The Coat Protein Is Dispensable for the Establishment of Systemic Infections by Pea Enation Mosaic Enamovirus

Abstract

Deletions in the coat protein (CP) open reading frame (ORF)-3 of pea enation mosaic enamovirus (PEMV) did not inhibit the systemic movement of PEMV. As early as 48 h postinoculation, truncated viral RNAs were detected in the roots and uninoculated leaves of infected plants. The detected concentrations of truncated RNAs varied significantly between experiments but were similar to those extracted from plants infected with wild-type (WT)-PEMV. Pea plants infected with CP-less mutants exhibited wilting and necrosis that appeared faster and were more severe than observed in infections with WT-PEMV. Moreover, the absence of the CP-ORF and its protein product did not affect the formation of either double-membrane bound vesicles or replication complexes characteristic of infections by PEMV. The potential role of these structures as the movement vehicles of the infectious entity of PEMV in plants is discussed.

Role of Pea Enation Mosaic Virus Coat Protein in the Host Plant and Aphid Vector

“…With this unique symbiotic model, PEMV1 is unable to move cell-to-cell or systemically via the phloem without PEMV2, which encodes the movement protein [10,13]. Skaf and collaborators [34] observed similar results on PEMV by studying the long-distance movement of deletion mutants in the CP. In fact, PEMV1 has the capacity to move long-distance via the phloem without being encapsidated by using a replication complex or double-membrane-bound vesicles associated with its genome [14].…”