Maize smart-canopy architecture enhances yield at high densities.

Increasing planting density is a key strategy to enhance maize yields1-3. An ideotype for dense planting requires a 'smart canopy' with leaf angles at different canopy layers differentially optimized to maximize light interception and photosynthesis4-6, amongst other features. Here, we identified leaf angle architecture of smart canopy 1 (lac1), a natural mutant possessing upright upper leaves, less erect middle leaves and relatively flat lower leaves. lac1 has improved photosynthetic capacity and weakened shade-avoidance responses under dense planting. lac1 encodes a brassinosteroid C-22 hydroxylase that predominantly regulates upper leaf angle. Phytochrome A photoreceptors accumulate in shade and interact with the transcription factor RAVL1 to promote its degradation via the 26S proteasome, thereby attenuating RAVL1 activation of lac1 and reducing brassinosteroid levels. This ultimately decreases upper leaf angle in dense fields. Large-scale field trials demonstrate lac1 boosts maize yields under high densities. To quickly introduce lac1 into breeding germplasm, we transformed a haploid inducer and recovered homozygous lac1 edits from 20 diverse inbred lines. The tested doubled haploids uniformly acquired smart-canopy-like plant architecture. We provide an important target and an accelerated strategy for developing high-density-tolerant cultivars, with lac1 serving as a genetic chassis for further engineering of a smart canopy in maize.

Phytochromes enhance SOS2-mediated PIF1 and PIF3 phosphorylation and degradation to promote Arabidopsis salt tolerance.

Soil salinity is one of the most detrimental abiotic stresses affecting plant survival, and light is a core environmental signal regulating plant growth and responses to abiotic stress. However, how light modulates the plant's response to salt stress remains largely obscure. Here, we show that Arabidopsis (Arabidopsis thaliana) seedlings are more tolerant to salt stress in the light than in the dark, and that the photoreceptors phytochrome A (phyA) and phyB are involved in this tolerance mechanism. We further show that phyA and phyB physically interact with the salt tolerance regulator SALT OVERLY SENSITIVE2 (SOS2) in the cytosol and nucleus, and enhance salt-activated SOS2 kinase activity in the light. Moreover, SOS2 directly interacts with and phosphorylates PHYTOCHROME-INTERACTING FACTORS PIF1 and PIF3 in the nucleus. Accordingly, PIFs act as negative regulators of plant salt tolerance, and SOS2 phosphorylation of PIF1 and PIF3 decreases their stability and relieves their repressive effect on plant salt tolerance in both light and dark conditions. Together, our study demonstrates that photoactivated phyA and phyB promote plant salt tolerance by increasing SOS2-mediated phosphorylation and degradation of PIF1 and PIF3, thus broadening our understanding of how plants adapt to salt stress according to their dynamic light environment.

SALT OVERLY SENSITIVE2 stabilizes phytochrome-interacting factors PIF4 and PIF5 to promote Arabidopsis shade avoidance.

Sun-loving plants trigger the shade avoidance syndrome (SAS) to compete against their neighbors for sunlight. Phytochromes are plant red (R) and far-red (FR) light photoreceptors that play a major role in perceiving the shading signals and triggering SAS. Shade induces a reduction in the level of active phytochrome B (phyB), thus increasing the abundance of PHYTOCHROME-INTERACTING FACTORS (PIFs), a group of growth-promoting transcription factors. However, whether other factors are involved in modulating PIF activity in the shade remains largely obscure. Here, we show that SALT OVERLY SENSITIVE2 (SOS2), a protein kinase essential for salt tolerance, positively regulates SAS in Arabidopsis thaliana. SOS2 directly phosphorylates PIF4 and PIF5 at a serine residue close to their conserved motif for binding to active phyB. This phosphorylation thus decreases their interaction with phyB and posttranslationally promotes PIF4 and PIF5 protein accumulation. Notably, the role of SOS2 in regulating PIF4 and PIF5 protein abundance and SAS is more prominent under salt stress. Moreover, phyA and phyB physically interact with SOS2 and promote SOS2 kinase activity in the light. Collectively, our study uncovers an unexpected role of salt-activated SOS2 in promoting SAS by modulating the phyB-PIF module, providing insight into the coordinated response of plants to salt stress and shade.

