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• In response to elevated ambient temperature Arabidopsis thaliana seedlings display a thermomorphogenic response that includes elongation of hypocotyls and petioles. Phytochrome B and cryptochrome 1 are two photoreceptors also playing a role in thermomorphogenesis. Downstream of both environmental sensors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) is essential to trigger this response at least in part through the production of the growth promoting hormone auxin. • Using a genetic approach, we identified PHYTOCHROME INTERACTING FACTOR 7 (PIF7) as a novel player for thermomorphogenesis and compared the phenotypes of pif7 and pif4 mutants. We investigated the role of PIF7 during temperature-regulated gene expression and the regulation of PIF7 transcript and protein by temperature. • Furthermore, pif7 and pif4 loss-of-function mutants were similarly unresponsive to increased temperature. This included hypocotyl elongation and induction of genes encoding auxin biosynthetic or signalling proteins. PIF7 bound to the promoters of auxin biosynthesis and signalling genes. In response to temperature elevation PIF7 transcripts decreased while PIF7 protein levels increased rapidly. • Our results reveal the importance of PIF7 for thermomorphogenesis and indicate that PIF7 and PIF4 likely dependon each other possibly by forming heterodimers. Elevated temperature rapidly enhances PIF7 protein accumulation, which may contribute to the thermomorphogenic response.

[...]this Research Topic wanted to embrace all aspects of plant physiology, giving a voice to less-represented scientists in this field. According to UNESCO, women represent only 30% of the world’s researchers. [...]by promoting their works through this dedicated Research Topic on Women in Plant Physiology, Frontiers wanted to support women’s careers, reducing the gender gap. Half of the papers in this collection focused on studying plant-environment interactions (Figure 1). Since plants are sessile organisms that cannot flee or change their habitats depending on the seasons and nutrient availability, they have evolved mechanisms to cope with the ever-changing environment by adapting their growth and development to it. The authors found that phosphorylation of the light-harvesting complex II, happening in low light, depends on the Cl− channel ClCe that regulates H+ flux and ATP synthase activities. [...]phenotypic analyses of the clc mutant demonstrates the importance of this channel in controlling the acclimation of plants under low light. [...]this Research Topic addresses a variety of questions in the plant physiology field and highlights the necessity of constant crosstalk between basic and applied research to move forward the knowledge in this field.

The seed habit is the most complex and successful method of sexual reproduction in vascular plants. It represents a remarkable moment in the evolution of plants that afterward spread on land. In particular, seed size had a pivotal role in evolutionary success and agronomic traits, especially in the field of crop domestication. Given that crop seeds constitute one of the primary products for consumption, it follows that seed size represents a fundamental determinant of crop yield. This adaptative feature is strictly controlled by genetic traits from both maternal and zygotic tissues, although seed development and growth are also affected by environmental cues. Despite being a highly exploited topic for both basic and applied research, there are still many issues to be elucidated for developmental biology as well as for agronomic science. This review addresses a number of open questions related to cues that influence seed growth and size and how they influence seed germination. Moreover, new insights on the genetic–molecular control of this adaptive trait are presented.

