.png){kind=icon}
.png){kind=icon}
Return
Shallot virus X p42 Protein Expressed in Concert with Virus Movement Proteins Is a Suppressor of Two Plant Antiviral Defense Mechanisms
.png){kind=icon}
PRE
AI
D
A
E
A
A
S
A
DOI：10.3390-plants14162552.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
The genomes of viruses in the Allexivirus genus encode the p42 protein, which is considered the hallmark of the genus. The functions of p42 have not yet been studied experimentally and cannot be predicted based on sequence similarity, as p42-related proteins are not found among known cell or viral proteins. Here, p42 of Shallot virus X (ShVX), the type allexivirus, is demonstrated to be translated via a leaky scanning mechanism on a template comprising three “triple gene block” (TGB) transport genes and the p42 gene. Sequence analysis shows that this p42 expression mechanism is conserved in the vast majority of allexiviruses. p42 binds single-stranded RNA (ssRNA) but not double-stranded RNA (dsRNA) in vitro and localizes to the cytoplasm in association with microtubules and microtubule-bound bodies. In transient expression assays, p42 exhibits weak but detectable suppression of silencing induced by ssRNA but not by dsRNA. In addition, p42 suppresses silencing in the context of virus infection. Furthermore, p42 inhibits nonsense-mediated RNA decay (NMD) induced by a long 3′-terminal untranslated region of mRNA. Taken together, these findings provide initial evidence that the ShVX TGB-p42 gene module functions as a single genomic unit in terms of protein expression, that p42 acts as a suppressor of NMD and silencing, and that it may have multiple roles, while the precise biological significance of p42 in these roles remains to be experimentally confirmed.
Keywords:
plant virus
plant defense response
RNA silencing
nonsense-mediated decay
virus protein
silencing suppressor
RNA binding
microtubules
expression mechanism
leaky scanning
Journal
IF:
4.1
Papers:
2.2W
Citations:
6.4W
Organization
No organization information available
Cited Papers