Establishing a role for shrimp fortilin in preventing cell death

• Published in: Aquaculture 2006-05, Vol.255 (1), p.157-164
• Main Authors: Graidist, Potchanapond, Fujise, Kenichi, Wanna, Warapond, Sritunyalucksana, Kallaya, Phongdara, Amornrat
• Format: Article
• Language: English
• Subjects: Animal aquaculture; Animal productions; animal proteins; Anti-apoptotic protein; Apoptosis; Aquaculture; Biological and medical sciences; complementary DNA; Crustacea; Fortilin; Fundamental and applied biological sciences. Psychology; gene expression regulation; General aspects; Hybridization; Invertebrates; Marine; molecular cloning; Penaeidae; Penaeus; Penaeus monodon; Penaeus monodon (Pm); Proteins; Shellfish; shrimp; shrimp culture; translationally controlled tumor protein; Translationally controlled tumor protein (TCTP); Viruses; white spot syndrome; White spot syndrome virus; White spot syndrome virus (WSSV)
• ISSN: 0044-8486; 1873-5622
• DOI: 10.1016/j.aquaculture.2005.12.023

White spot syndrome virus (WSSV) is a highly virulent and infectious virus to farmed shrimps and represents a serious threat to aquatic industries. Fortilin, also known as translationally controlled tumor protein (TCTP), protects mammalian cells under stress from cell death. A subtraction hybridization screening in our laboratory between healthy and moribund WSSV-infected Penaeus mondon shrimps has identified a fortilin gene whose messages critically decrease during the terminal stage of the WSSV-induced illness. Fortilin/TCTPs are highly conserved throughout the animal and plant kingdoms, and shrimp fortilin has a 64% identity in amino acid composition with human fortilin. In our previous work, the data clearly suggested that fortilin in shrimp protected WSSV-infected shrimps from death. Although human fortilin has a role in apoptosis regulation, it is not known if shrimp fortilin has any role in apoptosis regulation. We report that fortilin is greatly upregulated in shrimp haemolymph during the early phase of WSSV infection and that its expression abruptly decreases as the shrimp becomes moribund. Strikingly, shrimp fortilin, when overexpressed in mammalian cells, protected them from cell death induced by etoposide, staurosporine, cisplatin, hydroxyurea, and 5-fluorouracil (5-FU). These data suggest that shrimp fortilin, like mammalian fortilin, can protect cells under toxic conditions from death. In addition, since shrimp fortilin was capable of protecting cells in a mammalian environment, this indicates that shrimp and human fortilin use a common cellular pathway to achieve this. Shrimp fortilin may play a critical role in their response to WSSV-infection, through regulation of a cell death pathway that is common to shrimp and humans.