traits of Drosophila. In that regard, the effect for evolution is similar to having chromosomal duplication.

 

Most chemical things that affect the DNA usually do more harm than they do good. This should have raised at least a yellow flag with respect to the very slow progression theory of genetic mutations.

 

There never was a "progression theory of genetic mutations". And you are in error: most mutations are either neutral (the vast majority) or harmful. Only 2.8 per thousand mutations are out and out harmful.

 

One way to explain how fast genetic progression can be slowed down to fit the data, can be explained by the environment setting the standard for change.

 

Pioneer, how much about evolution have you actually read? This is not an insult, but a serious question. I ask because you seem to be trying to reinvent the wheel.

 

Let me review: natural selection is a two-step process.

1. Variation (of which mutations are one type)

2. Selection.

 

You must have BOTH steps for natural selection to work. And yes, it is the environment that sets the criteria for selection. Only those variations that do better in that particular environment will be selected.

 

It has long been known that there are 3 types of natural selection:

 

1. Directional. This is the one people most often associate with the term "natural selection". This happens in a changing environment and where natural selection picks new designs/adaptations and changes populations to fit that environment.

 

2. Purifying or stabilizing selection. Once a population is well-adapted to a particular environment, natural selection will actually act against changing the population. Once a population is at a fitness peak in the adaptive landscape, almost any change is going to make the individual LESS adapted. Therefore selection will work to stabilize or purifiy the genome to only those alleles that have the best adaptations for the particular environment.

 

3. Disruptive selection. This happens when a population covers a geographical area such that there are different environments in different parts of the range. Directional selection for the subpopulations tends to adapt the subpopulation for the particular environments but gene flow between the subpopulations tends to homogenize the population.

 

For example, if you look back at the age of dinosaurs, things were supersized.

 

Not really. You are using selective data. Dinos ranged in size from chickens to the giants you are thinking of.

 

If in the age of the dinosaurs, one of the dinos mutated into a smaller size, with a more modern brain to body ratio, even though this will be the direction of the future,

 

Again, not "the direction of the future". In evolution there is a principle called Cope's Rule. It states that, in any particular lineage, the trend is toward larger body size over time. The data strongly support this. Notice what happened to mammals and birds when the dinos suddenly went extinct at the KT boundary: lineages of mammals evolved into larger sizes to fill the empty ecological niches. Many mammalian species -- rhinos, hippos, elephants, etc., present and extinct -- overlap in size the range of size of the dinos. Blue whales are larger than any dino ever was.

[doG]

2. How many of the bacterial genes are expressed? Having the genome present in Drosophila does not mean the Drosophila cells are making the proteins from the bacterial genome.

 

From the article:

 

Werren says that several types of evidence indicate that gene transfers from Wolbachia to invertebrates occur frequently, including: 1) the team's discovery of Wolbachia DNA in so many randomly selected organisms; 2) the agreement between the team's laboratory analyses and computational analyses; and 3) the infection of approximately 70 percent of the world's terrestrial invertebrates by Wolbachia, which means that this parasite has had a virtually limitless number of opportunities to transfer its genes to its hosts.

 

It is not yet definitely known whether any transferred Wolbachia genes are functional. But Werren says that the frequent nature of Wolbachia lateral gene transfers indicates that this parasite has probably produced new functions in some animals. Moreover, the transfer of even a fragment of a Wolbachia genome would be significant if it contained even one functional gene.

 

It appears to be happening in many more species than just Drosophila. If it has caused new functions in animals has it caused functions that would not have evolved in those host species with the donation of Wolbachia's DNA? We don't know but it seemed like good food for thought.

[lucaspa]

OK, I found the paper and my answer as to how many of the genes are expressed: "In addition, RT-PCR followed by sequencing (11)

demonstrated that ~2% of Wolbachia genes (28 of 1206 genes

assayed; table S3) are transcribed in cured adult males and

females of D. ananassae Hawaii."