Background Diabetic retinopathy (DR) is a microvascular complication of diabetes with a heavy impact on the quality of life of subjects and with a dramatic burden for health and economic systems on a global scale. Although the pathogenesis of DR is largely unknown, several preclinical data have pointed out to a main role of Muller glia (MG), a cell type which spans across the retina layers providing nourishment and support for Retina Ganglion Cells (RGCs), in sensing hyper-glycemia and in acquiring a pro-inflammatory polarization in response to this insult. Results By using a validated experimental model of DR in vitro, rMC1 cells challenged with high glucose, we uncovered the induction of an early (within minutes) and atypical Nuclear Factor-kB (NF-kB) signalling pathway regulated by a calcium-dependent calmodulin kinase II (CamKII)-proteasome axis. Phosphorylation of proteasome subunit Rpt6 (at Serine 120) by CamKII stimulated the accelerated turnover of IkBα (i.e., the natural inhibitor of p65-50 transcription factor), regardless of the phosphorylation at Serine 32 which labels canonical NF-kB signalling. This event allowed the p65-p50 heterodimer to migrate into the nucleus and to induce transcription of IL-8, Il-1β and MCP-1. Pharmacological inhibition of CamKII as well as proteasome inhibition stopped this pro-inflammatory program, whereas introduction of a Rpt6 phospho-dead mutant (Rpt6-S120A) stimulated a paradoxical effect on NF-kB probably through the activation of a compensatory mechanism which may involve phosphorylation of 20S α4 subunit. Conclusions This study introduces a novel pathway of MG activation by high glucose and casts some light on the biological relevance of proteasome post-translational modifications in modulating pathways regulated through targeted proteolysis. Key Points High glucose quickly induces an atypical NF-kB pro-inflammatory program. CamKII phosphorylation of Rpt6 subunit of the proteasome stimulates IkBα turnover and p65-p50 release. Inhibition of either CamkII or proteasome blocks this pathway.

Background Polycomb repressive complex 2 (PRC2) is an epigenetic transcriptional repression system, whose catalytic subunit (ENHANCER OF ZESTE HOMOLOG 2, EZH2 in animals) is responsible for trimethylating histone H3 at lysine 27 (H3K27me3). In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported. Results We show here that the 1,5-bis (3-bromo-4-methoxyphenyl)penta-1,4-dien-3-one compound (RDS 3434), previously reported as an EZH2 inhibitor in human leukemia cells, is active on the Arabidopsis catalytic subunit of PRC2, since treatment with the drug reduces the total amount of H3K27me3 in a dose-dependent fashion. Consistently, we show that the expression level of two PRC2 targets is significantly increased following treatment with the RDS 3434 compound. Finally, we show that impairment of H3K27 trimethylation in Arabidopsis seeds and seedlings affects both seed germination and root growth. Conclusions Our results provide a useful tool for the plant community in investigating how PRC2 affects transcriptional control in plant development.

ABSTRACT Phototropic bending of plants towards a light source allows them to position their photosynthetic tissues to optimize light capture. In light‐grown (de‐etiolated) Arabidopsis seedlings, phototropic bending of the hypocotyl is inhibited by light with a high red:far‐red ratio (HRFR) and high levels of blue light (HBL). This occurs via activation of the phytochrome B (phyB) and cryptochrome 1 (cry1) photoreceptor signaling pathways. Both phyB and cry1 act upstream of PHYTOCHROME INTERACTING FACTOR (PIF) transcription factors, which are required for hypocotyl bending in light‐grown seedlings. Presently, it is not known whether other pathways are involved in the inhibition of PIF‐mediated phototropism in light‐grown seedlings. To address this, we conducted a screen to identify mutants with increased phototropic bending relative to wild type in HRFR + HBL conditions. Through this screen, we identified EARLY FLOWERING 3 (ELF3), a member of the Evening Complex (EC), as a key inhibitor of phototropic bending in green seedlings. We show that both ELF3 and LUX, another component of the EC, inhibit phototropic bending upstream of PIF4/PIF5. Furthermore, we show that phototropic bending in Arabidopsis seedlings is subject to circadian regulation in an ELF3‐dependent manner. Finally, we provide evidence that ELF3 in the grass Brachypodium distachyon also affects phototropism but in an opposite way than in Arabidopsis.

Light regulates Arabidopsis seed germination through the phyB/PIL5 (PHYTOCHROME INTERACTING FACTOR 3-LIKE 5) transduction pathway, and we have previously shown that the Dof transcription factor DOF AFFECTING GERMINATION1 (DAG1) is a component of this pathway. By means of microarray analysis of dag1 and wild type developing siliques, we identified the EARLY LIGHT-INDUCED PROTEIN1 and 2 (ELIP1 and ELIP2) genes among those deregulated in the loss-of-function dag1 mutant. We analysed seed germination of elip single and double mutants, of elip dag1 double mutants as well as of elip1 elip2 dag1 triple mutant under different environmental conditions. We show that ELIP1 and ELIP2 are involved in opposite ways in the control of this developmental process, in particular under abiotic (light, temperature, salt) stress conditions.

