CaNAC2c acts modulator in the tradeoff among pepper growth, adaptation
to high temperature stress and resistance to Ralstonia solanacearum
infection
Abstract
In their natural habitats, plants are inevitably exposed to different
biotic and abiotic stresses, to maximize fitness, their adaptation to
these stresses should be appropriately coordinated by trade-offs among
growth and stress response. However, the involved players and their
possible mode of action remain to be investigated. Herein, by approaches
of reverse genetics including virus induced gene silencing (VIGS),
transient overexpression in pepper or ecoptic overexpression in
Nicotiana benthamiana, ChIP-PCR and physiology, CaNAC2c was functionally
characterized in trade-offs between growth and immunity against
Ralstonia solanacearum inoculation (RSI) or thermotolerance. Our results
demonstrate that CaNAC2c remains lower level of transcripts in absence
of stress and functions negatively in pepper growth, but is upregulated
and functions positively in pepper response to high temperature stress
(HTS) and to RSI probably via signaling mediated by ABA and JA,
respectively. CaNAC2c functions by directly targeting CaHSFA5 and
decreasing H2O2 accumulation upon HTS. On the other hand, it acts
positively in pepper response to RSI by upregulating JA- and enhancing
accumulation of H2O2, while downregulating SA-signaling mediated PR
genes, but does not target or regulate CaHSFA5. In addition, CaNAC2c
exhibits redundancy with CaNAC2d in response to challenge of RSI but not
to that of HTS, indicating that immunity against RSI is more robust than
thermotolerance. These findings collectively unveil that tradeoff
between growth and thermotolerance/immunity mediated by CaNAC2c is
mainly determined by its differential transcription, while tradeoff
between thermotolerance and immunity mediated by CaNAC2c is conferred by
its context dependent post-translational regulation.