 

It's also not clear how biologically relevant the expressed proteins are:

"Analysis of the transcript levels of inserted

Wolbachia genes with qRT-PCR (11) revealed that they are

104-fold to107-fold less abundant than the fly’s highly

transcribed Actin gene (act5C; table S3). There is no cutoff

that defines a biologically relevant level of transcription, and

assessment of transcription in whole insects can obscure

important tissue specific transcription. Therefore, it is unclear

whether these transcripts are biologically meaningful, and

further work is needed to determine their significance."

 

Interestingly, the peer-reviewed article in Science doesn't mention ANYTHING about evolutionary implications! Instead, the focus is on methodology and excluding bacterial sequences when genomes are sequenced:

 

"Whole eukaryote genome sequencing projects routinely

exclude bacterial sequences on the assumption that these

represent contamination. For example, the publicly available

assembly of D. ananassae does not include any of the

Wolbachia sequences described here. Therefore, the argument

that the lack of bacterial genes in these assembled genomes

indicates that bacterial LGT does not occur is circular and

invalid. ... Because

W. pipientis is among the most abundant intracellular bacteria

(17, 18), and its hosts are among the most abundant animal

phyla, the view that prokaryote to eukaryote transfers are

uncommon and unimportant needs to be reevaluated."

 

From the article:

"It is not yet definitely known whether any transferred Wolbachia genes are functional. But Werren says that the frequent nature of Wolbachia lateral gene transfers indicates that this parasite has probably produced new functions in some animals. Moreover, the transfer of even a fragment of a Wolbachia genome would be significant if it contained even one functional gene. "

 

It appears to be happening in many more species than just Drosophila. If it has caused new functions in animals has it caused functions that would not have evolved in those host species with the donation of Wolbachia's DNA? We don't know but it seemed like good food for thought.

 

A problem I have with this data is that it contradicts other data that we have: phylogenetic analysis.

 

You see, if these inserted genes played a role in evolution, we would have discontinuity at the genetic level between ancestor-descendent. When the Wolbachia genes were inserted into female Drosophila genome the first time, we don't have "descent with modification" but gene engineering -- done by the Wolbachia bacteria.

 

Thinking about it some more, Werren and colleagues would argue that phylogenetic analysis excluded any bacterial sequences from the analysis -- thinking that they were contamination. (see quote in previous post from paper). So maybe the phylogenetic data doesn't contradict this because the sequences were excluded.

 

Oh, this paper is a nasty blow to IDers! IDers argue that the only way to get complex sequences of genes is for an intelligent agent to manufacture them. But here Drosophila (and other invertebrates) potentially get a complex sequence of genes without an intelligent agent. Yes, this does indeed knock a major prop out from under ID. Yes, you can have "genetic engineering" in multicelled organisms but not by an intelligent designer!

[CharonY]

Oh, this paper is a nasty blow to IDers! IDers argue that the only way to get complex sequences of genes is for an intelligent agent to manufacture them.

 

I wonder why they would argue like that at all. Genetic mobile elements (like transposons, viruses or integrons) are known for a long time to integrate new genes into organisms. What is surprising here is the sheer amount of genes in one go. On the other hand if one just takes a look at how many sequences found in databases are of putative viral origin it ain't that much after all.

 

Still, I see the problem of distinguishing sequences "real" chromosomal sequences from co-purified intracellular parasite sequences before any more conclusions can be drawn.

Also it would be interesting to see how stable these insertions are. As for instance plants bioengineered by Agrobacterium often do not inherit the additional information (as it harshly reduces fitness). Also, sequences from mobile genetic elements appear to be stable mostly in an (apparent) inactive form.

[lucaspa]

I wonder why they would argue like that at all. Genetic mobile elements (like transposons, viruses or integrons) are known for a long time to integrate new genes into organisms. What is surprising here is the sheer amount of genes in one go.

 

Transposons and viral elements are not sequences for functional proteins. Remember, Behe and other IDers state that a multicomponent biochemical sequence can arise only by getting all the individual genes to come into existence together. To them, this means ONLY manufacturing all of the genes at the same time.

