Gibberellins (GAs) and brassinosteroids (BRs) are important phytohormones that control plant development and responses to environmental cues by involving DELLA proteins and BRASSINAZOLE-RESISTANT1 (BZR1) respectively as key transcription factors. Here, we reveal a new role for JUNGBRUNNEN1 (JUB1) as a transcriptional regulator of GA/BR signalling in Arabidopsis thaliana. JUB1 directly represses the hormone biosynthesis genes GA3ox1 and DWARF4 (DWF4), leading to reduced levels of GAs and BRs and typical GA/BR deficiency phenotypes exhibiting short hypocotyls, dwarfism, late flowering and male sterility. JUB1 also directly represses PHYTOCHROME INTERACTING FACTOR4 (PIF4), a transcription factor connecting hormonal and environmental stimuli. On the other hand, JUB1 activates the DELLA genes GA INSENSITIVE (GAI) and RGA-LIKE 1 (RGL1). In addition, BZR1 and PIF4 act as direct transcriptional repressors upstream of JUB1, establishing a negative feedback loop. Thus, JUB1 forms the core of a robust regulatory module that triggers DELLA accumulation, thereby restricting cell elongation while concomitantly enhancing stress tolerance.

Kinetochores are supramolecular assemblies that link centromeres to microtubules for sister chromatid segregation in mitosis. For this, the inner kinetochore CCAN/Ctf19 complex binds to centromeric chromatin containing the histone variant CENP‐A, but whether the interaction of kinetochore components to centromeric nucleosomes is regulated by posttranslational modifications is unknown. Here, we investigated how methylation of arginine 37 (R37Me) and acetylation of lysine 49 (K49Ac) on the CENP‐A homolog Cse4 from Saccharomyces cerevisiae regulate molecular interactions at the inner kinetochore. Importantly, we found that the Cse4 N‐terminus binds with high affinity to the Ctf19 complex subassembly Okp1/Ame1 (CENP‐Q/CENP‐U in higher eukaryotes), and that this interaction is inhibited by R37Me and K49Ac modification on Cse4. In vivo defects in cse4‐R37A were suppressed by mutations in OKP1 and AME1, and biochemical analysis of a mutant version of Okp1 showed increased affinity for Cse4. Altogether, our results demonstrate that the Okp1/Ame1 heterodimer is a reader module for posttranslational modifications on Cse4, thereby targeting the yeast CCAN complex to centromeric chromatin.

We recently reported that NAC transcription factor (TF) JUNGBRUNNEN1 (JUB1; At2g43000; also called ANAC042) positively regulates longevity in Arabidopsis thaliana. JUB1 overexpression extends plant life span, while its inhibition leads to precocious senescence, 1 most likely through a gene regulatory network (GRN) that controls the level of intracellular hydrogen peroxide (H 2 O 2 ) concentration. Transcriptome profiling revealed more prominent induction, after H 2 O 2 treatment, of several known H 2 O 2 -responsive genes in JUB1 overexpressors ( JUB1ox) compared with wild-type (WT) and jub1-1 knockdown lines. These genes included DREB2A and HEAT SHOCK FACTOR (HSF) A2, both of which also encode TFs and are well known for their important role in abiotic stress signaling. 2-6Similarly, several HEAT SHOCK PROTEIN (HSP) genes, which are downstream targets of HSFs, and other H 2 O 2 -/reactive oxygen-species (ROS)-responsive genes such as GLUTATHIONE S-TRANSFERASES were more highly induced in JUB1ox than WT and jub1-1 plants after H 2 O 2 treatment.1 Notably, in addition to promoting juvenility, overexpression of JUB1 also leads to enhanced abiotic stress tolerance which is accompanied by changes in the metabolic profiles, including a lower H 2 O 2 level and elevated levels of proline and trehalose. Collectively, our data indicate that JUB1 obeys an important regulatory function that modulates cellular H 2 O 2 level and primes plants to combat stress.We recently reported that the NAC transcription factor JUNGBRUNNEN1 (JUB1; ANAC042) extends longevity and increases tolerance to heat stress in Arabidopsis thaliana when overexpressed, while the opposite is observed in jub1-1 knock-down lines. Here we extend our previous findings by demonstrating that JUB1 also positively regulates plant survival under heat stress when plants were treated by a prior moderate (and non-lethal) temperature regime (so-called priming). We further find that JUB1 shows thermomemory-related expression, similar to two other genes previously reported to be important for thermopriming, i.e., HSFA2, encoding a heat shock factor, and HSA32, encoding a heat shock protein. Our analysis also identifies ASCORBATE PEROXIDASE2 (APX2) and the heat shock protein genes HSP18.2 and HSP21 as thermomemory-expressed genes, revealing them as new candidates for studies to decode the molecular processes controlling thermopriming.