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Seth J Davis - One of the best experts on this subject based on the ideXlab platform.

  • a mobile ELF4 delivers circadian temperature information from shoots to roots
    Nature plants, 2020
    Co-Authors: Wei Wei Chen, Dmitri A Nusinow, Seth J Davis, Nozomu Takahashi, Yoshito Hirata, James Ronald, Silvana Porco, Steve A Kay
    Abstract:

    The circadian clock is synchronized by environmental cues, mostly by light and temperature. Explaining how the plant circadian clock responds to temperature oscillations is crucial to understanding plant responsiveness to the environment. Here, we found a prevalent temperature-dependent function of the Arabidopsis clock component EARLY FLOWERING 4 (ELF4) in the root clock. Although the clocks in roots are able to run in the absence of shoots, micrografting assays and mathematical analyses show that ELF4 moves from shoots to regulate rhythms in roots. ELF4 movement does not convey photoperiodic information, but trafficking is essential for controlling the period of the root clock in a temperature-dependent manner. Low temperatures favour ELF4 mobility, resulting in a slow-paced root clock, whereas high temperatures decrease movement, leading to a faster clock. Hence, the mobile ELF4 delivers temperature information and establishes a shoot-to-root dialogue that sets the pace of the clock in roots.

  • photoperiod sensing of the circadian clock is controlled by early flowering 3 and gigantea
    Plant Journal, 2020
    Co-Authors: Seth J Davis, Muhammad Usman Anwer, Amanda M Davis, Marcel Quint
    Abstract:

    ELF3 and GI are two important components of the Arabidopsis circadian clock. They are not only essential for the oscillator function but are also pivotal in mediating light inputs to the oscillator. Lack of either results in a defective oscillator causing severely compromised output pathways, such as photoperiodic flowering and hypocotyl elongation. Although single loss of function mutants of ELF3 and GI have been well studied, their genetic interaction remains unclear. We generated an elf3 gi double mutant to study their genetic relationship in clock-controlled growth and phase transition phenotypes. We found that ELF3 and GI repress growth differentially during the night and the day, respectively. Circadian clock assays revealed that ELF3 and GI are essential that enable the oscillator to synchronize the endogenous cellular mechanisms to external environmental signals. In their absence, the circadian oscillator fails to synchronize to the light-dark cycles even under diurnal conditions. Consequently, clock-mediated photoperiod-responsive growth and development are completely lost in plants lacking both genes, suggesting that ELF3 and GI together convey photoperiod sensing to the central oscillator. Since ELF3 and GI are conserved across flowering plants and represent important breeding and domestication targets, our data highlight the possibility of developing photoperiod-insensitive crops by adjusting the allelic combination of these two key genes.

  • photoperiod sensing of the circadian clock is controlled by early flowering 3 and gigantea
    bioRxiv, 2019
    Co-Authors: Seth J Davis, Muhammad Usman Anwer, Amanda M Davis, Marcel Quint
    Abstract:

    Summary ELF3 and GI are two important components of the Arabidopsis circadian clock. They are not only essential for the oscillator function but are also pivotal in mediating light inputs to the oscillator. Lack of either results in a defective oscillator causing severely compromised output pathways, such as photoperiodic flowering and hypocotyl elongation. Although single loss of function mutants of ELF3 and GI have been well-studied, their genetic interaction remains unclear. We generated an elf3 gi double mutant to study their genetic relationship in clock-controlled growth and phase transition phenotypes. We found that ELF3 and GI repress growth differentially during the night and the day, respectively. Circadian clock assays revealed that ELF3 and GI are essential Zeitnehmers that enable the oscillator to synchronize the endogenous cellular mechanisms to external environmental signals. In their absence, the circadian oscillator fails to synchronize to the light-dark cycles even under diurnal conditions. Consequently, clock-mediated photoperiod-responsive growth and development is completely lost in plants lacking both genes, suggesting that ELF3 and GI together convey photoperiod sensing to the central oscillator. Since ELF3 and GI are conserved across flowering plants and represent important breeding and domestication targets, our data highlight the possibility of developing photoperiod-insensitive crops by adjusting the allelic combination of these two key genes. One sentence summary ELF3 and GI are essential for circadian clock mediated photoperiod sensing.

