Stability of Begomoviral pathogenicity determinant βC1 is modulated by mutually antagonistic SUMOylation and SIM interactions

Nair, Ashwin; Chatterji, Kiran Sankar; Vikram, J; Das, Ranabir; Shivaprasad, P. V.

doi:10.1101/2020.06.05.135830

Cited by 2 publications

(13 citation statements)

References 77 publications

(75 reference statements)

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“…As controls, p35S::GFP was used along with an empty vector. As expected and previously observed (Nair et al, 2020), βC1 enhanced viral titre (Figure 7A). In the presence of Nt RecA1 and WT βC1, but not with βC1-DM mutant, the accumulation of viral replicons increased.…”

Section: Resultssupporting

confidence: 92%

“…Based on phenotype as well as changes in host DDR genes, we hypothesised that the cause for the deregulation of such a huge number of chloroplast genes is likely due to selective plastid DNA destabilization by βC1. Chloroplast localized SyYVCV βC1 was previously identified as the causal protein for the symptoms during viral infection (Nair et al, 2020). To further confirm that βC1 is the protein responsible to induce chlorosis during viral infection, we infected N. tabacum leaves with SyYVCV DNA-A alone or with DNA-β and DNA-β with point mutations in βC1 ORF (DNA-βmβC1 (mSIM2,3,4;,(Nair et al, 2020)).…”

Section: Resultsmentioning

confidence: 99%

“…Chloroplast localized SyYVCV βC1 was previously identified as the causal protein for the symptoms during viral infection (Nair et al, 2020). To further confirm that βC1 is the protein responsible to induce chlorosis during viral infection, we infected N. tabacum leaves with SyYVCV DNA-A alone or with DNA-β and DNA-β with point mutations in βC1 ORF (DNA-βmβC1 (mSIM2,3,4;,(Nair et al, 2020)). The point mutations in the SIM region of βC1 completely abolishes βC1 functions.…”

Section: Resultsmentioning

confidence: 99%

“…The expression of chloroplast-localized βC1, a geminiviral pathogenicity determinant, is toxic to plants (Cui et al, 2004; Yang et al, 2008). We and others had previously reported a multitude of growth defects observed in host plants upon ectopic expression of βC1 (Nair et al, 2020; Bhattacharyya et al, 2015; Cheng et al, 2011; Briddon et al, 2003). Here we show that Synedrella yellow vein clearing virus (SyYVCV) βC1 (Das et al, 2018) induces selective degradation of cpDNA during viral infection.…”

Section: Introductionmentioning

confidence: 91%

“…Similarly, DAMPs and PAMPs are recognised by cell surface receptors such as RECEPTOR LIKE KINASES (RLKs) and RECEPTOR LIKE PROTEINS (RLPs) (Teixeira et al, 2019; Niehl et al, 2016; Nicaise and Candresse, 2017; Zorzatto et al, 2015). In line with the role of chloroplast in antiviral defense, various viral effectors disrupt the key process of chloroplast metabolism to sabotage PTI activation (Fondong et al, 2007; Gnanasekaran et al, 2019; Bhattacharyya et al, 2015; Nair et al, 2020; Medina-Puche et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

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Geminiviral βC1 orchestrates organellar genomic instability to augment viral infection by hijacking host RecA

Shivaprasad

Nair

Harshith

et al. 2021

Preprint

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Chloroplast is the site for transforming light energy to chemical energy. It also acts as a production unit for a variety of defense-related molecules. These defense moieties are necessary to mount a successful counter defence against pathogens including viruses. Geminiviruses disrupt chloroplast homeostasis as a basic strategy for their successful infection inducing vein-clearing, mosaics and chlorosis in infected plants. Here we show that a geminiviral pathogenicity determinant protein βC1 directly interferes with plastid homeostasis. βC1 was capable of inducing organelle-specific nuclease to degrade plastid genome as well as diverted functions of RecA1 protein, a major player in plastid genome maintenance. βC1 interacted with RecA1 in plants and its homolog in bacteria to reduce the ability of host cells to maintain genomic integrity under stresses. Further, reduction in the coding capacity of plastids severely affected retrograde signalling necessary for viral perception and activation of defense. Induction of chloroplast-specific nuclease by βC1 is similar to phosphate starvation-response in which nucleotides are recycled to augment synthesis of new, potentially viral, DNA. These results indicate the presence of a novel strategy in which a viral protein alters host defence by targeting regulators of chloroplast DNA. We predict that the mechanism identified here might have similarities in other plant-pathogen interactions.

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Geminiviral βC1 orchestrates organellar genomic instability to augment viral infection by hijacking host RecA

Shivaprasad

Nair

Harshith

et al. 2021

Preprint

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Plant responses to geminivirus infection: guardians of the plant immunity

Gupta

Reddy

Bhattacharyya

et al. 2021

Virol J

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Background Geminiviruses are circular, single-stranded viruses responsible for enormous crop loss worldwide. Rapid expansion of geminivirus diversity outweighs the continuous effort to control its spread. Geminiviruses channelize the host cell machinery in their favour by manipulating the gene expression, cell signalling, protein turnover, and metabolic reprogramming of plants. As a response to viral infection, plants have evolved to deploy various strategies to subvert the virus invasion and reinstate cellular homeostasis. Main body Numerous reports exploring various aspects of plant-geminivirus interaction portray the subtlety and flexibility of the host–pathogen dynamics. To leverage this pool of knowledge towards raising antiviral resistance in host plants, a comprehensive account of plant’s defence response against geminiviruses is required. This review discusses the current knowledge of plant’s antiviral responses exerted to geminivirus in the light of resistance mechanisms and the innate genetic factors contributing to the defence. We have revisited the defence pathways involving transcriptional and post-transcriptional gene silencing, ubiquitin-proteasomal degradation pathway, protein kinase signalling cascades, autophagy, and hypersensitive responses. In addition, geminivirus-induced phytohormonal fluctuations, the subsequent alterations in primary and secondary metabolites, and their impact on pathogenesis along with the recent advancements of CRISPR-Cas9 technique in generating the geminivirus resistance in plants have been discussed. Conclusions Considering the rapid development in the field of plant-virus interaction, this review provides a timely and comprehensive account of molecular nuances that define the course of geminivirus infection and can be exploited in generating virus-resistant plants to control global agricultural damage.

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Stability of Begomoviral pathogenicity determinant βC1 is modulated by mutually antagonistic SUMOylation and SIM interactions

Cited by 2 publications

References 77 publications

Geminiviral βC1 orchestrates organellar genomic instability to augment viral infection by hijacking host RecA

Geminiviral βC1 orchestrates organellar genomic instability to augment viral infection by hijacking host RecA

Plant responses to geminivirus infection: guardians of the plant immunity

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