Reconstitution of phytochrome A-mediated light modulation of the ABA signaling pathways in yeast.

Abscisic acid (ABA), a classical plant hormone, plays an essential role in plant adaptation to environmental stresses. The ABA signaling mechanisms have been extensively investigated, and it was shown that the PYR1 (PYRABACTIN RESISTANCE1)/PYL (PYR1-LIKE)/RCAR (REGULATORY COMPONENT OF ABA RECEPTOR) ABA receptors, the PP2C coreceptors, and the SnRK2 protein kinases constitute the core ABA signaling module responsible for ABA perception and initiation of downstream responses. We recently showed that ABA signaling is modulated by light signals, but the underlying molecular mechanisms remain largely obscure. In this study, we established a system in yeast cells that was not only successful in reconstituting a complete ABA signaling pathway, from hormone perception to ABA-responsive gene expression, but also suitable for functionally characterizing the regulatory roles of additional factors of ABA signaling. Using this system, we analyzed the roles of several light signaling components, including the red and far-red light photoreceptors phytochrome A (phyA) and phyB, and the photomorphogenic central repressor COP1, in the regulation of ABA signaling. Our results showed that both phyA and phyB negatively regulated ABA signaling, whereas COP1 positively regulated ABA signaling in yeast cells. Further analyses showed that photoactivated phyA interacted with the ABA coreceptors ABI1 and ABI2 to decrease their interactions with the ABA receptor PYR1. Together, data from our reconstituted yeast ABA signaling system provide evidence that photoactivated photoreceptors attenuate ABA signaling by directly interacting with the key components of the core ABA signaling module, thus conferring enhanced ABA tolerance to light-grown plants.

Molecular mechanisms underlying coordinated responses of plants to shade and environmental stresses.

Shade avoidance syndrome (SAS) is triggered by a low ratio of red (R) to far-red (FR) light (R/FR ratio), which is caused by neighbor detection and/or canopy shade. In order to compete for the limited light, plants elongate hypocotyls and petioles by deactivating phytochrome B (phyB), a major R light photoreceptor, thus releasing its inhibition of the growth-promoting transcription factors PHYTOCHROME-INTERACTING FACTORs. Under natural conditions, plants must cope with abiotic stresses such as drought, soil salinity, and extreme temperatures, and biotic stresses such as pathogens and pests. Plants have evolved sophisticated mechanisms to simultaneously deal with multiple environmental stresses. In this review, we will summarize recent major advances in our understanding of how plants coordinately respond to shade and environmental stresses, and will also discuss the important questions for future research. A deep understanding of how plants synergistically respond to shade together with abiotic and biotic stresses will facilitate the design and breeding of new crop varieties with enhanced tolerance to high-density planting and environmental stresses.

TIME FOR COFFEE regulates phytochrome A-mediated hypocotyl growth through dawn-phased signaling.

To enhance plant fitness under natural conditions, the circadian clock is synchronized and entrained by light via photoreceptors. In turn, the circadian clock exquisitely regulates the abundance and activity of photoreceptors via largely uncharacterized mechanisms. Here we show that the clock regulator TIME FOR COFFEE (TIC) controls the activity of the far-red light photoreceptor phytochrome A (phyA) at multiple levels in Arabidopsis thaliana. Null mutants of TIC displayed dramatically increased sensitivity to light irradiation with respect to hypocotyl growth, especially to far-red light. RNA-sequencing demonstrated that TIC and phyA play largely opposing roles in controlling light-regulated gene expression at dawn. Additionally, TIC physically interacts with the transcriptional repressor TOPLESS (TPL), which was associated with the significantly increased PHYA transcript levels in the tic-2 and tpl-1 mutants. Moreover, TIC interacts with phyA in the nucleus, thereby affecting phyA protein turnover and the formation of phyA nuclear speckles following light irradiation. Genetically, phyA was found to act downstream of TIC in regulating far red light-inhibited growth. Taken together, these findings indicate that TIC acts as a major negative regulator of phyA by integrating transcriptional and post-translational mechanisms at multiple levels.