  • background dependent effects of polyglutamine variation in the arabidopsis thaliana gene elf3
    Proceedings of the National Academy of Sciences of the United States of America, 2012
    Co-Authors: Soledad Undurraga, Maximilian O Press, Seth J Davis, Nora Bujdoso, Matthieu Legendre, Jacob B Bale, Hui Wang, Kevin J Verstrepen, Christine Queitsch
    Abstract:

    Tandem repeats (TRs) have extremely high mutation rates and are often considered to be neutrally evolving DNA. However, in coding regions, TR copy number mutations can significantly affect phenotype and may facilitate rapid adaptation to new environments. In several human genes, TR copy number mutations that expand polyglutamine (polyQ) tracts beyond a certain threshold cause incurable neurodegenerative diseases. PolyQ-containing proteins exist at a considerable frequency in eukaryotes, yet the phenotypic consequences of natural variation in polyQ tracts that are not associated with disease remain largely unknown. Here, we use Arabidopsis thaliana to dissect the phenotypic consequences of natural variation in the polyQ tract encoded by EARLY FLOWERING 3 (ELF3), a key developmental gene. Changing ELF3 polyQ tract length affected complex ELF3-dependent phenotypes in a striking and nonlinear manner. Some natural ELF3 polyQ variants phenocopied elf3 loss-of-function mutants in a common reference background, although they are functional in their native genetic backgrounds. To test the existence of background-specific modifiers, we compared the phenotypic effects of ELF3 polyQ variants between two divergent backgrounds, Col and Ws, and found dramatic differences. In fact, the Col-ELF3 allele, encoding the shortest known ELF3 polyQ tract, was haploinsufficient in Ws × Col F1 hybrids. Our data support a model in which variable polyQ tracts drive adaptation to internal genetic environments.

  • a reduced function allele reveals that early flowering3 repressive action on the circadian clock is modulated by phytochrome signals in arabidopsis
    The Plant Cell, 2011
    Co-Authors: Elsebeth Kolmos, Ferenc Nagy, Eva Herrero, Nora Bujdoso, Peter Gyula, Andrew J Millar, Reka Toth, Seth J Davis
    Abstract:

    Arabidopsis thaliana EARLY FLOWERING3 (ELF3) is essential for the generation of circadian rhythms. ELF3 has been proposed to restrict light signals to the oscillator through phytochrome photoreceptors, but that has not been explicitly shown. Furthermore, the genetic action of ELF3 within the clock had remained elusive. Here, we report a functional characterization of ELF3 through the analysis of the elf3-12 allele, which encodes an amino acid replacement in a conserved domain. Circadian oscillations persisted, and unlike elf3 null alleles, elf3-12 resulted in a short circadian period only under ambient light. The period shortening effect of elf3-12 was enhanced by the overexpression of phytochromes phyA and phyB. We found that elf3-12 was only modestly perturbed in resetting of the oscillator and in gating light-regulated gene expression. Furthermore, elf3-12 essentially displayed wild-type development. We identified targets of ELF3 transcriptional repression in the oscillator, highlighting the action at the morning gene PSEUDO-RESPONSE REGULATOR9. Taken together, we identified two separable roles for ELF3, one affecting the circadian network and the other affecting light input to the oscillator. This is consistent with a dual function of ELF3 as both an integrator of phytochrome signals and a repressor component of the core oscillator.

Hirofumi Kai - One of the best experts on this subject based on the ideXlab platform.

  • roles and regulations of the ets transcription factor ELF4 mef
    Journal of Molecular Cell Biology, 2016
    Co-Authors: Mary Ann Suico, Tsuyoshi Shuto, Hirofumi Kai
    Abstract:

    Most E26 transformation-specific (ETS) transcription factors are involved in the pathogenesis and progression of cancer. This is in part due to the roles of ETS transcription factors in basic biological processes such as growth, proliferation, and differentiation, and also because of their regulatory functions that have physiological relevance in tumorigenesis, immunity, and basal cellular homoeostasis. A member of the E74-like factor (ELF) subfamily of the ETS transcription factor family-myeloid elf-1-like factor (MEF), designated as ELF4-has been shown to be critically involved in immune response and signalling, osteogenesis, adipogenesis, cancer, and stem cell quiescence. ELF4 carries out these functions as a transcriptional activator or through interactions with its partner proteins. Mutations in ELF4 cause aberrant interactions and induce downstream processes that may lead to diseased cells. Knowing how ELF4 impinges on certain cellular processes and how it is regulated in the cells can lead to a better understanding of the physiological and pathological consequences of modulated ELF4 activity.

