bZIP17 regulates heat stress tolerance at reproductive stage in Arabidopsis

High temperature elicits a well-conserved response called the unfol ded protein response(UPR)to bring protein homeostasis in the endoplasmic reticulum(ER).Two key UPR regulators bZIP28 and bZIP60 have been shown to be essential for maintaining fertility under heat stress conditions in Arabidopsis,however,the function of transcriptional activator bZIP17,a paralog of bZIP28,in heat stress response at reproductive stage is not reported.Here we found that bzip17 mutant plants were sensitive to heat stress in terms of silique length and fertility comparing to that of wildtype(WT)Arabidopsis plants,and transcri ptomic analysis showed that 1380 genes were specifically up-regulated and 493 genes were specifically down-regulated by heat stress in the flowers of WT plants comparing to that in bzip17 mutant plants.These bZIP17-dependent up-regulated genes were enriched in responses to a biotic stresses such as water deprivation and salt stress.Further chromatin immuno-preci pitation coupled with high-throughput sequencing(ChIP-Seq)uncovered 1645 genes that were direct targets of bZIP17 in MYC-bZIP17 expressing seedlings subjected to heat stress.Among these 1645 genes,ERSE-II cis-element was enriched in the binding peaks of their promoters,and the up-regulation of 113 genes by heat stress in flowers was dependent on bZIP17.Our results revealed direct targets of bZIP17 in flowers during heat stress responses and demonstrated the important role of bZIP17 in maintai ning fertility upon heat stress in plants.

A vicinal oxygen chelate protein facilitates viral infection by triggering the unfolded protein response in Nicotiana benthamiana

Vicinal oxygen chelate(VOC)proteins are members of an enzyme superfamily with dioxygenase or non-dioxygenase activities.However,the biological functions of VOC proteins in plants are poorly understood.Here,we show that a VOC in Nicotiana benthamiana(NbVOC1)facilitates viral infection.NbVOC1 was significantly induced by infection by beet necrotic yellow vein virus(BNYVV).Transient overexpression of NbVOC1 or its homolog from Beta vulgaris(BvVOC1)enhanced BNYVV infection in N.benthamiana,which required the nuclear localization of VOC1.Consistent with this result,overexpressing NbVOC1 facilitated BNYVV infection,whereas,knockdown and knockout of NbVOC1 inhibited BNYVV infection in transgenic N.benthamiana plants.NbVOC1 interacts with the basic leucine zipper transcription factors bZIP17/28,which enhances their self-interaction and DNA binding to the promoters of unfolded protein response(UPR)-related genes.We propose that bZIP17/28 directly binds to the NbVOC1 promoter and induces its transcription,forming a positive feedback loop to induce the UPR and facilitating BNYVV infection.Collectively,our results demonstrate that NbVOC1 positively regulates the UPR that enhances viral infection in plants.