Identification and characterization of the XPG gene of the frog Rana Grylio virus

The RGV(9808) is one of three Rana Grylio viruses which were isolated from the cultured pig frogs with lethal syndrome obtained from different provinces in China, which belongs to the iridoviridae family. In RGV(9808), an open reading frame (ORF), whose deduced amino acid sequence(aa) shows identity with Xeroderma pigmentosum G (XPG) protein, was identified. XPG is one of the nucleotide excision repair (NER) genes, whose encoded protein plays a critical role in NER system as a nuclease. The ORF of RGV(9808) has 1092bp in length, G+C content of 60.62% and encodes a putative protein of 363 aa with a predicted molecular mass of 40.6 kDa, whose isoelectric point (pI) is 7.33. Compared with the XPGs found in other 12 species, the higher homology among RGV(9808) and the four ranavirus is present as more than 97%, and RGV(9808) has the lowest identity with Chilo iridescent virus (CIV), coming to 22.6%. This indicated that there exist large differences among distinct genus viruses, although the gene is identical in iridoviridae family. Key words: Rana grylio virus; Aquatic animal disease; Viral pathogeny; Iridovirus; XPG gene. In the past ten years, many virulent iridoviruses have been isolated and characterized from fish, reptiles, amphibians and turtles. These viruses cause serious systematic diseases and high mortality rates in cultured aquatic animals, and have been factors restricting aquaculture development for the special animals in the world (Chinchar V G., 2002). Iridoviruses are large icosahedral viruses whose genomes consist of linear, double-stranded DNA(dsDNA) that is both circularly permuted and terminally redundant (Zhang et al., 2004; Fauquet C M et al., 2005). According to the report of the International Committee on the Taxonomy of Viruses (ICTV) (Fauquet C M et al., 2005), the family iridoviridae has been subdivided into four genera, including Iridovirus, Chloriridavirus, Ranavirus and Lymphocystivirus. autosomal recessive disease that is characterized by the extreme sensitivity of the skin of human to sunlight(Steeg et al., 1999). Genetic and molecular analysis have revealed that the repair of ultraviolet (UV)-induced DNA damage is impaired in XPG patients owing to mutations in XPG gene that form part of a DNA-repair pathway known as nucleotide excision repair. Studies have confirmed that human XPG protein makes the 3' incision during the NER of DNA, acting as a structure-specific endonuclease (Evans et al., 1997). We have known that the replication strategy of iridovirus is unique in that the virus utilizes both the host cell nucleus and cytoplasm for its nucleic acid synthesis but assembles in the cytoplasm (Goorha et al., 1982). During the first stage, the smaller replicating DNA molecules are synthesized, then extremely large replicating complexes are synthesized only in the cytoplasm in the second stage. The large precursor DNA was cleaved by some nuclesase to form mature viral DNA size molecules. The unique features of genomes for iridovirus that are both circularly permuted and terminally redundant may result from this cleavage (Yin et al., 1992). Whether the XPG in RGV(9808) is also a nuclease, and whether it plays an essential role in this pathway is not evident. Further studies that are currently in progress may provide beneficial information on genome maturation of iridoviridae, which is necessary for the control of iridovirious infection