Monika R, PSG College of Technology, Coimbatore
Geminiviruses are plant viruses that cause economically important plant diseases worldwide. These viruses are proliferating globally and have attracted considerable scientific interest during the past 30 years. These viruses have circular ssDNA genomes and initiate infection with the discharge of viral ssDNA into the nucleus of the host, subsequently resulting in the replication, transcription, and translation of the viral genome. The viral proteins help to facilitate virus replication, movement and counteract plant host defence responses.
Recent findings have provided new insights into the structure and function of those proteins and have identified numerous host-interacting patterns. Most of the viral proteins are multifunctional and have evolved coordinated interactions with host proteins to confirm a successful infection.
Geminiviruses present a new threat to global food security and sustainability, by causing heavy losses on food and cash crops, like cassava, tomatoes, grain legumes, vegetables, and cotton. During the last 20 years, newly emerging geminiviruses have threatened crop production. Because of these reasons, geminiviruses have been characterized extensively at the molecular level.
Recently a review was presented by Neha Gupta and Kishorekumar Reddy, supported by the Molecular Virology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi. “Our review deals with past and up-to-date findings of major plant immune responses operated against the geminiviruses and a short discussion on anti-host defense responses,” said Kishore, an employee at the National Institute of Plant Genome Research. Here, an up-to-date review of viral protein function and their dynamic competition with host responses are presented, and a few areas requiring further research are also identified.
Plant’s defense strategies against Geminivirus
Plants have evolved to develop very complex defense strategies against geminiviral infection. RNA silencing is one of the prominent mechanisms. While transcriptional gene silencing (TGS) carries out viral genome methylation, resulting in the repression of viral proteins, post-transcriptional gene silencing (PTGS) mediates the degradation of the viral mRNAs, thereby inhibiting the virus infection. Several chromatin re-modelers have evolved in plants that perform repressive modifications on the host genome and divert targeting the viral genome. miRNAs ad R-genes also mediate defense against the geminiviruses, highlighted recently. Several other host defense regulatory mechanisms like autophagy, ubiquitination, hormonal signaling, protein kinases also play a major role in guarding and shielding the host from geminivirus.
Neha said, “Although there’s a large array of defense mechanisms, the geminivirus deploys various suppressor proteins and evolved sophisticated strategies against them, and emphasizes the dynamic relationship between the host and the pathogens.”
The dynamic relationship between the host and the virus
Due to the coevolution of plants and pathogenic viruses, plants acquired multiple strategies to defend and counter virus infection and pathogenesis via multiple host factors. However, viruses co-evolve to beat such resistance responses via viral factors.
Fig 1: Schematic overview of the dynamic relationship for co-evolution.
GRAB, RPT4a, EML1, SnRK1, RFP1, ATG8h, MEKK1, MKK2, MPK4, NIK-1 are host factors whereas Rep-A, VSRs, Rep, TrAP, βC1, C4 are the viral factors, whose interactions lead to a dynamic relationship for coevolution.
- In the host Triticum monococcum, GRAB interacts with RepA and interferes with the replication whereas RPT4a and EML1 obstruct the RNA Pol-II on virus euchromatin hampering the geminivirus active transcription. Additionally, the host induces RNAi via TGS and PTGS to suppress the viral gene expression. Virus-encoded VSRs potentially suppress the RNAi. This was concluded from research conducted by Islam and his colleagues.
- Similarly, in A. thaliana, Geminivirus activates SnRK1 which further activates the viral Rep, TrAP, and βC1 protein. Phosphorylation of Rep and TrAP causes a delay in the infection. βC1 phosphorylation hampers the TGS and PTGS suppressor functionalities and also reduces expression via suppression of AS1-βC1. Phosphorylated βC1 can also direct to autophagy.
- In N. tabacum, RFP1 interacts with βC1 via ubiquitin-mediated 26S proteasomal pathway prompts the βC1 degradation.
- In S. lycopersicum, ATG8h interacts with nuclear C1 and translocates to the cytosol, which is then recruited into autophagosomes with the help of ATG5 and ATG7 for vacuolar degradation.
- In N. benthamiana, the defense-regulated MEKK1-MKK1/MKK2-MPK4 module exerts the basal defense response. However, the βC1 protein directly interacts with MKK2 and MPK4, thereby suppressing the broad spectrum of defense reactions.
- In A. thaliana, NIK-1 from the plasma membrane triggers dimerization and autophosphorylation, while activated upon the geminivirus infection. Alternatively, PTI-induced DAMPs may cause NIK-1 activation. Active NIK-1 phosphorylates and translocates L10 into the nucleus where it binds to LIMYB to block the transcription and prevents the translation of viral genes.
Thus, the viruses have evolved multifunctional proteins that maintain a coevolutionary relationship with the host to invade the host defense machinery.
CRISPR-Cas9 for resistance against Geminivirus
The application of advanced genetic engineering methods like CRISPR-Cas9 has helped to beat the constraints of labor-intensive traditional approaches for developing resistant plants. It employs a bacterial adaptive immune strategy against invasive foreign nucleic acids that has been exploited to focus on plant viruses.
But in the case of Geminivirus, recombination allows swapping of genomic sequences during mixed infections and enables it to escape the CRISPR induced cleavage, subsequently resulting in CRISPR resistance.
In controlling global agricultural damage
Due to mixed virus infections, success is yet to be reached, although various conventional methods and molecular approaches are adopted to manage geminiviral infections. Identifying the appropriate host factors involved in the resistance during plant-geminivirus interaction can aid in the development of disease-free plants.
Though many of those interactions and their biological functions are elucidated, many are still poorly understood and more information will continue to be discovered to provide new opportunities in the design of virus control strategies.
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Source: Gupta, N., Reddy, K., Bhattacharyya, D., & Chakraborty, S. (2021). Plant responses to geminivirus infection: Guardians of the plant immunity. Virology Journal, 18(1), 143. https://doi.org/10.1186/s12985-021-01612-1
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About the author: Monika Raman is an undergraduate student pursuing her final year B. Tech in Biotechnology. She is an enthusiastic Biotech student aspiring for an opportunity to develop skills and grow professionally in the research field. Extremely motivated and possess strong interpersonal skills.
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