 

In this case, the bacterial genome already many hundreds/thousands of sequences for functional proteins. It is already a set of "irreducibly complex" systems. Now, consider that those functional proteins are in addition to the functional proteins already in the Drosophila genome, and you can see that you can suddenly get, without manufacture, several sets of complex biochemical sequences all at the same time.

 

Still, I see the problem of distinguishing sequences "real" chromosomal sequences from co-purified intracellular parasite sequences before any more conclusions can be drawn.

 

A major point of the authors is that it has been assumed that bacterial sequences found during the human genome project (for instance) were from contamination and they were ignored. The authors think that some, or all, of those sequences were actually IN the human genome.

 

Also it would be interesting to see how stable these insertions are.

 

Considering that the DNA was isolated from members of Drosophila captured in the wild, it is likely that this is stable. It would be very improbable that this insertion happened just a few generations ago. Also, the authors tested for inheritance of the Wolbachia genes:

"Crosses between Wolbachia-free Hawaii males (with the

insert) and Wolbachia-free Mexico females (without the

insert) revealed that the insert is paternally inherited by

offspring of both sexes, confirming that Wolbachia genes are

inserted into an autosome. Since Wolbachia infections are

maternally inherited this also confirms that PCR

amplification in the antibiotic treated line is not due to a low

level infection. Furthermore, the Hawaii and Mexico crosses

revealed Mendelian, autosomal inheritance of Wolbachia

inserts (paternal N = 57, k = 0.49; maternal N = 40, k = 0.58)."

 

Also, sequences from mobile genetic elements appear to be stable mostly in an (apparent) inactive form.

 

In this case, only about 2% of the Wolbachia genes were transcribed to mRNA and then only in very small amounts:

"In addition, RT-PCR followed by sequencing (11)

demonstrated that ~2% of Wolbachia genes (28 of 1206 genes

assayed; table S3) are transcribed in cured adult males and

females of D. ananassae Hawaii. The complete 5' sequence

of one of the transcripts, WD_0336, was obtained with 5'-

RACE on uninfected flies (11) suggesting that this transcript

has a 5' mRNA cap, a form of eukaryotic post-transcriptional

modification. Analysis of the transcript levels of inserted

Wolbachia genes with qRT-PCR (11) revealed that they are

10-4fold to10-7 fold less abundant than the fly’s highly

transcribed Actin gene (act5C; table S3)."

[CharonY]

Transposons and viral elements are not sequences for functional proteins.

Well, genes encoded within transposons and viral components (unless deactivated) are coding for functional proteins of course. But agreed, probably the promoters of ID are more referring to genes coding for more complex cellular features than that.

 

A major point of the authors is that it has been assumed that bacterial sequences found during the human genome project (for instance) were from contamination and they were ignored. The authors think that some, or all, of those sequences were actually IN the human genome.

That I understood, but as I meant that this is just an assumption. I have for instance not found any data as of how much of the library contained bacterial sequences. If it was truly inserted in the genome, one would expect a similar frequency as for human inserts.

Undeniably in almost any eukaryotic library you will find bacterial DNA that are really contaminations and just claiming all of them to be inserts is imo a bit far fetched.

 

The inheritence of Wolbachia sequences is somewhat convincing, the sequencing of a wild-capture is not. The latter by itself does not give information about stability, not about presence as you cannot track down the time of infection. Moreover, apparently not all Drosophila lines were cured of Wolbachia, first (S2).

As Drosophila are commonly infected with WolbachiaTracking more (cured) generations would be a better indicator of stability.

 

Regarding the expression of genes, apparently the authors normalized the Wolbachia genes against the act5 gene (unless I misunderstood it), but this is technically not correct as it does not account for sequence dependent differences in the PCR efficiency. I'd love to see the cut-off.