  • sumo down regulates the activity of ELF4 myeloid elf 1 like factor
    Biochemical and Biophysical Research Communications, 2006
    Co-Authors: Mary Ann Suico, Tsuyoshi Shuto, Hideaki Nakamura, Hisato Saitoh, Mitsuyoshi Nakao, Hirofumi Kai
    Abstract:

    Myeloid elf-1-like factor (MEF) or ELF4 is an ETS protein known to regulate the basal expression of the anti-microbial peptides, lysozyme and human beta-defensin-2, in epithelial cells and activate the transcription of perforin in natural killer cells. The numerous target genes of MEF and its biological functions signify the importance of this Ets transcription factor. Here we show that MEF is modified by conjugation with SUMO-1/-2 (small ubiquitin-related modifier) both in mammalian cells and in Escherichia coli overexpressing human SUMO-1/-2. We identified by point mutation that lysine 657 of MEF is the site for sumoylation. This modification down-regulated MEF activity on lysozyme and perforin promoters, and decreased the lysozyme mRNA expression. Chromatin immuno-precipitation analysis revealed that SUMO-conjugation diminished the recruitment of MEF to the lysozyme promoter, which partly explains the down-regulation of MEF activity by SUMO. These findings contribute to our understanding of the regulation of the ETS factor MEF.

Daniel H Lacorazza - One of the best experts on this subject based on the ideXlab platform.

  • transcription factor ELF4 promotes development and function of memory cd8 t cells in listeria monocytogenes infection
    European Journal of Immunology, 2014
    Co-Authors: Maksim Mamonkin, Monica Puppi, Daniel H Lacorazza
    Abstract:

    Most differentiated CD8(+) T cells die off at the end of an infection, revealing two main subsets of memory T cells - central and effector memory - which can be found in lymphoid tissues or circulating through nonlymphoid organs, respectively. The cell intrinsic regulation of the differentiation of CD8(+) T cells to effector and central memory remains poorly studied. Herein, we describe a novel role of the ETS transcription factor ELF4 in the development and function of memory CD8(+) T cells following infection with Listeria monocytogenes. Adoptively transferred ELF4(-/-) naive CD8(+) T cells produced lower numbers of effector memory CD8(+) T cells despite a normal pool of central memory. This was caused by suboptimal priming and decreased survival of CD8(+) T cells at the peak of response while enhanced Notch1 signaling and upregulation of eomesodermin correlated with "normal" development of ELF4(-/-) central memory. Finally, loss of ELF4 impaired the expansion of both central and effector memory CD8(+) T cells in a recall response by also activating Notch1 signaling. Altogether, ELF4 emerges as a novel transcriptional regulator of CD8(+) T-cell differentiation in response to infection.

  • the transcription factor ELF4 promotes survival of myeloid leukemic stem cells
    Blood, 2010
    Co-Authors: Chun Shik Park, Koramit Suppipat, Daniel H Lacorazza
    Abstract:

    Abstract 1209 Chronic myeloid leukemia (CML) is a myeloproliferative disease that originate in hematopoietic stem cells (HSCs) as a result of the t(9;22) translocation, giving rise to the Ph (Philadelphia chromosome) and BCR-ABL oncoprotein. Although treatment of CML patients with tyrosine kinase inhibitor can efficiently eliminate most leukemic cells, chemoresistant leukemic stem cells (LSCs) can survive and drive recurrence of CML in these patients. A number of genes have been described to promote or inhibit proliferation of LSCs. Some of them have similar roles in normal HSCs. The transcription factor ELF4 promotes cell cycle entry of quiescent HSCs during homeostasis (Lacorazza et al., 2006). Thus, to investigate the function of ELF4 in CML initiation and maintenance, we developed a BCR-ABL-induced CML-like disease using retroviral transfer of BCR-ABL in ELF4-null bone marrow (BM) cells. We first investigated whether ELF4 is required for the induction of CML. Recipient mice of BCR-ABL-transduced WT BM cells developed CML and died with a latency 16–23 days, whereas recipient mice of BCR-ABL-transduced ELF4 -/- BM cells showed longer latency of 45–47 days (n=20; p + leukemic cells expanded the first two weeks after BM transplantation followed by a decline at expense of a secondary expansion of B220 + cells. In contrast, Gr-1 + leukemic cells continuously expanded in mice receiving BCR-ABL-transduced WT BM cells. These results suggest that loss of ELF4 causes a profound abrogation in BCR-ABL-induced CML, while allowing progression of B-cell acute lymphocytic leukemia. Since loss of ELF4 led to impaired maintenance of myeloid leukemic cells, we postulated that ELF4 may affect survival of LSCs. Thus, we analyzed the frequency of Lin - c-Kit + Sca-1 + (LSK) cells that are BCR-ABL positive in BM and spleen. We found that BCR-ABL + LSK cells were significantly reduced in recipients of BCR-ABL-transduced ELF4 -/- BM cells. These studies indicate that ELF4 is essential to maintain the LSC pool in CML acting as a molecular switch between myeloid and lymphoid blast crisis. Disclosures: No relevant conflicts of interest to declare.

