During an infection with cowpea mosaic virus (CPMV) both virion assembly and formation of tubules associated with plasmodesmata are required for cell-to-cell movement. These functions are encoded by the M-RNA of CPMV. To study the mechanism of CPMV movement, mutant N123 was used in complementation studies with sunn-hemp mosaic virus (SHMV), a legume-infecting tobamovirus. Previous studies have shown that N123 fails to spread in cowpea plants because of mutation(s) in its M-RNA. However, the mutant was efficiently replicated in cowpea protoplasts, in which virions were formed and tubular transport structures were induced. After high-dose inoculation of cowpeas with N123, only a few infected protoplasts could be isolated, indicating that cell-to-cell transport of N123 was greatly impaired, if not completely abolished. Upon coinoculation 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 lacking the tubule-inducing function, were complemented by SHMV to only low levels. It is concluded that SHMV-facilitated spread of CPMV in the non-virion tobamovirus mode is inefficient and that spread of mutant N123 is probably in the CPMV mode, SHMV providing an as yet unidentified helper function.


Article metrics loading...

Loading full text...

Full text loading...


Most cited this month Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error