Begomovirus-Associated Betasatellite Virulence Factor βC1 Attenuates Tobacco Defense to Whiteflies via Interacting With Plant SKP1

Abstract

Plant-mediated interactions between plant viruses and their vectors are important determinants of the population dynamics of both types of organisms in the field. The whitefly Bemisia tabaci can establish mutualism with begomoviruses via their shared host plants. This mutualism is achieved by the interaction between virulence factors and their host proteins. While the virulence factor bC1 encoded by tomato yellow leaf curl China betasatellite (TYLCCNB), a subviral agent associated to the begomovirus tomato yellow leaf curl China virus (TYLCCNV), may interact with plant protein MYC2, thereby establishing the indirect mutualism between TYLCCNV and whitefly, whether other mechanisms are involved remains unknown. Here, we found the in vitro and in vivo interactions between bC1 and tobacco protein S-phase kinase associated protein 1 (NtSKP1). Silencing the expression of NtSKP1 enhanced the survival rate and fecundity of whiteflies on tobacco plants. NtSKP1 could activate the transcription of genes in jasmonic acid (JA) pathways by impairing the stabilization of JAZ1 protein. Moreover, bC1-NtSKP1 interaction could interfere JAZ1 degradation and attenuate the plant JA defense responses. These results revealed a novel mechanism underlying the better performance of whiteflies on TYLCCNV/TYLCCNB-infected plants.

Virus‐induced phytohormone dynamics and their effects on plant–insect interactions

“…First, by interacting with the plant transcription factor MYC2, βC1 interferes with the plant’s JA‐signaling pathway to reduce downstream terpenoid synthesis (Li et al ., 2014). Second, βC1 interacts with tobacco protein S‐phase kinase‐associated protein 1, resulting in enhanced JAZ1 stability and the attenuation of the plant’s JA defense responses (Zou et al ., 2020). Finally, within the phloem, βC1 binds to the plant transcription factor WRKY20.…”

“…Methods: Genomics, transcriptomics, metabolomics and molecular biology Results: (a) βC1 encoded by TYLCCNV interferes with plant JA pathway (Zhang et al, 2012) (b) βC1 suppresses terpenoid synthesis (Luan et al, 2013) (c) βC1 interacts with the plant transcription factor MYC2 (Li et al, 2014) (d) βC1 binds to WRKY20 to redeploy plant defenses including JA pathway, thereby benefiting vector whitefly but negatively affecting two non-vector competitors (Zhao et al, 2019) (e) βC1 interacts with tobacco protein S-phase kinase associated protein 1, thereby interfering with JAZ1 degradation and JA pathway (Zou et al, 2020) (f) βC1 binds to PIFs to compromise terpene synthesis (Zhao et al, 2021)…”

“…This enhanced whitefly performance is a result of the viral satellite βC1 protein, which suppresses JA biosynthesis/catabolism, JA signaling and terpenoid biosynthesis/catabolism (Zhang et al ., 2012; Luan et al ., 2013b). Mechanistically, interactions between βC1 and several plant proteins are known, including three transcription factors (MYC2, WRKY20 and PHYTOCHROME‐INTERACTING FACTOR) and the S‐phase kinase‐associated protein 1 (Li et al ., 2014; Zou et al ., 2020; Zhao et al ., 2019, 2021). Similarly, the infection by tomato yellow leaf curl virus (TYLCV) in tomato interferes with JA signaling, leading to suppression of plant defenses and, in turn, enhanced performance of its whitefly vector (Su et al ., 2016).…”

Tomato chlorosis virus–encoded p22 suppresses auxin signalling to promote infection via interference with SKP1‐Cullin‐F‐boxTIR1 complex assembly

“…The βC1 protein encoded by CLCuMuV betasatellite is known to interact with the N-terminus of NbSKP1.1 to destabilize the integrity of SCF COI1 complex and to subvert ubiquitination, leading to suppressed responses to JA and GA (Jia et al, 2016). Tomato yellow leaf curl China betasatellite (TYLCCNB)-encoded βC1 interacts with NtSKP1 to interfere JAZ1 degradation and attenuate the plant JA defense responses and may enhance the survival rate and fecundity of whiteflies on tobacco plants (Zou et al, 2020). In the case of ToCV p22, another possibility is that p22 may contain a cryptic F-box motif and form a new ligase complex with SKP1.1 and CUL1 (Figure 7), thus mediating target proteins to be ubiquitinated and degraded through 26S proteasome pathway.…”

Inhibition of browning problem during the callogenesis of Spartium junceum L.

“…Also, in order to investigate isoflavone compounds, the stem and nodal segments with axillary buds were cultured on medium MS containing 0.5 mg L -1 BA. After one month, shoot proliferation was found (Clematisa et al, 2014). Since browning disorder is occurred during all phases of in vitro culture of S. junceum and causes plant material to be lose, the present study was done with the purpose of control and preventing explants from browning during disinfection and Callogenesis phases using exposure time of sterilants (ethanol and sodium hypochlorite), antioxidant compounds (PVP, activated charcoal, Curcumin), plant growth regulators (2,4-D and BA), and by changing light/ dark conditions was designed.…”