COP1 positively regulates ABA signaling during Arabidopsis seedling growth in darkness by mediating ABA-induced ABI5 accumulation.

CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1), a well-characterized E3 ubiquitin ligase, is a central repressor of seedling photomorphogenic development in darkness. However, whether COP1 is involved in modulating abscisic acid (ABA) signaling in darkness remains largely obscure. Here, we report that COP1 is a positive regulator of ABA signaling during Arabidopsis seedling growth in the dark. COP1 mediates ABA-induced accumulation of ABI5, a transcription factor playing a key role in ABA signaling, through transcriptional and post-translational regulatory mechanisms. We further show that COP1 physically interacts with ABA-hypersensitive DCAF1 (ABD1), a substrate receptor of the CUL4-DDB1 E3 ligase targeting ABI5 for degradation. Accordingly, COP1 directly ubiquitinates ABD1 in vitro, and negatively regulates ABD1 protein abundance in vivo in the dark but not in the light. Therefore, COP1 promotes ABI5 protein stability post-translationally in darkness by destabilizing ABD1 in response to ABA. Interestingly, we reveal that ABA induces the nuclear accumulation of COP1 in darkness, thus enhancing its activity in propagating the ABA signal. Together, our study uncovers that COP1 modulates ABA signaling during seedling growth in darkness by mediating ABA-induced ABI5 accumulation, demonstrating that plants adjust their ABA signaling mechanisms according to their light environment.

Mutual upregulation of HY5 and TZP in mediating phytochrome A signaling.

Phytochrome A (phyA) is the far-red (FR) light photoreceptor in plants that is essential for seedling de-etiolation under FR-rich environments, such as canopy shade. TANDEM ZINC-FINGER/PLUS3 (TZP) was recently identified as a key component of phyA signal transduction in Arabidopsis thaliana; however, how TZP is integrated into the phyA signaling networks remains largely obscure. Here, we demonstrate that ELONGATED HYPOCOTYL5 (HY5), a well-characterized transcription factor promoting photomorphogenesis, mediates FR light induction of TZP expression by directly binding to a G-box motif in the TZP promoter. Furthermore, TZP physically interacts with CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), an E3 ubiquitin ligase targeting HY5 for 26S proteasome-mediated degradation, and this interaction inhibits COP1 interaction with HY5. Consistent with those results, TZP post-translationally promotes HY5 protein stability in FR light, and in turn, TZP protein itself is destabilized by COP1 in both dark and FR light conditions. Moreover, tzp hy5 double mutants display an additive phenotype relative to their respective single mutants under high FR light intensities, indicating that TZP and HY5 also function in largely independent pathways. Together, our data demonstrate that HY5 and TZP mutually upregulate each other in transmitting the FR light signal, thus providing insights into the complicated but delicate control of phyA signaling networks.

Novel and multifaceted regulations of photoperiodic flowering by phytochrome A in soybean.

Photoperiod is an important environmental cue. Plants can distinguish the seasons and flower at the right time through sensing the photoperiod. Soybean is a sensitive short-day crop, and the timing of flowering varies greatly at different latitudes, thus affecting yields. Soybean cultivars in high latitudes adapt to the long day by the impairment of two phytochrome genes, PHYA3 and PHYA2, and the legume-specific flowering suppressor, E1. However, the regulating mechanism underlying phyA and E1 in soybean remains largely unknown. Here, we classified the regulation of the E1 family by phyA2 and phyA3 at the transcriptional and posttranscriptional levels, revealing that phyA2 and phyA3 regulate E1 by directly binding to LUX proteins, the critical component of the evening complex, to regulate the stability of LUX proteins. In addition, phyA2 and phyA3 can also directly associate with E1 and its homologs to stabilize the E1 proteins. Therefore, phyA homologs control the core flowering suppressor E1 at both the transcriptional and posttranscriptional levels, to double ensure the E1 activity. Thus, our results disclose a photoperiod flowering mechanism in plants by which the phytochrome A regulates LUX and E1 activity.

