This release is also available in Spanish
A team of researchers from the Universitat Aut˛noma de Barcelona (UAB) has discovered that transposons, small DNA sequences that travel through the genomes, can silence the genes adjacent to them by inducing a molecule called antisense RNA. This is a new mechanism for evolution that has been unknown until now. The research has been recently published in the journal Proceedings of the National Academy of Sciences (PNAS).
Transposons are repeated DNA sequences that move through the genomes. For a long time they have been considered as a useless part of genetic material, DNA left overs. However, it is more and more clear that transposons can cause favourable changes for the adaptation and survival of the organism.
In this research project, the UAB scientists have demonstrated that a transposon inserted in the genome of the Drosophila (a model used for a lot of genetic studies) silenced a gene adjacent to it, that is, it reduced its level of expression significantly. The expression of a gene consists in using the DNA as a mould to synthesise a molecule called a messenger RNA, which in its own environment will be used to synthesise a particular protein. According to what the researchers have seen, the transposon stimulates the synthesis of a molecule that is complementary to the normal messenger RNA. This new complementary molecule (that the scientists have called antisense RNA) joins with the normal RNA of the gene obstructing it from synthesising the protein. Even though the research has been carried out on the species Drosophila buzzatii, the researchers state that transposons, that in the human genomes represent 45% of the genetic material, could be provoking the same type of silencing effect in our species.
The work now published is a continuation of previous studies. In 1999, the research team headed by Dr. Alfredo Ruiz, from the Department of Genetics and Microbiology at the UAB, published an article in Science where they demonstrated that a chromosomal inversion in Drosophila buzzatii was generated by the transposon activity. The inversions are formed by turning a chromosome segment upside down so that it is orientated in the opposite direction. In Drosophila it has been demonstrated that the chromosomal inversions often have an adaptive value, that is, that the individuals that have chromosomes with the inversion show some advantages over those that don't, even though it still unclear what is the mechanism used by the inversions to cause these differences.
In the case of the of Drosophila buzzatii a lot of transposons were found inserted in the break points, but only in the chromosomes with the inversion and not the normal ones (without an inversion). One of these transposons, called Kepler, is responsible for this silencing of the genetic expression, discovered recently. The fact that this transposon is present only in the chromosomes with the inversion implies that the gene is silenced only in the individuals that have these inverted chromosomes, and not in those with normal chromosomes. It is known that flies with this inversion are larger and develop over a longer period of time than the flies without the inversion. It could be, even though it is not yet proved, that these differences are caused by silencing the gene adjacent to the Kepler. If this is so, this newly discovered mechanism could explain the adaptive value of the chromosomal inversion.
The participants in the research project are Marta Puig, from the Department of Genetics and Microbiology from the UAB; Mario Cßceres, from the Department of Human Genetics from the Emory University School of Medicine in Atlanta (USA); and Alfredo Ruiz, director of the research project and in charge of the Group of Genomic, Biocomputing and Evolution (Grup de Gen˛mica, BioinformÓtica i Evoluciˇ) at the UAB.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
Published on PsychCentral.com. All rights reserved.
If you talk to God, you are praying.
If God talks to you, you have schizophrenia.
-- Thomas Szasz