Geminiviruses rely heavily on the host cellular machinery and interact with a wide range of plant proteins and processes during infection. They change host gene expression patterns, inhibit cell death pathways, and interfere with cell signalling and protein turnover to redirect or block host defences and hormone signalling.
Protein modification by ubiquitin (Ub) modulate protein function, regulate many plant processes including development, the cell cycle, and responses to abiotic and biotic stresses. We will present the recent progress made in understanding geminivirus interactions with ubiquitination pathway and their consequences on viral infection and propagation. The interaction of C2 protein with the signalosome catalytic subunit CSN5, that alters CUL1-based SCF ubiquitin E3 ligases will be used as an example. Although response to hormones controlled by SCF ligases (jasmonates, auxins, gibberellins, ethylene, and abscisic acid) is altered in transgenic plants expressing C2, transcriptomic analysis highlights the response to jasmonates as the main SCF-dependent process affected by C2. The fact that C2 also interacts with a JAZ protein, suggests, that geminiviruses reduce the sensitivity to jasmonate by a dual mechanism. Transgenic plants expressing C2 are less sensitive to jasmonate treatment and increase the vector survival. Besides infection of jasmonate impaired coi1 mutants shows that disturbance of the jasmonate-response pathway also alter viral infection.
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