Induction of plant defenses in response to Citrus leprosis virus C and Brevipalpus
spp., the components of citrus leprosis pathosystem. GD Arena1,2,3; PL Ramos3; VM
Novelli3; MA Nunes3; AJ Soares3; T Sinico3; J Freitas-Astúa4; MA Machado3.
1
ESALQ/USP, Piracicaba-SP. 2Unicamp, Campinas-SP. 3Centro APTA Citros Sylvio
Moreira/IAC, Cordeirópolis-SP. 4Embrapa Cassava and Fruits, Cruz das Almas-BA.
Financial support: INCT Citrus, FAPESP (2012/18771-0, 2014/00366-8) and CNPq
(573848/08-4 and 375843/2012-4)
Citrus leprosis is an atypical and economically important disease caused by Citrus
leprosis virus C (CiLV-C) and transmitted by Brevipalpus spp. mites. CiLV-C can
infect citrus and other 40 plant species always inducing chlorotic and necrotic lesions
around the mite feeding sites and systemic infection is never accomplished. To unveil
the mechanisms underlying such singular interaction, we evaluated the activity of plant
defenses along a time course during mite feeding and viral infection in Arabidopsis
thaliana and Citrus sinensis. We searched for reactive oxygen species (ROS)
production and cell death by histochemical analyses, and evaluated expression patterns
of genes associated to plant defense pathways by RT-qPCR. When non-viruliferous
mites were used, ROS accumulation and salicylic acid (SA) pathway were induced.
Only the branch of the jasmonate/ethylene (JA/ET) pathways that confers resistance to
necrotrophic pathogens -and not to herbivorous- was activated, suggesting a
manipulation of plant signaling by mites. Upon mite mediated-infection of CiLV-C,
ROS bursts were enhanced and dead cells were detected. In infected leaves, both SA
pathway and RNA silencing were up-regulated, whereas the expression of JAdependent genes was suppressed. Results indicate a coordinated action of SA response
and RNA silencing to counteract viral infection, an antagonistic SA-JA interplay and
the activation of an HR-like response in cells surrounding the feeding sites of
viruliferous mites. Hence, we suggest that the typical leprosis symptoms are indeed a
delayed HR. This work validates the use of A. thaliana as a CiLV-C experimental host
and proposes a model to study mite/CiLV-C/plant interaction.