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Molecular Parasite / Parasitic Genetic Element
Molecular parasites or parasitic genetic elements are genes, parts of genes, or groups of genes that similar to other parasites have their own lifecycle. Molecular parasites live inside a host cell, inside the host's genome, or inside a host gene. At least initially the molecular parasite does not increase the fitness of the organismal host, and many have developed mechanisms to minimize the damage to the host, by removing themselves from the product of the invaded gene through self splicing at the RNA or protein level. The decrease in fitness to the host (i.e the infected host produces fewer viable offspring than the uninfected host) is overcome by invasion of previously uninfected organisms.

Molecular parasites are often labeled as selfish genes, selfish DNA or selfish genetic elements; however, it may be more accurate to call them parasitic rather than selfish. According to Dawkins' gene centered view of evolution, all genes are selfish, even those that cooperate with other genes to build the organism that carries the genes into the next generation. Most selfish genes are "selfish" only insofar as they compete with other genes or alleles but usually they fulfill a function for the organisms, whereas "parasitic genetic elements", at least initially, do not make a positive contribution to the fitness of the organism.

Something on the grey zone separating molecular parasites from parasites, especially non-cellular parasites.

A paragraph on the genome as ecosystem.

The following are examples for parasitic genetic elements:

Introns
Introns are nucleotide sequences within the genome that that are spliced out at the RNA level in the processing of genes. There is much evidence in their life cycle that justifies their consideration for molecular parasitism.

1) Group 1 Introns:
Group I catalytic introns are characterized by self-splicing RNA catalysis, they are found in lower eukaryotes, higher plants, and rarely in bacteria. They often have homing endonucleases suggesting their existence as mobile genetic elements and also a cyclical model of invasion, degeneration and loss, followed by re-invasion. 'Homing' can be described as the lateral transfer of an intervening sequence. A study done by Matthew Goddard and Austin Burt looked at introns in twenty species of yeast and was suggestive of horizontal transmission.

2) Group 2 Introns:
Group II introns are also characterized by self-splicing catalyzed by the RNA within the sequence itself and also by the formation of a lariat structure after splicing. These introns have been found in organellar genomes of plants and lower eukaryotes, and more recently in the intergenic regions of bacterial genomes. This suggests that they are mobile entities since this area of the genome is under less selective pressure to remain conserved. Group II introns in bacteria often also contain active retroelements or derivatives of retroelements, this suggests that they are more mobile as opposed to other types of group II introns mentioned.

3) Spliceosomal Introns:
This third type of Intron is seen throughout eukaryotes, but mainly found in 'crown eukaryotes'. These introns require the assistance of a spliceosome to be removed from the RNA transcript during processing of the gene. Like group II introns, spliceosomal introns also form a lariat structure when excised from the transcript. This is evidence that they share some common evolutionary history. This idea is further supported by evidence that non functioning group II introns will splice in the presence of the missing part provided by a spliceosome. The reverse is also true. The idea of introns as molecular parasites finds support in the evidence for the Intron Late Theory. The positions of introns in the triose phosphate isomerase gene suggest late invasion.

Inteins
Inteins are parasitic elements in a host genome in that they do not contribute to the fitness of the host. Inteins consist of two main domains, a self-splicing domain that allows them to catalyze splicing post-translationally, and also a homing endonuclease domain. They are transcribed and translated with the gene that serves as their host and then splice out at the protein level and ligate the two exteins together. This splicing is vital for the proper functioning of the protein, while the homing endonuclease domain may degrade if the intein is fixed in a population, the self-splicing domain is always under high selective pressure. Sometimes, by the process of gratuitous complexity they may become fixed in the genome, and their splicing out of the sequence relied upon for proper function of the gene.

Homing endonucleases
Homing endonucleases are types of genes typically found in intron and intein sequences that allow them to replicate laterally through a population through super mendelian inheritance. These genes function by making a double strand cut in the host genome when they encounter an allele that is not already occupied by an intein or intron. The parasite sequence is then incorporated into the host genome upon repair of the strand breakage. The inteins or introns are often very specific about where in the host genome they invade. The homing cycle is useful in describing the life cycle of these two types of molecular parasites.

Transposons
Transposons are DNA sequences that can change their relative position in the genome of a cell by two different mechanisms.

1)Retrotransposons (Class 1):
Retrotransposons move within the genome by “Copy and paste” mechanism. They make a copy of their DNA through transcription into RNA, and then reverse transcription back into DNA, creating a second DNA molecule, which is inserted into another site within the genome. Behave similarly to retroviruses, which enter host cells and reverse transcribe their RNA into DNA to be integrated into the host genome
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RNA intermediate used by both retrotransposons and retroviruses
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2)DNA transposons (Class 2):
DNA transposons move within the genome by “Cut and paste” mechanism. Transposase enzymes cut the transposon sequence out of the DNA and ligates it elsewhere in the genome at a target site.

Function
Most transposons create silent mutations but some can act as mutagens and damage the host cell. New investigations are also occurring that are attempting to show transposons can have a beneficial role in spreading genetic innovations and regulating gene expression.

Uses
Transposons are widely used for mutatgenesis research, gene therapy, and cell tracking within an organism. See following link for more information:

http://www.springerlink.com/content/r1x5894635n0v733/