The cold response regulator CBF1 promotes Arabidopsis hypocotyl growth at ambient temperatures.

Light and temperature are two core environmental factors that coordinately regulate plant growth and survival throughout their entire life cycle. However, the mechanisms integrating light and temperature signaling pathways in plants remain poorly understood. Here, we report that CBF1, an AP2/ERF-family transcription factor essential for plant cold acclimation, promotes hypocotyl growth under ambient temperatures in Arabidopsis. We show that CBF1 increases the protein abundance of PIF4 and PIF5, two phytochrome-interacting bHLH-family transcription factors that play pivotal roles in modulating plant growth and development, by directly binding to their promoters to induce their gene expression, and by inhibiting their interaction with phyB in the light. Moreover, our data demonstrate that CBF1 promotes PIF4/PIF5 protein accumulation and hypocotyl growth at both 22°C and 17°C, but not at 4°C, with a more prominent role at 17°C than at 22°C. Together, our study reveals that CBF1 integrates light and temperature control of hypocotyl growth by promoting PIF4 and PIF5 protein abundance in the light, thus providing insights into the integration mechanisms of light and temperature signaling pathways in plants.

The CRY2-COP1-HY5-BBX7/8 module regulates blue light-dependent cold acclimation in Arabidopsis.

Light and temperature are two key environmental factors that coordinately regulate plant growth and development. Although the mechanisms that integrate signaling mediated by cold and red light have been unraveled, the roles of the blue light photoreceptors cryptochromes in plant responses to cold remain unclear. In this study, we demonstrate that the CRYPTOCHROME2 (CRY2)-COP1-HY5-BBX7/8 module regulates blue light-dependent cold acclimation in Arabidopsis thaliana. We show that phosphorylated forms of CRY2 induced by blue light are stabilized by cold stress and that cold-stabilized CRY2 competes with the transcription factor HY5 to attenuate the HY5-COP1 interaction, thereby allowing HY5 to accumulate at cold temperatures. Furthermore, our data demonstrate that B-BOX DOMAIN PROTEIN7 (BBX7) and BBX8 function as direct HY5 targets that positively regulate freezing tolerance by modulating the expression of a set of cold-responsive genes, which mainly occurs independently of the C-repeat-binding factor pathway. Our study uncovers a mechanistic framework by which CRY2-mediated blue-light signaling enhances freezing tolerance, shedding light on the molecular mechanisms underlying the crosstalk between cold and light signaling pathways in plants.

14-3-3 proteins regulate photomorphogenesis by facilitating light-induced degradation of PIF3.

14-3-3s are highly conserved phosphopeptide-binding proteins that play important roles in various developmental and signaling pathways in plants. However, although protein phosphorylation has been proven to be a key mechanism for regulating many pivotal components of the light signaling pathway, the role of 14-3-3 proteins in photomorphogenesis remains largely obscure. PHYTOCHROME-INTERACTING FACTOR3 (PIF3) is an extensively studied transcription factor repressing photomorphogenesis, and it is well-established that upon red (R) light exposure, photo-activated phytochrome B (phyB) interacts with PIF3 and induces its rapid phosphorylation and degradation. PHOTOREGULATORY PROTEIN KINASES (PPKs), a family of nuclear protein kinases, interact with phyB and PIF3 in R light and mediate multisite phosphorylation of PIF3 in vivo. Here, we report that two members of the 14-3-3 protein family, 14-3-3λ and κ, bind to a serine residue in the bHLH domain of PIF3 that can be phosphorylated by PPKs, and act as key positive regulators of R light-induced photomorphogenesis. Moreover, 14-3-3λ and κ preferentially interact with photo-activated phyB and promote the phyB-PIF3-PPK complex formation, thereby facilitating phyB-induced phosphorylation and degradation of PIF3 upon R light exposure. Together, our data demonstrate that 14-3-3λ and κ work in close concert with the phyB-PIF3 module to regulate light signaling in Arabidopsis.

