Summary auto-generated
This study examined the role of the C-terminal region of cowpea chlorotic mottle virus (CCMV) movement protein (MP) in cell-to-cell and long-distance viral movement. Researchers engineered six deletions removing 10-80 amino acids from the C-terminus of the MP gene and tested them in three plant species: Nicotiana benthamiana, Chenopodium quinoa, and cowpea. Results showed that most MP deletion mutants severely impaired viral movement when coat protein (CP) was absent. Notably, the ∆MP43 mutant, lacking 43 C-terminal amino acids, retained near-normal cell-to-cell movement capability. When these mutants were tested with wild-type CP present, movement patterns were significantly restored and varied dramatically between plant species. The ∆MP43 mutant achieved systemic spread in cowpea despite infection appearing benign. These findings demonstrate that the C-terminal region of CCMV MP contains critical functional elements necessary for movement, and that both MP and CP proteins must interact cooperatively with host factors to achieve efficient viral spread. The host plant species significantly influences how effectively mutant MPs facilitate viral movement.
Key findings
- C-terminal deletions of 10-80 amino acids in CCMV movement protein severely impaired cell-to-cell viral spread, except for the ∆MP43 mutant which retained near-normal movement despite removing 43 amino acids
- The presence of wild-type coat protein substantially restored movement capacity of most defective MP mutants, indicating MP and CP function cooperatively
- The same MP mutant behaved differently across the three plant species tested, with N. benthamiana being more permissive to viral movement than cowpea, suggesting host-specific factors regulate movement
- The ∆MP80 mutant showed complete loss of movement capacity, suggesting the RNA-binding domain of MP may reside within this region
- Long-distance movement requires functional MP C-terminal sequences, while coat protein can partially compensate for MP defects in local spread
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Abstract
In order to elucidate the function of the C-terminal region of cowpea chlorotic mottle bromovirus (CCMV) movement protein (MP) in cell-to-cell movement, a set of deletions ranging from 10 to 80 amino acids (DeltaMP10, DeltaMP20, DeltaMP33, DeltaMP43, DeltaMP60 and DeltaMP80) was engineered into the MP gene encoded by the biologically active clone C3/DeltaCP-EGFP, a variant of CCMV RNA3 that contained wild-type (wt) MP and the enhanced green fluorescent protein (EGFP) gene in place of the coat protein (CP). The effect of each MP deletion on cell-to-cell movement was examined in three susceptible host plants: Chenopodium quinoa, Nicotiana benthamiana and cowpea (Vigna sinensis cv. Black Eye). The results indicate that, except for mutant DeltaMP43, infections resulting from the deletion mutants remained subliminal. Interestingly, infections resulting from inoculating mutant DeltaMP43, which lacked the 43 most C-terminal amino acids, spread rapidly between cells and the number of infected cells expressing EGFP approached that of control inoculations made with C3/DeltaCP-EGFP. To verify whether the presence of wt CP altered the movement behaviour of these mutants, each MP deletion was also incorporated into the genetic background of wt CCMV RNA3 (pCC3) and inoculated independently to all three hosts. The results suggest that the overall movement process exhibited by each MP mutant is influenced profoundly by the presence of CP and the particular host plant tested.