Open AccessActivation of senescence‐associated Dark‐inducible ( DIN ) genes during infection contributes to enhanced susceptibility to plant viruses
Author(s) -
FernándezCalvino Lourdes,
GuzmánBenito Irene,
Toro Francisco J.,
Donaire Livia,
CastroSanz Ana B.,
RuízFerrer Virginia,
Llave César
Publication year - 2016
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12257
Subject(s) - biology , nicotiana benthamiana , virus , rna interference , virology , gene silencing , gene , potato virus x , tobacco rattle virus , potexvirus , senescence , arabidopsis thaliana , gene expression , plant virus , genetics , microbiology and biotechnology , rna , mutant , coat protein
Summary Virus infections in plants cause changes in host gene expression that are common to other environmental stresses. In this work, we found extensive overlap in the transcriptional responses between A rabidopsis thaliana plants infected with T obacco rattle virus ( TRV ) and plants undergoing senescence. This is exemplified by the up‐regulation during infection of several senescence‐associated Dark‐inducible ( DIN ) genes, including At DIN1 ( S enescence 1 , SEN1 ), At DIN6 ( A sparagine synthetase 1 , At ASN1 ) and At DIN11 . DIN1 , DIN6 and DIN11 homologues were also activated in N icotiana benthamiana in response to TRV and P otato virus X ( PVX ) infection. Reduced TRV levels in RNA interference ( RNAi ) lines targeting At DIN11 indicate that DIN11 is an important modulator of susceptibility to TRV in A rabidopsis. Furthermore, low accumulation of TRV in A rabidopsis protoplasts from RNAi lines suggests that At DIN11 supports virus multiplication in this species. The effect of DIN6 on virus accumulation was negligible in Arabidopsis, perhaps as a result of gene or functional redundancy. However, TRV ‐induced silencing of Nb ASN , the DIN6 homologue in N . benthamiana , compromises TRV and PVX accumulation in systemically infected leaves. Interestingly, Nb ASN inactivation correlates with the appearance of morphological defects in infected leaves. We found that DIN6 and DIN11 regulate virus multiplication in a step prior to the activation of plant defence responses. We hypothesize on the possible roles of DIN6 and DIN11 during virus infection.