  • the mtor pathway inhibits expression of the tumor suppressors ELF4 and klf4 downstream of tcr signaling to induce t cell proliferation
    Blood, 2009
    Co-Authors: Takeshi Yamada, Kirsten Gierach, Daniel H Lacorazza
    Abstract:

    Abstract Abstract 3688 Poster Board III-624 Quiescence of circulating naive T cells is maintained by the transcription factors ELF4 and KLF4 downstream of T-cell receptor (TCR) signaling. Hence, loss of ELF4 leads to increased proliferation of CD8+ T cells in response to homeostatic and antigen driven stimuli (Yamada et al, Nature Immunology, 2009). The identification of signals that suppress this restraint of proliferation will aid to enhance immunological memory during vaccination and to better understand development of T-cell acute lymphoblastic leukemias. Consistent with lower threshold of activation by ELF4 deletion in unstimulated naive T cells, we identified a significant downregulation of the dual-specificity phosphatases DUSP1 and DUSP5 in a global gene expression study, which was confirmed at a protein level. Consequently, ELF4−/− CD8 T cells showed sustained phosphorylation of Erk1/2 upon TCR activation. In addition, we found that the PD98059 and LY294002 inhibitors, but not Cyclosporin A, blocked inhibition of ELF4 transcription upon TCR activation independently of CD28 co-stimulation and signals emanating from IL-2R. Furthermore, rapamycin also prevented downregulation of ELF4 transcripts following T cell activation, suggesting that mTORC1 inhibits ELF4 transcription downstream of MAPK and PI3K/Akt pathways. We conclude that the transcription factor ELF4 sets a proliferation threshold in naive T cells by activating DUSPs and that ELF4 suppression upon TCR activation is mediated by mTORC1 downstream of MAPK and PI3K/Akt pathways. Our findings provide important targets of this novel control of T cell proliferation to enhance immune response to vaccination and to prevent expansion of pre-leukemic clones in pediatric patients that fail to respond to current therapies. Disclosures: No relevant conflicts of interest to declare.

  • transcription factor ELF4 controls the proliferation and homing of cd8 t cells via the kruppel like factors klf4 and klf2
    Nature Immunology, 2009
    Co-Authors: Takeshi Yamada, Chun Shik Park, Maksim Mamonkin, Daniel H Lacorazza
    Abstract:

    The transcription factor ELF4 controls hematopoietic stem cell quiescence. Lacorazza and colleagues show that ELF4 is also needed to maintain the quiescence of naive T cells during steady-state conditions and after antigen stimulation.

  • hemangiogenic role of ELF4 in bone marrow post myeloablation
    Blood, 2006
    Co-Authors: Mariela Sivina, Takeshi Yamada, Natalie Dang, Daniel H Lacorazza
    Abstract:

