未折叠蛋白应答(UPR)和热激应答(HSR)是两个进化上保守的保护植物免受热胁迫的系统。UPR和HSR发生在不同的细胞隔间，这两种反应都是由错误折叠的蛋白质引起的，这些蛋白质在恶劣的环境条件下积累，如热应激。虽然UPR和HSR似乎是独立运行的，但我们在玉米(Zea Mays)中发现了它们之间的联系，涉及碱性亮氨酸ZIPPER60(BZIP60)转录因子的产生，这是UPR对热胁迫的关键反应。令人惊讶的是，一个突变体(bzip60-2)下调了bZIP60的表达，使HSR在高温下变钝，并阻止了一组热休克蛋白基因在高温下的正常上调。关键的热休克因子转录因子FCTOR13(HSFTF13，热休克因子A6b[HSFA6B]家族成员)在bzip60-2中的表达受到抑制，并且HSFTF13启动子被证明是bZIP60在玉米原生质体中的靶标。此外，在bzip60-2中，参与叶绿素分解代谢和叶绿体蛋白周转的基因在高温下表达上调，这些基因也被发现是bZIP60的靶标。
因此，UPR，一种与内质网相关的反应，出人意料地促进了玉米的核质HSR。
The unfolded protein response (UPR) and the heat shock response (HSR) are two evolutionarily conserved systems that protect plants from heat stress. The UPR and HSR occur in different cellular compartments and both responses are elicited by misfolded proteins that accumulate under adverse environmental conditions such as heat stress. While the UPR and HSR appear to operate independently, we have found a link between them in maize (Zea mays) involving the production of the BASIC LEUCINE ZIPPER60 (bZIP60) transcription factor, a pivotal response of the UPR to heat stress. Surprisingly, a mutant (bzip60-2) knocking down bZIP60 expression blunted the HSR at elevated temperatures and prevented the normal upregulation of a group of heat shock protein genes in response to elevated temperature. The expression of a key HEAT SHOCK FACTOR TRANSCRIPTION FACTOR13 (HSFTF13, a HEAT SHOCK FACTOR A6B [HSFA6B] family member) was compromised in bzip60-2, and the HSFTF13 promoter was shown to be a target of bZIP60 in maize protoplasts. In addition, the upregulation by heat of genes involved in chlorophyll catabolism and chloroplast protein turnover were subdued in bzip60-2, and these genes were also found to be targets of bZIP60. Thus, the UPR, an endoplasmic-reticulum–associated response, quite unexpectedly contributes to the nuclear/cytoplasmic HSR in maize.
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