IbBBX24 Promotes the Jasmonic Acid Pathway and Enhances Fusarium Wilt Resistance in Sweet Potato.

Cultivated sweet potato (Ipomoea batatas) is an important source of food for both humans and domesticated animals. Here, we show that the B-box (BBX) family transcription factor IbBBX24 regulates the jasmonic acid (JA) pathway in sweet potato. When IbBBX24 was overexpressed in sweet potato, JA accumulation increased, whereas silencing this gene decreased JA levels. RNA sequencing analysis revealed that IbBBX24 modulates the expression of genes involved in the JA pathway. IbBBX24 regulates JA responses by antagonizing the JA signaling repressor IbJAZ10, which relieves IbJAZ10's repression of IbMYC2, a JA signaling activator. IbBBX24 binds to the IbJAZ10 promoter and activates its transcription, whereas it represses the transcription of IbMYC2 The interaction between IbBBX24 and IbJAZ10 interferes with IbJAZ10's repression of IbMYC2, thereby promoting the transcriptional activity of IbMYC2. Overexpressing IbBBX24 significantly increased Fusarium wilt disease resistance, suggesting that JA responses play a crucial role in regulating Fusarium wilt resistance in sweet potato. Finally, overexpressing IbBBX24 led to increased yields in sweet potato. Together, our findings indicate that IbBBX24 plays a pivotal role in regulating JA biosynthesis and signaling and increasing Fusarium wilt resistance and yield in sweet potato, thus providing a candidate gene for developing elite crop varieties with enhanced pathogen resistance but without yield penalty.

MYB30 Is a Key Negative Regulator of Arabidopsis Photomorphogenic Development That Promotes PIF4 and PIF5 Protein Accumulation in the Light.

Phytochromes are red (R) and far-red (FR) light photoreceptors in plants, and PHYTOCHROME-INTERACTING FACTORS (PIFs) are a group of basic helix-loop-helix family transcription factors that play central roles in repressing photomorphogenesis. Here, we report that MYB30, an R2R3-MYB family transcription factor, acts as a negative regulator of photomorphogenesis in Arabidopsis (Arabidopsis thaliana). We show that MYB30 preferentially interacts with the Pfr (active) forms of the phytochrome A (phyA) and phytochrome B (phyB) holoproteins and that MYB30 levels are induced by phyA and phyB in the light. It was previously shown that phytochromes induce rapid phosphorylation and degradation of PIFs upon R light exposure. Our current data indicate that MYB30 promotes PIF4 and PIF5 protein reaccumulation under prolonged R light irradiation by directly binding to their promoters to induce their expression and by inhibiting the interaction of PIF4 and PIF5 with the Pfr form of phyB. In addition, our data indicate that MYB30 interacts with PIFs and that they act additively to repress photomorphogenesis. In summary, our study demonstrates that MYB30 negatively regulates Arabidopsis photomorphogenic development by acting to promote PIF4 and PIF5 protein accumulation under prolonged R light irradiation, thus providing new insights into the complicated but delicate control of PIFs in the responses of plants to their dynamic light environment.

Purification and biochemical characterization of a novel ene- reductase from Kazachstania exigua HSC6 for dihydro-ß-ionone from ß-ionone.

PURPOSE: We purified and characterized a novel ene-reductase (KaDBR1) from Kazachstania exigua HSC6 for the synthesis of dihydro-ß-ionone from ß-ionone. METHODS: KaDBR1 was purified to homogeneity by ammonium sulfate precipitation and phenyl-Sepharose Fast Flow and Q-Sepharose chromatography. The purified enzyme was characterized by measuring the amount of dihydro-ß-ionone from ß-ionone with LC-MS analysis method. RESULTS: The molecular mass of KaDBR1 was estimated to be 45 kDa by SDS-PAGE. The purified KaDBR1 enzyme had optimal activity at 60 °C and pH 6.0. The addition of 5 mM Mg2+, Ca2+, Al3+, Na+, and dithiothreitol increased the activity of KaDBR1 by 25%, 18%, 34%, 20%, and 23%, respectively. KaDBR1 favored NADH over NADPH as a cofactor, and its catalytic efficiency (kcat/Km) toward ß-ionone using NADH was 8.1-fold greater than when using NADPH. CONCLUSION: Owing to its unique properties, KaDBR1 is a potential candidate for the enzymatic biotransformation of ß-ionone to dihydro-ß-ionone in biotechnology applications.

