Fig. 1
From: Plant responses to geminivirus infection: guardians of the plant immunity
Schematic overview of plant immune strategies against geminiviruses. Geminivirus infection initiates with the release of viral ssDNA into the nucleus, subsequently leads to the replication, transcription and translation of viral genome. (A) Plants counteract geminivirus genetic life cycle via multiple host factors. GRAB interacts with RepA and interferes with the replication. RPT4a and EML1 hamper the geminivirus active transcription by obstructing the RNA Pol-II on virus euchromatin. Additionally, host induces RNAi via TGS and PTGS to suppress the viral gene expression. Virus-encoded VSRs potentially suppresses the RNAi. (B) Geminivirus induced GRIK1 autophosphorylates and activates SnRK1 which interact and phosphorylates the viral Rep, TrAP (AL2/C2) and βC1 protein. Phosphorylation of Rep and TrAP impedes Rep binding and causes a delay in the infection, respectively. βC1 phosphorylation hampers the TGS and PTGS suppressor functionalities and attenuates symptom expression via suppression of AS1-βC1 mediated downstream responses. Phosphorylated βC1 may also direct to autophagy. (C) Tobacco RFP1 interacts with βC1 and prompts the βC1 degradation via ubiquitin-mediated 26S proteasomal pathway and causes the symptom attenuation. (D) ATG8h interacts with nuclear C1 and translocate to cytosol XpoI dependent manner. The ATG8h-C1 complex is then recruited into autophagosomes with the aid of ATG5 and ATG7 for vacuolar degradation. (E) Defence regulated MEKK1-MKK1/MKK2-MPK4 module induced, activated by geminivirus infection and exerts the basal defence response. However, βC1 protein directly interacts with MKK2 and MPK4, thereby suppress the broad spectrum of downstream defence reactions. (F) NIK-1 from plasma membrane activated upon the geminivirus infection triggers dimerization and autophosphorylation. Alternatively, PTI induced DAMPs secreted from ER in response to virus attack may cause NIK-1 activation. Active NIK-1 phosphorylates and translocate L10 into the nucleus where it binds to LIMYB to block the transcription of ribosomal biosynthesis genes which affects the global translation and prevents the translation of viral genes