SummaryA model is presented describing the gene regulatory network surrounding three similar NAC
transcription factors that have roles in Arabidopsis leaf senescence and stress responses.
ANAC019, ANAC055 and ANAC072 belong to the same
clade of NAC domain genes and have overlapping expression patterns. A combination of promoter
DNA/protein interactions identified using yeast 1-hybrid analysis and modelling using gene
expression time course data has been applied to predict the regulatory network upstream of these
genes. Similarities and divergence in regulation during a variety of stress responses are predicted
by different combinations of upstream transcription factors binding and also by the modelling.
Mutant analysis with potential upstream genes was used to test and confirm some of the predicted
interactions. Gene expression analysis in mutants of ANAC019 and
ANAC055 at different times during leaf senescence has revealed a distinctly
different role for each of these genes. Yeast 1-hybrid analysis is shown to be a valuable tool that
can distinguish clades of binding proteins and be used to test and quantify protein binding to
predicted promoter motifs.
Cells naïve to stress can display the effects of stress, such as DNA damage and apoptosis, when they are exposed to signals from stressed cells; this phenomenon is known as the bystander effect. We previously showed that bystander effect induced by ionising radiation are mediated by extracellular vesicles (EVs). Bystander effect can also be induced by other types of stress, including heat shock, but it is unclear whether EVs are involved. Here we show that EVs released from heat shocked cells are also able to induce bystander damage in unstressed populations. Naïve cells treated with media conditioned by heat shocked cells showed higher levels of DNA damage and apoptosis than cells treated with media from control cells. Treating naïve cells with EVs derived from media conditioned by heat shocked cells also induced a bystander effect when compared to control, with DNA damage and apoptosis increasing whilst the level of cell viability was reduced. We demonstrate that treatment of naïve cells with heat shocked cell-derived EVs leads to greater invasiveness in a trans-well Matrigel assay. Finally, we show that naïve cells treated with EVs from heat-shocked cells are more likely to survive a subsequent heat shock, suggesting that these EVs mediate an adaptive response. We propose that EVs released following stress mediate an intercellular response that leads to apparent stress in neighbouring cells but also greater robustness in the face of a subsequent insult.
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