The coat protein of tobacco mosaic virus as an anti-tobacco mosaic virus: a molecular dynamics simulation

Abstract

The Coat Protein (CP) of the Tobacco Mosaic Virus (TMV) executes an important duty in the protection of virus RNA. The interaction between the virus CP and host plant proteins induces infection in the host and creates dark and light green mosaics on crops, which disturb the growth and function of the plant. The interaction between the virus CP and the modified CP, expressed in transgenic plants, causes Coat Protein-Mediated Resistance (CP-MR), which reduces virus infection in transgenic plants. In this study, a model is suggested for resistance as “stop assembly of CP” in the virus. It is based on the fact that the CP, when mutated, acts as a dead-end in virus assembly. For evaluation of the model, we investigated the effect of four mutants including CB_T28I, AB_T42W, AB_D77R, and AB_T89W complexes on plant resistance against TMV infection by molecular dynamics simulation. Previous studies had shown the influence of such mutations on the CP-MR. The MD results of in the present study further confirmed the mentioned effect and demonstrated how the mutations could be the cause of CP-MR. The results are calculated by the RMSD, Rg, H-bond, and g-MMPBSA scripts. The change in binding energy between two chains is consistent with CP-MR such that with increase in binding energy, the affinity between two chains was reduced and the CP-MR increased. Based on this model, it is possible to design mutants with a high level of efficiency.

Communicated by Ramaswamy H. Sarma

Keywords:

• Tobacco mosaic virus
• coat protein
• coat protein-mediated resistance
• molecular dynamics simulation

Acknowledgment

The authors wish to thank the support from Yazd University and Tarbiat Modares University.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.