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Identifies AtDJB3's role in heat shock response and thermotolerance in plants, suggesting its importance for stress resilience.
Heat stress disrupts protein homeostasis, triggering the heat shock response (HSR) to maintain cellular proteostasis. A key aspect of this response is the release of heat shock factors (HSFs) from HSP70-mediated attenuation under heat shock conditions, making HSP70 a central regulator of HSR. However, the role of HSP70 co-chaperones in this process remains largely unexplored in plants. Our study identifies AtDJB3, a heat-inducible class II J-domain protein (JDP), as a critical modulator of HSR. Microscopy and cell fractionation show that loss of AtDJB3 impairs HSC70-1 recruitment to heat-induced protein aggregates, maintaining HSFA1d bound to HSC70-1 in the cytoplasm. Chromatin immunoprecipitation (ChIP) and promoter luciferase assays revealed that AtDJB3 is required for HSFA1d enrichment at promoters of key heat-inducible genes, linking AtDJB3 to transcriptional activation of genes, including HSC70-1, HSP90, HSP17.6, FES1A, and HOP3. Consistent with this, atdjb3 mutants displayed compromised thermotolerance, evidenced by their inability to survive prolonged heat stress of 37°C. Conversely, overexpression of AtDJB3 conferred enhanced thermotolerance, supporting its positive regulatory role in HSR. We propose that AtDJB3 not only contributes to the solubilization of heat-induced protein aggregates but also promotes HSFA1d activation by diverting HSC70-1 to aggregates, thereby releasing HSFA1d to drive the transcriptional heat shock response.
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Satheesh et al. (2026) studied this question.
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