DEFECTIVE CELL-TO-CELL MOVEMENT OF COWPEA MOSAIC-VIRUS MUTANT N123 ISEFFICIENTLY COMPLEMENTED BY SUNN-HEMP MOSAIC-VIRUS

During an infection with cowpea mosaic virus (CPMV) both virion assemb ly and formation of tubules associated with plasmodesmata are required for cell-to-cell movement. These functions are encoded by the M-RNA o f CPMV. To study the mechanism of CPMV movement, mutant N123 was used in complementation studies with sunn-hemp mosaic virus (SHMV), a legum e-infecting tobamovirus. Previous studies have shown that N123 fails t o spread in cowpea plants because of mutation(s) in its M-RNA. However , the mutant was efficiently replicated in cowpea protoplasts, in whic h virions were formed and tubular transport structures were induced. A fter high-dose inoculation of cowpeas with N123, only a few infected p rotoplasts could be isolated, indicating that cell-to-cell transport o f N123 was greatly impaired, if not completely abolished. Upon coinocu lation with SHMV, mutant N123 infected cowpea plants systemically and accumulated to levels which were comparable to those of wild-type CPMV . In contrast, separate B-RNA of CPMV and a CPMV deletion mutant lacki ng the tubule-inducing function, were complemented by SHMV to only low levels. It is concluded that SHMV-facilitated spread of CPMV in the n on-virion tobamovirus mode is inefficient and that spread of mutant N1 23 is probably in the CPMV mode, SHMV providing an as yet unidentified helper function.