The UBC27-AIRP3 ubiquitination complex modulates ABA signaling by promoting the degradation of ABI1 in Arabidopsis.

Abscisic acid (ABA) is the key phytohormone in plant drought tolerance and stress adaptation. The clade A protein phosphatase 2Cs (PP2Cs) like ABI1 (ABA-INSENSITIVE 1) work as coreceptors of ABA and regulate multiple ABA responses. Ubiquitination of ABI1 has been proven to play important regulatory roles in ABA signaling. However, the specific ubiquitin conjugating enzyme (E2) involved is unknown. Here, we report that UBC27 is an active E2 that positively regulates ABA signaling and drought tolerance. UBC27 forms the E2-E3 pair with the drought regulator RING E3 ligase AIRP3. Both UBC27 and AIRP3 interact with ABI1 and affect the ubiquitination and degradation of ABI1. ABA activates the expression of UBC27, inhibits the proteasome degradation of UBC27, and enhances the interaction between UBC27 and ABI1 to increase its activity. These findings uncover a regulatory mechanism in ABA signaling and drought response and provide a further understanding of the plant ubiquitination system and ABA signaling pathway.

CsTFL1 inhibits determinate growth and terminal flower formation through interaction with CsNOT2a in cucumber.

Cucumber (Cucumis sativus L.) is an important vegetable crop that carries on vegetative growth and reproductive growth simultaneously. Indeterminate growth is favourable for fresh market under protected environments, whereas determinate growth is preferred for pickling cucumber in the once-over mechanical harvest system. The genetic basis of determinacy is largely unknown in cucumber. In this study, map-based cloning of the de locus showed that the determinate growth habit is caused by a non-synonymous SNP in CsTFL1CsTFL1 is expressed in the subapical regions of the shoot apical meristem, lateral meristem and young stems. Ectopic expression of CsTFL1 rescued the terminal flower phenotype in the Arabidopsis tfl1-11 mutant and delayed flowering in wild-type Arabidopsis Knockdown of CsTFL1 resulted in determinate growth and formation of terminal flowers in cucumber. Biochemical analyses indicated that CsTFL1 interacts with a homolog of the miRNA biogenesis gene CsNOT2a; CsNOT2a interacts with FDP. Cucumber CsFT directly interacts with CsNOT2a and CsFD, and CsFD interacts with two 14-3-3 proteins. These data suggest that CsTFL1 competes with CsFT for interaction with CsNOT2a-CsFDP to inhibit determinate growth and terminal flower formation in cucumber.

Transcriptomic comparison sheds new light on regulatory networks for dimorphic flower development in response to photoperiod in Viola prionantha.

BACKGROUND: Chasmogamous (CH)-cleistogamous (CL) dimorphic flowers are developed in Viola prionantha. However, the environmental and genetic factors necessary for the CH-CL transition are unknown. RESULTS: In the present work, short-day (SD) conditions induced CH flowers, whereas long days (LDs) triggered CL flowers in V. prionantha. Compared to fully developed CH flowers, CL flowers had less mature stamens, no nectar glands, and immature petals. Comparative transcriptomics revealed differentially expressed genes (DEGs) during CL and CH development. Core genes in the photoperiod pathway, such as V. prionantha orthologs of GIGANTEA (GI), CONSTANS (CO), and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1), which promote floral induction, were highly expressed in CL flowers, whereas UNUSUAL FLORAL ORGANS (UFO) and B-class MADS-box genes for floral organ identity and development showed an opposite alteration. Moreover, genes in the glycolytic process, sucrose metabolic process, and fatty acid biosynthetic process were all highly expressed in CH flowers. Interestingly, V. prionantha orthologs of the B-class MADS-box genes APETALA3 (AP3) and PISTILLATA (PI) might relate to these sugar-fatty acid processes and were co-expressed with GAIP-B-like and YABBY5 (YAB5), which regulate the development of the petal, stamen, and nectary. Compared to CH flowers, DEGs and hub genes in the most significantly correlated modules of the gene co-expression network, which are involved in abiotic and biotic responses, were upregulated in CL flowers. CONCLUSIONS: We proposed an integrative model for transcription regulation of genes in the photoperiod pathway, floral organ development, stress response, and sugar-fatty acid processes to determine CH-CL flower development in V. prionantha. Particularly, under LDs, activated GI may induce genes involved in the stress-response pathways, and then downregulated AP3 and PI or UFO to inhibit the sugar-fatty acid metabolic processes, together forming CL flowers. In contrast, CH flowers were produced under SDs. This work provides novel insights into the developmental evolution of dimorphic flowers in Viola.

