Ambivalent roles of nonsense-mediated mRNA decay in heat stress tolerance

NMD-deficient Arabidopsis thaliana upf1-5 and upf3-1 show a biphasic heat-stress memory phenotype: transiently higher tolerance early recovery, then increased sensitivity during late recovery.

• Why it matters: RNA degradation pathways are known to shape gene regulation, but how nonsense-mediated mRNA decay (NMD) tunes the shift from stress response to later recovery is unclear.
• What they did: Using a long-term acquired thermotolerance assay, the study compared heat tolerance in NMD mutants (upf1-5, upf3-1) and analyzed genetic interactions with upf3;hsfa2 and upf3;hsfa3, plus transcriptome profiling under non-treated and triggering stress.
• The result: NMD deficiency likely causes early tolerance via baseline priming of heat-shock transcripts, while later sensitivity aligns with reduced HsfA2-I and attenuated HsfA2-dependent thermomemory regulon, alongside immune upregulation and repression of developmental/cell-wall pathways.

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