Science in Society Archive

Horizontal gene transfer - new evidence 5.12.98

Dr. Mae-Wan Ho

A group of researchers in Indiana University of the United States have just reported [1] that a genetic parasite belonging to yeast has suddenly jumped into many unrelated species of higher plants recently.

This parasite is a piece of DNA called a "group I intron" that can splice itself in and out of a particular gene in the genome of mitochondria. Mitochondria are little power houses of the cell that oxidize food in order to turn it into a form of energy that can be used for all living processes. Until 1995, this parasite was thought to be largely confined to yeast and only one genus of higher plants out of the 25 surveyed had the parasite.

But in a new survey of species from 335 genera of higher plants, 48 were found to have the parasite. These 48 genera were in five different families: Asterids, Rosids, Monocots, Piperales, and Magnoliales. Moreover, all the higher plants that have gained the group I intron had the same one, as the DNA base sequence is more than 92% identical.

When this intron jumps into a genome, it also adds to its tail end an extra stretch of DNA that does not belong to the host. By comparing this extra tail, the researchers are able to conclude that almost all of the horizontal gene transfer events were independent and occurred very recently. "This massive wave of lateral transfers is of entirely recent occurrence, perhaps triggered by some key shift in the intron's invasiveness within angiosperms [i.e., higher plants]." Two possible scenarios presented themselves, either an original yeast group I intron jumped into a higher plant, and from there, infected all other genera independently, or the same yeast intron has jumped independently to all the plants. The present data cannot distinguish between the two possibilities

So, what triggered the recent "explosive invasion" of the higher plants by this genetic parasite? It could have got into the plant cells by being carried in viruses, insects or bacteria. In order to get into the genome, however, it has to overcome genetic barriers that keep species distinct. For example, the genome has to have a specific site of about 20 base pairs that is recognized by the parasite. Furthermore, in order for the splicing gene carried by the parasite to become expressed, it has to have a signal that is recognized by the host. [2]

The researchers themselves raise concerns about releasing transgenic crops into the environment, given that horizontal gene transfer is now found to be so widespread.

Additional comments:

• Only two months ago, it was reported in the Journal Nature that genes transferred into transgenic plants can be up to 30 times more likely to escape than the plant’s own genes. [3]

• Is it possible that the recent massive horizontal gene transfer from yeast to higher plants was triggered by commercial genetic engineering biotechnology?

• Genetic engineering makes use of artificial genetic parasites as gene carriers, to transfer genes horizontally between unrelated species. These artificial parasites are made from parts of the most aggressive naturally occurring parasites, like the group 1 intron discussed here.

• The same kinds of explosive horizontal gene transfer have already been documented among viruses and bacteria which are responsible for the recent resurgence of drug and antibiotic resistant diseases. [4]

Article first published 26/07/00


  1. 1. Cho, Y., Qiu, Y.-L., Kuhlman, P. and Palmer, J.D. (1998). Explosive invasion of plant mitochondria by a group I intron. Proc. Natl. Acad. Sci. USA 95, 14244-9.
  2. 2. Gray, M.W. (1998). Mass migration of a group I intron: Promiscuity on a grand scale. Proc. Natl. Acad. Sci. USA 95, 14003-5.
  3. 3. Bergelson, J., Purrington,c.B. and Wichmann, G. (1998). Promiscuity in transgenic plants. Nature 395, 25.
  4. 4. Ho, M.W., Traavik, T., Olsvik, O., Tappeser, B., Howard, C.V., von Weizsacker, C. and McGavin, G. (1998). Gene technology and gene ecology of infectious diseases. Microbial Ecology in Health and Disease 10, 33-59.

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