From The Gypsy Database

The Gypsy-like-Integrase Type 1 (GIN-1) (Llorens & Marin 2001) is an intron-exon host integrase (INT) gene of 1.2-2.0 kb, exclusively found in the genomes of vertebrates. GIN-1 originally drawed attention because of the similarity of its encoded product to the INTs coded by the Ty3/Gypsy LTR retrotransposons. The GIN1 product shows the typical INT core preceded by a GPY/F module thought to mediate multimerization (Ebina et al. 2008), as it is typically observed among LTR retroelement INTs. For simplicity´s sake the figure below shows the genomic structure without introns.


Subsequent approaches have revealed a putative vertebrate paralog of GIN-1, called GIN-2 (Bao et al. 2010; Marin 2010) as well as other related pools of exon-intron Solo-transposase (TR) transposons called GINGER1 (Bao et al. 2010), GINA and GINO (Marin 2010) with which GIN-1 share direct ancestry. In this regard, phylogenetic analyses reveal that GIN-1 and GIN-2 are not true paralogs but that GIN-1 is counterpart of GINO and that GIN-2 is phylogenetically close to GINA within a phylogenetic cluster where GINGER1 elements occupy the most basal position. In other words, both GIN-1 and GIN-2 are host genes evolved from domesticated GINGER1-like transposons (note that we use the name of the most basal position to describe the whole pool). This evidence does not invalidate however the original hypothesis (Llorens & Marin 2001) of Ty3/Gypsy ancestry because phylogenetic analyses significantly relate the whole GINGER1 cluster to the INTs coded by certain Ty3/Gypsy LTR retroelements (for more details see the Section describing the GINGER1 transposons).

There are two complementary classifications for the GINGER1 elements. Based on sequence these elements can be classified as DDE TRs and INTs. Based on INT-like structural potential similarities, the INT coded by GINGER1 elements are members of the Retroviral Integrase Superfamily (Nowotny 2009) of nucleic acid-processing enzymes involved in; a) selfish evolution; b) replication and repair of DNA; c) recombination and gene fusion; d) RNA-mediated gene silencing; and e) oncogenesis.

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