The transition from juvenility through maturation to senescence is a complex process that involves the regulation of longevity. Here, we identify JUNGBRUNNEN1 (JUB1), a hydrogen peroxide (H 2 O 2 )-induced NAC transcription factor, as a central longevity regulator in Arabidopsis thaliana. JUB1 overexpression strongly delays senescence, dampens intracellular H 2 O 2 levels, and enhances tolerance to various abiotic stresses, whereas in jub1-1 knockdown plants, precocious senescence and lowered abiotic stress tolerance are observed. A JUB1 binding site containing a RRYGCCGT core sequence is present in the promoter of DREB2A, which plays an important role in abiotic stress responses. JUB1 transactivates DREB2A expression in mesophyll cell protoplasts and transgenic plants and binds directly to the DREB2A promoter. Transcriptome profiling of JUB1 overexpressors revealed elevated expression of several reactive oxygen species-responsive genes, including heat shock protein and glutathione S-transferase genes, whose expression is further induced by H 2 O 2 treatment. Metabolite profiling identified elevated Pro and trehalose levels in JUB1 overexpressors, in accordance with their enhanced abiotic stress tolerance. We suggest that JUB1 constitutes a central regulator of a finely tuned control system that modulates cellular H 2 O 2 level and primes the plants for upcoming stress through a gene regulatory network that involves DREB2A.

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The ability of plants to cope with abiotic environmental stresses such as drought, salinity, heat, cold or flooding relies on flexible mechanisms for re-programming gene expression. Over recent years it has become apparent that transcriptional regulation needs to be understood within its structural context. Chromatin, the assembly of DNA with histone proteins, generates a local higher-order structure that impacts on the accessibility and effectiveness of the transcriptional machinery, as well as providing a hub for multiple protein interactions. Several studies have shown that chromatin features such as histone variants and post-translational histone modifications are altered by environmental stress, and they could therefore be primary stress targets that initiate transcriptional stress responses. Alternatively, they could act downstream of stress-induced transcription factors as an integral part of transcriptional activity. A few experimental studies have addressed this 'chicken-and-egg' problem in plants and other systems, but to date the causal relationship between dynamic chromatin changes and transcriptional responses under stress is still unclear. In this review we have collated the existing information on concurrent epigenetic and transcriptional responses of plants to abiotic stress, and we have assessed the evidence using a simple theoretical framework of causality scenarios. This article is part of a Special Issue entitled: Plant Gene Regulatory Mechanisms and Networks, edited by Dr. Erich Grotewold and Dr. Nathan Springer.

Intrinsically disordered proteins can adopt multiple conformations, thereby enabling interaction with a wide variety of partners. They often serve as hubs in protein interaction networks. We have previously shown that the Histone Deacetylase Complex 1 (HDC1) protein from Arabidopsis (Arabidopsis thaliana) interacts with histone deacetylases and quantitatively determines histone acetylation levels, transcriptional activity, and several phenotypes, including abscisic acid sensitivity during germination, vegetative growth rate, and flowering time. HDC1-type proteins are ubiquitous in plants, but they contain no known structural or functional domains. Here, we explored the protein interaction spectrum of HDC1 using a quantitative bimolecular fluorescence complementation assay in tobacco (Nicotiana benthamiana) epidermal cells. In addition to binding histone deacetylases, HDC1 directly interacted with histone H3-binding proteins and corepressor-associated proteins but not with H3 or the corepressors themselves. Surprisingly, HDC1 also was able to interact with variants of the linker histone H1. Truncation of HDC1 to the ancestral core sequence narrowed the spectrum of interactions and of phenotypic outputs but maintained binding to a H3-binding protein and to H1. Thus, HDC1 provides a potential link between H1 and histone-modifying complexes.Regulation of gene transcription underpins plant development and dynamic responses to the environment. Transcription occurs in the context of chromatin, a highly condensed structure in which the DNA is wrapped around nucleosomes composed of histones H2A/B, H3, and H4 and further stabilized by linker histone H1 (Over and Michaels, 2014;Hergeth and Schneider, 2015). Alteration of chromatin structure plays an important part in transcriptional regulation and is achieved through multiprotein complexes that recognize and instigate biochemical modifications of the DNA and/or the histones (Pfluger and Wagner, 2007;Derkacheva et al., 2013). For example, binding of repressors to so-called corepressors recruits histone deacetylases (HDAs) to the gene region (Song et al., 2005). The HDAs in turn interact with histonebinding proteins (Mehdi et al., 2016). Removal of acetyl groups from Lys residues of the core histones leads to chromatin compaction and inhibition of transcription (Kouzarides, 2007;Roudier et al., 2009). Specific recruitment at both 'ends' of the repressive protein complex generates a double lock between DNA and the nucleosome: the repressors recognize certain DNA motifs in the gene promoters, and the histone-binding proteins recognize ('read') certain histone residues and their modifications (Liu et al., 2010). A minimal HDAC complex therefore needs to combine at least three protein functions: repressor binding, histone binding, and catalytic activity. Biochemical studies in yeast (Saccharomyces cerevisiae) and in animal systems have provided evidence for large multiprotein complexes linking a corepressor and a HDA with several histone-binding proteins and a range of associate...

HighlightAnalysis of salt-challenged, tocopherol-deficient potato plants revealed that stress-induced blocking of sugar export is not caused by plasmodesmatal plugging, but rather by direct effects of sugar signalling on export.