    Bone marrow suppression is an important cause of death in patients exposed to radiation or in cancer patients treated with conventional chemotherapeutic agents. Myeloablative treatments (i.e. 5-fluorouracil administration) lead to apoptosis of blood forming cells and to regression of blood vessels in bone marrow. It is well known that hematological recovery post-bone marrow insult depends on the capacity of hematopoietic stem cells to regenerate the entire hematopoietic system, however, the transcriptional machinery involved in the regeneration of sinusoidal blood vessels in bone marrow from endothelial progenitor cells is largely unknown. Endothelial cells express the Tie2 receptor tyrosine kinase (a.k.a. Tek), which is involved in the angiogenic remodeling and vessel stabilization. Gene targeting of Tie2 showed that it is not required for differentiation and proliferation of definitive hematopoietic lineages in the embryo although Tie2 is needed during postnatal bone marrow hematopoiesis. ELF is a subgroup of the ETS family of transcription factors composed by ELF1, ELF2 (a.k.a. NERF), ELF3, ELF4 (a.k.a. MEF) and ELF5. ELF1 and ELF2 have been shown to regulate Tie2 expression in vitro . Recently we showed that ELF4 modulates the exit of hematopoietic stem cells (HSC) from quiescence (Lacorazza et al., Cancer Cell 2006, 9:175–187). Given the high homology between ELF1 and ELF4 and the same origin of HSC and endothelial progenitor cells, we hypothesize that ELF4 regulates proliferation and Tie2 expression of endothelial cells. We used a luciferase gene reporter system in COS-7 and HEK cells to examine the capacity of ELF proteins to activate Tie2. ELF4 is the strongest activator of Tie2 expression following the hierarchy ELF4>ELF1>ELF2 variant 1>ELF2 variant 2. Site directed mutagenesis of each of the five ETS-binding sites (EBS) present in the Tie2 promoter shows that ELF4 binds preferentially to EBS 1, 3 and 5. Binding of ELF4 to the Tie2 promoter was confirmed by chromatin immunoprecipitation and EMSA. Although Elf1 gene expression is essentially normal in ELF4−/− bone marrow cells collected after 5-FU treatment, we detected diminished Tie2 expression compared to ELF4+/+ bone marrow cells. The association of this effect to human endothelial cells derived from umbilical cord (HUVEC cells) was investigated. All-trans retinoic acid (ATRA) and vascular-endothelial growth factor (VEGF) induced ELF4 expression in HUVEC cells in a dose and time dependent manner which was followed by increased Tie2 expression, suggesting that expression of ELF4 is modulated by angiogenic signals. Moreover, endothelial cells treated with ATRA showed rapid wound colonization in a wound assay. Expression of the pan-endothelial marker MECA-32 was determined by immunohistochemistry to correlate Tie2 with the regeneration of blood vessels: myeloablated ELF4−/− femurs exhibited a reduction of MECA-32 positive arterioles. Finally, temporal and spatial expression of Tie2 during hematological recovery post ablation was measured in bone marrow using transgenic Tie2-LacZ mice crossed to ELF4−/− mice. Collectively, our data suggests that ELF4 regulates Tie2 expression in endothelial cells but most importantly their proliferative capacity in response to angiogenic signals.

Elsebeth Kolmos - One of the best experts on this subject based on the ideXlab platform.

  • early flowering4 recruitment of early flowering3 in the nucleus sustains the arabidopsis circadian clock
    The Plant Cell, 2012
    Co-Authors: Eva Herrero, Elsebeth Kolmos, Nora Bujdoso, Ye Yuan, Mengmeng Wang, Markus C Berns, Heike Uhlworm, George Coupland, Reena Saini, Mariusz Jaskolski
    Abstract:

    The plant circadian clock is proposed to be a network of several interconnected feedback loops, and loss of any component leads to changes in oscillator speed. We previously reported that Arabidopsis thaliana EARLY FLOWERING4 (ELF4) is required to sustain this oscillator and that the ELF4 mutant is arrhythmic. This phenotype is shared with both elf3 and lux. Here, we show that overexpression of either ELF3 or LUX ARRHYTHMO (LUX) complements the ELF4 mutant phenotype. Furthermore, ELF4 causes ELF3 to form foci in the nucleus. We used expression data to direct a mathematical position of ELF3 in the clock network. This revealed direct effects on the morning clock gene PRR9, and we determined association of ELF3 to a conserved region of the PRR9 promoter. A cis-element in this region was suggestive of ELF3 recruitment by the transcription factor LUX, consistent with both ELF3 and LUX acting genetically downstream of ELF4. Taken together, using integrated approaches, we identified ELF4/ELF3 together with LUX to be pivotal for sustenance of plant circadian rhythms.