[lucaspa]

Well, genes encoded within transposons and viral components (unless deactivated) are coding for functional proteins of course. But agreed, probably the promoters of ID are more referring to genes coding for more complex cellular features than that.

 

The point IDers make is that, say, the flagellum, is a complex structure of many different proteins and thus many different genes. They don't see how this multitude of different genes for one structure could have come about thru a step-by-step process that is their strawman of natural selection. (They can, because natural selection is not their strawman of it.) However, here what we have is the importation of hundreds/thousands of genes at one fell swoop! So, you could have 30 of these bacterial genes, say, and just ONE of the host genes and suddenly you have the 31 genes you need for a flagellum. Now do you see why I say this is really bad for ID?

 

That I understood, but as I meant that this is just an assumption. I have for instance not found any data as of how much of the library contained bacterial sequences.

 

Your pronoun "this" is vague. I can see 2 "assumptions"

1. That of the Human Genome Project that any bacterial DNA sequences were contamination from stray bacteria in the test tubes, reagents, etc.

2. An "assumption" by the authors of this paper that the bacterial sequences found in the Human Genome Project were part of the human genome.

 

So which are you referring to?

 

Which "library". The Drosophila or the Human? In the human library, you won't find any data because no one kept track of it and didn't publish it. You'd have had to be involved and look at the original data.

 

If it was truly inserted in the genome, one would expect a similar frequency as for human inserts.

 

Not necessarily. This is coming from a parasite. Humans may not have had similar parasites or those parasites may not have inserted their genome into the human genome. I'm not sure what the insertion mechanism is, but it looks to be contingent -- the bacteria/host have to have the correct enzymes to do the inserting.

 

Undeniably in almost any eukaryotic library you will find bacterial DNA that are really contaminations and just claiming all of them to be inserts is imo a bit far fetched.

 

That isn't the claim. You haven't read the paper, have you? You really should before you impute claims to them.

"Whole eukaryote genome sequencing projects routinely

exclude bacterial sequences on the assumption that these

represent contamination. For example, the publicly available

assembly of D. ananassae does not include any of the

Wolbachia sequences described here. Therefore, the argument

that the lack of bacterial genes in these assembled genomes

indicates that bacterial LGT does not occur is circular and

invalid. Recent bacterial LGT to eukaryotic genomes will

continue to be difficult to detect if bacterial sequences are

routinely excluded from assemblies without experimental

verification. And these LGT events will remain understudied

despite their potential to provide novel gene functions and

impact arthropod and nematode genome evolution. Because

W. pipientis is among the most abundant intracellular bacteria

(17, 18), and its hosts are among the most abundant animal

phyla, the view that prokaryote to eukaryote transfers are

uncommon and unimportant needs to be reevaluated."

 

The inheritence of Wolbachia sequences is somewhat convincing, the sequencing of a wild-capture is not. The latter by itself does not give information about stability, not about presence as you cannot track down the time of infection.

 

Finding these Wolbachia sequences in ALL wild captures makes it very unlikely that the time of infection was recent. Since the genes are not expressed, you don't have natural selection fixing the capture in the population. Instead, it must have occurred by genetic drift, and that takes a LOT of time in a large population like this. So, if it were unstable, then sometime during the time it took genetic drift to fix the captured genome, it would have been discarded.

 

Regarding the expression of genes, apparently the authors normalized the Wolbachia genes against the act5 gene (unless I misunderstood it), but this is technically not correct as it does not account for sequence dependent differences in the PCR efficiency. I'd love to see the cut-off.

 

Not "normalized" but "compared":

"Analysis of the transcript levels of inserted Wolbachia genes with qRT-PCR (11) revealed that they are 10-4fold to10-7 fold less abundant than the fly’s highly transcribed Actin gene (act5C; table S3)"

 

And yes, RT-PCR does correct for differences in PCR efficiency, as I understand the procedure. They chose the actin gene because actin is expressed in nearly all cells and is expressed at a fairly high level. I have seen actin used as the comparison in RT-PCR in many animal and human studies.