Some transposable elements affect the genes they mutate by bringing their expression under the control of a second unlinked locus that is termed a modifier. The modifier gene is referred to as an enhancer or a suppressor locus, depending on the type of effect exerted by mutations in this gene on the phenotype of the transposable element-induced mutation. This type of phenomenon has been documented extensively in yeast and Drosophila (for reviews, see Roeder and Fink 1983;Rubin 1983;Kubli 1986; Parkhurst and Corces 1986b;Rutledge et al. 1988

PVC-211 murine leukemia virus (MuLV) is a replication-competent, ecotropic type C retrovirus that was isolated after passage of the Friend virus complex through F344 rats. Unlike viruses in the Friend virus complex, it does not cause erythroleukemia but causes a rapidly progressive hind limb paralysis when injected into newborn rats and mice. We have isolated an infectious DNA clone (clone 3d) of this virus which causes neurological disease in animals as efficiently as parental PVC-211 MuLV. The restriction map of clone 3d is very similar to that of the nonneuropathogenic, erythroleukemogenic Friend murine leukemia virus (F-MuLV), suggesting that PVC-211 MuLV is a variant of F-MuLV and that no major structural alteration was involved in its derivation. Studies with chimeric viruses between PVC-211 MuLV clone 3d and wild-type F-MuLV clone 57 indicate that at least one determinant for neuropathogenicity resides in the 2.1-kb XbaI-ClaI fragment * Corresponding author. PVC-211 MuLV plays no significant role in neuropathogenicity but may be responsible for the failure of this virus to cause erythroleukemia. MATERIALS AND METHODS Cells and viruses. PVC-211 MuLV-producing normal rat kidney (NRK) cells (18) were obtained from B. Pogo, The Mount Sinai Medical Center, New York, N.Y., with the permission of K. Kai, Yamaguchi University, Yamaguchi, Japan. Supernatant from these cells was used to infect NIH 3T3 cells, and the virus-producing culture (104 to 105 XC-PFU/ml) was used for these studies. NIH 3T3 cells transfected with an infectious DNA clone (clone 57 [25]) of F-MuLV was used as a producer of wild-type F-MuLV (105 to 106 XC-PFU/ml). All the cells were grown on Dulbecco's modified Eagle's medium supplemented with 10% fetal calf serum. Virus titer, infectivity, and host range were determined by XC cell fusion (33), mink S+Lcell focus induction (27), and reverse transcriptase (19) assays. Animals. Although PVC-211 MuLV also causes neurological disease in NFS/N mice (15), the disease had a more rapid onset and progression in F344 rats. Therefore, the ability of viruses to cause neurological disease was assessed by using newborn F344 rats obtained from Harlan Sprague Dawley, Indianapolis, Ind., and housed in the Small Animal Facility,

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