Vesicle transport between the ER and Golgi apparatus via SLOH4/MIP3 involves in long-term heat tolerance of Arabidopsis

Plants are often exposed not only to short-term (S-) heat stress but also to diurnal long-term (L-) heat stress over several consecutive days. To reveal the mechanisms underlying L-heat stress tolerance, we here employed a forward genetic screening of mutants that were sensitive to long-term heat (sloh). We isolated sloh4 that was hypersensitive to L-heat stress but not to S-heat stress. The causal gene of sloh4 was identical to MIP3 encoding a member of MAG2 tethering complex localized at the endoplasmic reticulum (ER) membrane. The ER stress and the following unfolded protein response (UPR) were drastically facilitated in sloh4 under the L-heat stress compared with WT. Interestingly, in sloh4, the expression levels of bZIP60-regulated UPR genes were specifically and drastically induced under L-heat stress, whereas those of bZIP28- and bZIP28/60-regulated genes were comparable with WT. In addition, the accumulation of the spliced bZIP60 transcript and the regulated IRE1-dependent decay (RIDD) was observed in sloh4 in response to the L-heat stress. These findings suggested that the misfolded proteins generated in sloh4 under the L-heat stress may be recognized by IRE1 but not bZIP28, resulting in initiation of the UPR via activated bZIP60. Then, vesicle transport between the ER and Golgi apparatus via MAG2-SLOH4/MIP3 complex plays an important role in L-heat tolerance, and IRE1-bZIP60 regulates the UPR pathway in response to the L-heat stress.