Insight into aphid mediated Potato Virus Y transmission: A molecular to bioinformatics prospective

Abstract

Potato, the world's most popular crop is reported to provide a food source for nearly a billion people. It is prone to a number of biotic stressors that affect yield and quality, out of which Potato Virus Y (PVY) occupies the top position. PVY can be transmitted mechanically and by sap-feeding aphid vectors. The application of insecticide causes an increase in the resistant vector population along with detrimental effects on the environment; genetic resistance and vector-virus control are the two core components for controlling the deadly PVY. Using transcriptomic tools together with differential gene expression and gene discovery, several loci and genes associated with PVY resistance have been widely identified. To combat this virus we must increase our understanding on the molecular response of the PVY-potato plant-aphid interaction and knowledge of genome organization, as well as the function of PVY encoded proteins, genetic diversity, the molecular aspects of PVY transmission by aphids, and transcriptome profiling of PVY infected potato cultivars. Techniques such as molecular and bioinformatics tools can identify and monitor virus transmission. Several studies have been conducted to understand the molecular basis of PVY resistance/susceptibility interactions and their impact on PVY epidemiology by studying the interrelationship between the virus, its vector, and the host plant. This review presents current knowledge of PVY transmission, epidemiology, genome organization, molecular to bioinformatics responses, and its effective management.

Keywords: Potato Virus Y (PVY); aphid; bioinformatics; genome; molecular; potato; transcriptome; vector.

Figure 1

In the former, coat protein (CP) of virus interact directly with the binding sites (receptors) present in the stylet of aphid; in later, an additional non-structural protein namely HC-Pro (helper component proteinase) induces the binding between CP and aphid receptor component, thus creates a reversible “molecular bridge” that leads to effective infection by the aphid vector. In relation to aphid transmission, HC-Pro N-terminal domain (KITC—Lysine/Isoleucine/Threonine/Cysteine) is involved in specific binding to an aphid's stylet tip (acrostyle); while it's C-terminal domain (PTK-Proline/Threonine/Lysine) is involved either directly or indirectly in HC-Pro binding to the DAG motif (Aspartic acid/Alanine/Glycine) at the CP N-terminus.

Figure 2

Potyvirus proteins and their functions (Mishra et al., 2014). P1 Proteinase—Cell to cell movement; HC-Pro— Aphid mediated transmission, cell to cell movement; P3—Role in replication; CI—Genome replication (RNA helicase), membrane attachment, ATPase activity, cell to cell movement; VPg—Genome replication (Primer for initiation of RNA synthesis); NIa—Major Proteinase; NIb—Genome replication (RNA-dependent RNA polymerase [RdRp]); CP—RNA encapsidation, involved in vector transmission, cell to cell movement; 6K1, 6K2—Possible roles in RNA replication, regulatory function, inhibiting NIa nuclear translocation.

Figure 3

Interaction between potato and Potato Virus Y depicting incompatible and compatible resistance and susceptibility reaction in different potato varieties. Differential reactions (Extreme resistance, hypersensitive resistance, tolerance and sensitivity) are determined by the host genotype, viral strain, and environmental factors, and appear as varied responses in terms of virus replication and disease morphologies. Images representing symptoms on leaves 6 days after inoculation in selected cultivars of potato in optimum environment condition (Modified from Baebler et al., 2020).

Figure 4

EPG studies on potato-aphid interactions showing PVY transmission. (A) Depicts EPG system set-up with waveform pattern, (B) Represents typical waveforms corresponding to different feeding phase and several potential drop (pd) phases are depicted according to different feeding functions. (Adopted from Martin et al., 1997).

Figure 5

RNAi mediated gene silencing and direct dsRNA uptake for management of PVY. (A) Foliar spray of artificial exogenous dsRNA to the potato plant, (B) Piercing-sucking stylets acquire the virus from the phloem tissues of the plant, (C) Uptake of dsRNA to the cells of aphid, (D) The cellular RNAi mechanism of gene silencing in insects is illustrated. The RNAi molecular mechanism began in the cell with the Dicer 2 (Dcr2) enzyme cleaving dsRNA into short 21-24 nucleotide small interfering RNA (siRNA) duplexes. Following that, siRNAs are bound by Argonaute 2 (Ago2) proteins, which assemble the siRNA duplexes into the RNA-induced silencing complex (RISC), a multiprotein-siRNA structure. The RISC then mediates the cleavage of mRNA transcripts complementary to the integrated guide strand, thereby silencing the target gene and blocking protein translation (Modified from Cooper et al., 2019).