FHY3 interacts with phytochrome B and regulates seed dormancy and germination.

Seed dormancy and germination are fundamental processes for plant propagation, both of which are tightly regulated by internal and external cues. Phytochrome B (phyB) is a major red/far-red-absorbing photoreceptor that senses light signals that modulate seed dormancy and germination. However, the components that directly transduce that signal downstream of phyB are mostly unknown. Here, we show that the transposase-derived transcription factor FAR-RED ELONGATED HYPOCOTYL3 (FHY3) inhibits seed dormancy and promotes phyB-mediated seed germination in Arabidopsis thaliana. FHY3 physically interacts with phyB in vitro and in vivo. RNA-sequencing and reverse transcription-quantitative polymerase chain reaction analyses showed that FHY3 regulates multiple downstream genes, including REVEILLE2 (RVE2), RVE7, and SPATULA (SPT). Yeast one-hybrid, electrophoresis mobility shift, and chromatin immunoprecipitation assays demonstrated that FHY3 directly binds these genes via a conserved FBS cis-element in their promoters. Furthermore, RVE2, RVE7, and GIBBERELLIN 3-OXIDASE 2 (GA3ox2) genetically act downstream of FHY3. Strikingly, light and phyB promote FHY3 protein accumulation. Our study reveals a transcriptional cascade consisting of phyB-FHY3-RVE2/RVE7/SPT-GA3ox2 that relays environmental light signals and thereby controls seed dormancy and germination.

The Transcription Factor MYB59 Regulates K+/NO3 - Translocation in the Arabidopsis Response to Low K+ Stress.

Potassium and nitrogen are essential nutrients for plant growth and development. Plants can sense potassium nitrate (K+/NO3 -) levels in soils, and accordingly they adjust root-to-shoot K+/NO3 - transport to balance the distribution of these ions between roots and shoots. In this study, we show that the transcription factorMYB59 maintains this balance by regulating the transcription of the Arabidopsis (Arabidopsis thaliana) Nitrate Transporter1.5 (NRT1.5)/ Nitrate Transporter/Peptide Transporter Family7.3 (NPF7.3) in response to low K+ (LK) stress. The myb59 mutant showed a yellow-shoot sensitive phenotype when grown on LK medium. Both the transcript and protein levels of NPF7.3 were remarkably reduced in the myb59 mutant. LK stress repressed transcript levels of both MYB59 and NPF7.3 The npf7.3 and myb59 mutants, as well as the npf7.3 myb59 double mutant, showed similar LK-sensitive phenotypes. Ion content analyses indicated that root-to-shoot K+/NO3 - transport was significantly reduced in these mutants under LK conditions. Moreover, chromatin immunoprecipitation and electrophoresis mobility shift assay assays confirmed that MYB59 bound directly to the NPF7.3 promoter. Expression of NPF7.3 in root vasculature driven by the PHOSPHATE 1 promoter rescued the sensitive phenotype of both npf7.3 and myb59 mutants. Together, these data demonstrate that MYB59 responds to LK stress and directs root-to-shoot K+/NO3 - transport by regulating the expression of NPF7.3 in Arabidopsis roots.