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. 1998 Nov;72(11):8765-71.
doi: 10.1128/JVI.72.11.8765-8771.1998.

Walleye retroviruses associated with skin tumors and hyperplasias encode cyclin D homologs

L A LaPierre  1 , J W Casey, D L Holzschu
Affiliations

Walleye retroviruses associated with skin tumors and hyperplasias encode cyclin D homologs

L A LaPierre et al. J Virol. 1998 Nov.

Abstract

Walleye dermal sarcoma (WDS) and walleye epidermal hyperplasia (WEH) are skin diseases of walleye fish that appear and regress on a seasonal basis. We report here that the complex retroviruses etiologically associated with WDS (WDS virus [WDSV]) and WEH (WEH viruses 1 and 2 [WEHV1 and WEHV2, respectively]) encode D-type cyclin homologs. The retroviral cyclins (rv-cyclins) are distantly related to one another and to known cyclins and are not closely related to any walleye cellular gene based on low-stringency Southern blotting. Since aberrant expression of D-type cyclins occurs in many human tumors, we suggest that expression of the rv-cyclins may contribute to the development of WDS or WEH. In support of this hypothesis, we show that rv-cyclin transcripts are made in developing WDS and WEH and that the rv-cyclin of WDSV induces cell cycle progression in yeast (Saccharomyces cerevisiae). WEHV1, WEHV2, and WDSV are the first examples of retroviruses that encode cyclin homologs. WEH and WDS and their associated retroviruses represent a novel paradigm of retroviral tumor induction and, importantly, tumor regression.

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Figures

FIG. 1
FIG. 1
(A) Genomic organization of WDSV, WEHV1, and WEHV2. (B) Amino acid sequence alignment of the rv-cyclins encoded by WDSV, WEHV1, and WEHV2 with human (Hum) cyclins D1, D2, and D3. Identical and similar amino acids are shaded. The 10 α-helices that comprise the cyclin box are bracketed (A to E′), and conserved lysine and glutamate residues in helices C and E are marked by asterisks.
FIG. 2
FIG. 2
Hybridization of walleye genomic DNA with rv-cyclin probes. (A) Panel of three Southern blots hybridized with a WEHV1, WEHV2, or WDSV rv-cyclin probe, respectively. Lanes: 1, 1-kb DNA ladder (L); 2 and 4, DNA isolated from a pool of hyperplasias containing WEHV1 (H1) and WEHV2 (H2); 6, DNA isolated from a dermal sarcoma (DS); 3, 5, and 7, walleye sperm DNA (S) used a negative control. (B) Southern blot hybridized with walleye cellular kinase probe (KIN). The lane designations are the same as in panel A.
FIG. 3
FIG. 3
Analysis of rv-cyclin activity in yeast. (A) BY613 transformants grown on galactose minimal medium. Rows: 1, transformants containing the MET3 promoter plasmid backbone; 2, transformants expressing the WEHV1 rv-cyclin; 3, transformants expressing the WEHV2 rv-cyclin; 4 and 5, transformants containing independently derived plasmids expressing the WDSV rv-cyclin. (B) Glucose minimal medium replica plate of transformants from panel A. (C) Galactose-supplemented rich medium replica plate of transformants from panel A. (D) Glucose-supplemented rich medium replica plate of transformants from panel A.
FIG. 4
FIG. 4
Analysis of rv-cyclin expression. One microgram of poly(A)-enriched RNA from fall lesions (left panel) or 10 μg of total RNA from spring lesions (right panel) was hybridized to cognate rv-cyclin probes. H1, RNA isolated from hyperplasias hybridized to the WEHV1 rv-cyclin probe; H2, RNA from hyperplasias hybridized with the WEHV2 rv-cyclin probe; DS, RNA from dermal sarcomas hybridized with WDSV rv-cyclin probe. The fall blots were exposed to film for 4 days, while the spring blots were exposed to film for 24 h.
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