Home » horizontal gene transfer » Lateral gene transfer from bacteria to humans?

Lateral gene transfer from bacteria to humans?

In other words, gene swapping. From The Scientist , June 20:

“It really does seem that human genome sequence data from somatic cells show signs of LGT events from bacteria, and so do cancer cells,” said Jonathan Eisen from University of California, Davis, who coordinated the peer review of the new study but was not involved in the work. “Wild stuff does happen.”

“LGT is incredibly important in evolution but many claims of specific cases of LGT have been seriously flawed,” said Eisen. “I came into this as a serious skeptic. It just seemed so improbable.”

But the team won him over. They ran an extensive set of checks to make sure that these bacterial sequences were not laboratory artifacts and had not come from contaminating microbes.

If lateral (horizontal) gene transfer turns out to be an important factor in evolution, as is increasingly likely (it has already been identified in plants and animals), it could raise merry hay with Darwinian attempts to postdict the history of life using Darwin’s natural selection alone.

  • Delicious
  • Facebook
  • Reddit
  • StumbleUpon
  • Twitter
  • RSS Feed

11 Responses to Lateral gene transfer from bacteria to humans?

  1. In other words, evolutionary phylogenetics is completely non-falsifiable. If researchers find a gene that’s not supposed to be there.. well it was just later transfer, of course, if not an orphan gene.

  2. *lateral transfer

  3. Certainly it’s falsifiable.

    If you test the null of LGT-only and get a strong HGT signal, you’ve falsified the null of LGT-only.

    That’s how HGT was discovered. Then the issue was postulating a mechanism and testing that. That’s how the role of viruses was discovered, and now other mechanisms, including quasi-sexual mechanisms in bacteria, and with it, a possible precursor to sexual reproduction.

    After all, sexual reproduction involves HGT.

    Science is awesome.

  4. Sorry, I was using “LGT” to stand for “longitudinal gene transfer” i.e. transgenerational gene transfer. I see the OP uses it to mean what I am used to seeing referred to as HGT.

  5. The claim that this study has anything positive to say about Darwinian evolution is certainly exaggerated since they excluded the study of gamete cells.

    The trillions of bacteria in our bodies regularly exchange DNA with each other, but the idea that their genes could end up in human DNA has been very controversial. In 2001, the team that sequenced the first human genome claimed to have found 113 cases of such lateral gene transfers (LGT), but their conclusion was later refuted.
    This high-profile error “had a chilling effect on the field,” according to Julie Dunning Hotopp who led the new study. Although her team has since found several cases of LGT between bacteria and invertebrates, “it’s still difficult to convince people that it may be happening in the human genome,” she said.
    Rather than looking for bacterial genes that had become permanent parts of the human genome, Dunning Hotopp’s team searched for traces of microbial DNA in somatic cells—the cells of the body that do not form gametes.
    Lab members David Riley and Karsten Sieber scanned publicly available data from the 1000 Genomes Project and found more than 7,000 instances of LGT from bacteria, affecting around a third of the people they studied. When they analyzed sequences from the Cancer Genome Atlas, they discovered 691,000 more instances of LGT 99.9 percent of these came from tumor samples rather than normal tissues.
    http://www.the-scientist.com/?.....n-Genomes/

    Moreover, any reasonable person should conclude that since 99.9 percent of the 7,000 transfers were directly associated with cancer, then perhaps mutating gamete cells in such a transfer fashion would also be deleterious? Just saying!

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
    http://www.saddleback.com/mc/m/7ece8/

    Modern Synthesis of Neo-Darwinism Is Dead – No Evidence For Body Plan Morphogenesis From Embryonic Mutations – Paul Nelson – video
    http://www.metacafe.com/watch/5548184/

  6. The article in The Scientist uses “lateral gene transfer.”

  7. of related note: Immunity bacteria are shown to be species specific (Regardless of the surprising result, Darwinists still insist evolution did it.)

    Our Microbes, Ourselves: Billions of Bacteria Within, Essential for Immune Function, Are Ours Alone – ScienceDaily (June 21, 2012)
    Excerpt: A new study reports that the superabundance of microbial life lining our GI tracts,, are not immunologically functional in other mammals.,,,
    Chung repeated the experiment, only this time populating a third group of mice with microbes common to rats. This new group showed the same immune system deficiency as the humanized mice. “I was very surprised to see that,” Chung said. “Naturally, I would have expected more of a half-way response.”
    http://www.sciencedaily.com/re.....130643.htm

  8. Elizabeth Liddle,

    The amount of evolutionary explanations has made the inference to Common Descent through genetics non-falsifiable. No matter what is discovered it can be explained via HGT/LGT or Orphans. Why should molecular phylogenetics be considered supporting evidence for Evolution when it has no conditions to be falsified?

  9. The amount of evolutionary explanations has made the inference to Common Descent through genetics non-falsifiable. No matter what is discovered it can be explained via HGT/LGT or Orphans. Why should molecular phylogenetics be considered supporting evidence for Evolution when it has no conditions to be falsified?

    This just isn’t true, lifepsy. Phylogenetics is a rigorous discipline, it’s not just making patterns in sand. And phylogenetic model fits are statistically tested.

    And oth phylogenetic analysis based on both morphological and genetic analysis both give a strong “tree” signal – transgenerational gene transfer, with remarkable congruence.

    But the genetic phylogenies show an overlay of a different signal that demands explanation. Some genetic material appears to be tranferred “horizontally”. So mechanisms were sought – and found.

    Would you rather that scientists had just abandoned the whole story and started again from scratch? Why should they do this, when they have already got a model that fits the data very well, and the modification not only has empirical support, but improves the model-fit even more?

    To take an analogy:

    Let’s say we are looking to see whether there is a connection between energy-drink consumption and obesity.

    We fit a linear model where we plot energy-drink consumption against BMI and get a significant positive correlation. But it’s not very good – lots of data points are a long way of the best fit line. In particular, we have a bunch of data points in the bottom right where consumption is high, but BMI is very low.

    So we think: what is causing this additional signal? So we fit an improved model whereby we also model the amount of exercise each person takes, and we include an interaction term. Now we have a much better fitting model – we find that for low-exercise people, energy-drink consumption is stongly and positively correlated with BMI, whereas for high-exercise people, the slope goes the other way – the more they drink the lower the BMI. Why could this be? Well, we take a further look, and we find that these very low, high-exercise people are elite athletes, who take energy drinks because their energy stores are low.

    But we still have some data points that are far from our linear model, improved though it is. These people have low-exercise, low BMI, and high energy-drink consumption. So we add yet another variable to the model: cancer patients.

    Now our model is very good.

    This is how phylogenetic analysis works. It is rigorous, and it fits models to data. If the model doesn’t fit, it may need additional terms.

    That is certainly making the simple model of Common Descent more complicated, but it’s making the Evolutionary model a better fit, not worse – the explanatory power is constantly increasing.

    On the other hand (as sometime happens) if adding more terms to the model makes the model fit worse, then we know we are heading in the wrong direction.

  10. Until we know what makesd an organism what it is Universal Common Descent is a non-starter as a scientific hypothesis.

  11. Don’t be picky, Joe…

Leave a Reply