Boea hygrometrica resurrection plants require a period of acclimation by slow soil-drying in order to survive a subsequent period of rapid desiccation. The molecular basis of this observation was investigated by comparing gene expression profiles under different degrees of water deprivation. Transcripts were clustered according to the expression profiles in plants that were air-dried (rapid desiccation), soil-dried (gradual desiccation), rehydrated (acclimated) and air-dried after acclimation. Although phenotypically indistinguishable, it was shown by principal component analysis that the gene expression profiles in rehydrated, acclimated plants resemble those of desiccated plants more closely than those of hydrated acclimated plants. Enrichment analysis based on gene ontology was performed to deconvolute the processes that accompanied desiccation tolerance. Transcripts associated with autophagy and α-tocopherol accumulation were found to be activated in both air-dried, acclimated plants and soil-dried non-acclimated plants. Furthermore, transcripts associated with biosynthesis of ascorbic acid, cell wall catabolism, chaperone-assisted protein folding, respiration and macromolecule catabolism were activated and maintained during soil-drying and rehydration. Based on these findings, we hypothesize that activation of these processes leads to the establishment of an optimal physiological and cellular state that enables tolerance during rapid air-drying. Our study provides a novel insight into the transcriptional regulation of critical priming responses to enable survival following rapid dehydration in B. hygrometrica.

The conversion of lignocellulosic feedstocks to fermentable sugar for biofuel production is inefficient, and most strategies to enhance efficiency directly target lignin biosynthesis, with associated negative growth impacts. Here we demonstrate, for both laboratory- and field-grown plants, that expression of Pag-miR408 in poplar (Populus alba × P. glandulosa) significantly enhances saccharification, with no requirement for acid-pretreatment, while promoting plant growth. The overexpression plants show increased accessibility of cell walls to cellulase and scaffoldin cellulose-binding modules. Conversely, Pag-miR408 loss-of-function poplar shows decreased cell wall accessibility. Overexpression of Pag-miR408 targets three Pag-LACCASES, delays lignification, and modestly reduces lignin content, S/G ratio and degree of lignin polymerization. Meanwhile, the LACCASE loss of function mutants exhibit significantly increased growth and cell wall accessibility in xylem. Our study shows how Pag-miR408 regulates lignification and secondary growth, and suggest an effective approach towards enhancing biomass yield and saccharification efficiency in a major bioenergy crop.

Abiotic stresses disrupt protein folding and induce endoplasmic reticulum (ER) stress, which in turn activates the unfolded protein response (UPR) to aid in the refolding or degradation of misfolded proteins. The phytohormone ABA regulates many aspects of plant development and plays a central role in the stress response; however, the role of ABA in transducing stress signals to activate the UPR has not been recognized. In this study, a gene encoding the maize ortholog of AtbZIP17, a transmembrane transcription factor functioning as an ER stress transducer, was identified from the MaizeGDB database, and designated ZmbZIP17. ZmbZIP17 was induced by both ABA and ER stress-eliciting agents such as dithiotreitol (DTT) and tunicamycin (TM). Transiently expressed yellow fluorescent protein (YFP)–ZmbZIP17 co-localized with the ER marker HDEL–mCherry under control conditions, but partially translocated into the nucleus upon TM treatment or removal of the transmembrane domain. TM-induced processing of ZmbZIP17 was confirmed by Western blot analysis. When overexpressed in Arabidopsis, ZmbZIP17 triggered ER stress response gene expression and tolerance to DTT and TM, elevated ABA-responsive gene expression and ABA sensitivity both pre- and post-germination. Additionally, ABA was found to induce ER stress response gene expression, alone or synergistically with ZmbZIP17, in the absence of DTT or TM; while ZmbZIP17 was capable of interacting with ABA-responsive cis-elements (ABREs) that exist in promoters of known ABA-responsive genes. Together, our results reveal a direct link between ER stress and ABA signaling pathways involving the ZmbZIP17 transcription factor.