Hypocotyl elongation is influenced by light and hormones, but the molecular mechanisms underlying this process are not yet fully elucidated. We had previously suggested that the Arabidopsis DOF transcription factor DAG1 may be a negative component of the mechanism of light-mediated inhibition of hypocotyl elongation, as light-grown dag1 knock-out mutant seedlings show significant shorter hypocotyls than the wild type. By using high-throughput RNA-seq, we compared the transcriptome profile of dag1 and wild type hypocotyls and seedlings. We identified more than 250 genes differentially expressed in dag1 hypocotyls, and their analysis suggests that DAG1 is involved in the promotion of hypocotyl elongation through the control of ABA, ethylene and auxin signaling. Consistently, ChIP-qPCR results show that DAG1 directly binds to the promoters of WRKY18 encoding a transcription factor involved in ABA signaling, of the ethylene- induced gene ETHYLENE RESPONSE FACTOR ( ERF2 ), and of the SMALL AUXIN UP RNA 67 ( SAUR67 ), an auxin-responding gene encoding a protein promoting hypocotyl cell expansion.

Abstract Hypocotyl elongation of Arabidopsis seedlings is influenced by light and numerous growth factors. Light induces inhibition of hypocotyl elongation (photomorphogenesis), whereas in the dark hypocotyl elongation is promoted (skotomorphogenesis). Abscisic acid (ABA) plays a major role in inhibition of hypocotyl elongation, but the molecular mechanism remains unclear. We investigated the effect of ABA during photo- and skotomorphogenesis, making use of appropriate mutants, and we show that ABA negatively controls hypocotyl elongation acting on gibberellin (GA) metabolic genes, increasing the amount of the DELLA proteins GAI and RGA, thus affecting GA signalling, and (ultimately) repressing auxin biosynthetic genes. In this manuscript, we provide a molecular framework for the effect of abscisic acid (ABA) on hypocotyl elongation in Arabidopsis seedlings, independently of light conditions. Our results show that ABA negatively controls hypocotyl elongation by acting on gibberellin (GA) metabolic genes, increasing the amount of the DELLA proteins, thus affecting GA signalling, and (ultimately) repressing auxin biosynthetic genes.

Glaucoma is chronic optic neuropathy whose pathogenesis has been associated with the altered metabolism of Trabecular Meshwork Cells, which is a cell type involved in the synthesis and remodeling of the trabecular meshwork, the main drainage pathway of the aqueous humor. Starting from previous findings supporting altered ubiquitin signaling, in this study, we investigated the ubiquitin-mediated turnover of myocilin (MYOC/TIGR gene), which is a glycoprotein with a recognized role in glaucoma pathogenesis, in a human Trabecular Meshwork strain cultivated in vitro in the presence of dexamethasone. This is a validated experimental model of steroid-induced glaucoma, and myocilin upregulation by glucocorticoids is a phenotypic marker of Trabecular Meshwork strains. Western blotting and native-gel electrophoresis first uncovered that, in the presence of dexamethasone, myocilin turnover by proteasome particles was slower than in the absence of the drug. Thereafter, co-immunoprecipitation, RT-PCR and gene-silencing studies identified STUB1/CHIP as a candidate E3-ligase of myocilin. In this regard, dexamethasone treatment was found to downregulate STUB1/CHIP levels by likely promoting its proteasome-mediated turnover. Hence, to strengthen the working hypothesis about global alterations of ubiquitin-signaling, the first profiling of TMCs ubiquitylome, in the presence and absence of dexamethasone, was here undertaken by diGLY proteomics. Application of this workflow effectively highlighted a robust dysregulation of key pathways (e.g., phospholipid signaling, β-catenin, cell cycle regulation) in dexamethasone-treated Trabecular Meshwork Cells, providing an ubiquitin-centered perspective around the effect of glucocorticoids on metabolism and glaucoma pathogenesis.