  • a reduced function allele reveals that early flowering3 repressive action on the circadian clock is modulated by phytochrome signals in arabidopsis
    The Plant Cell, 2011
    Co-Authors: Elsebeth Kolmos, Ferenc Nagy, Eva Herrero, Nora Bujdoso, Peter Gyula, Andrew J Millar, Reka Toth, Seth J Davis
    Abstract:

    Arabidopsis thaliana EARLY FLOWERING3 (ELF3) is essential for the generation of circadian rhythms. ELF3 has been proposed to restrict light signals to the oscillator through phytochrome photoreceptors, but that has not been explicitly shown. Furthermore, the genetic action of ELF3 within the clock had remained elusive. Here, we report a functional characterization of ELF3 through the analysis of the elf3-12 allele, which encodes an amino acid replacement in a conserved domain. Circadian oscillations persisted, and unlike elf3 null alleles, elf3-12 resulted in a short circadian period only under ambient light. The period shortening effect of elf3-12 was enhanced by the overexpression of phytochromes phyA and phyB. We found that elf3-12 was only modestly perturbed in resetting of the oscillator and in gating light-regulated gene expression. Furthermore, elf3-12 essentially displayed wild-type development. We identified targets of ELF3 transcriptional repression in the oscillator, highlighting the action at the morning gene PSEUDO-RESPONSE REGULATOR9. Taken together, we identified two separable roles for ELF3, one affecting the circadian network and the other affecting light input to the oscillator. This is consistent with a dual function of ELF3 as both an integrator of phytochrome signals and a repressor component of the core oscillator.

  • integrating ELF4 into the circadian system through combined structural and functional studies
    Hfsp Journal, 2009
    Co-Authors: Elsebeth Kolmos, Monika Nowak, Maria Werner, Katrin Fischer, Guenter Schwarz, Sarah Mathews, Heiko Schoof, Ferenc Nagy, Janusz M Bujnicki, Seth J Davis
    Abstract:

    The circadian clock is a timekeeping mechanism that enables anticipation of daily environmental changes. In the plant Arabidopsis thaliana, the circadian system is a multiloop series of interlocked transcription‐translation feedbacks. Several genes have been arranged in these oscillation loops, but the position of the core‐clock gene ELF4 in this network was previously undetermined. ELF4 lacks sequence similarity to known domains, and functional homologs have not yet been identified. Here we show that ELF4 is functionally conserved within a subclade of related sequences, and forms an alpha‐helical homodimer with a likely electrostatic interface that could be structurally modeled. We support this hypothesis by expression analysis of new ELF4 hypomorphic alleles. These weak mutants were found to have expression level phenotypes of both morning and evening clock genes, implicating multiple entry points of ELF4 within the multiloop network. This could be mathematically modeled. Furthermore, morning‐expression...

  • ELF4 as a central gene in the circadian clock
    Plant Signaling & Behavior, 2007
    Co-Authors: Elsebeth Kolmos, Seth J Davis
    Abstract:

    The light-dark cycle of the environment serves as one of the major Zeitgebers in entrainment of the circadian clock. The circadian system consists of interconnected feedback loops in which the CCA1/LHY-TOC1 loop has a central position. Genetic analyses of the ELF4 mutant suggested that it is a positive regulator of CCA1 and LHY expression. Recently, we refined the mode-of-action of ELF4 in entrainment of the clock, and here hypothesize that ELF4 expression is interlocked with the CCA1/LHY-TOC1 loop.

  • ELF4 is required for oscillatory properties of the circadian clock
    Plant Physiology, 2007
    Co-Authors: Harriet G Mcwatters, Elsebeth Kolmos, Ferenc Nagy, Mark R Doyle, Richard M Amasino, Anthony Hall, Peter Gyula, Andrew J Millar, Seth J Davis
    Abstract:

    Circadian clocks are required to coordinate metabolism and physiology with daily changes in the environment. Such clocks have several distinctive features, including a free-running rhythm of approximately 24 h and the ability to entrain to both light or temperature cycles (zeitgebers). We have previously characterized the EARLY FLOWERING4 (ELF4) locus of Arabidopsis (Arabidopsis thaliana) as being important for robust rhythms. Here, it is shown that ELF4 is necessary for at least two core clock functions: entrainment to an environmental cycle and rhythm sustainability under constant conditions. We show that ELF4 demonstrates clock input defects in light responsiveness and in circadian gating. Rhythmicity in ELF4 could be driven by an environmental cycle, but an increased sensitivity to light means the circadian system of ELF4 plants does not entrain normally. Expression of putative core clock genes and outputs were characterized in various ELF4 backgrounds to establish the molecular network of action. ELF4 was found to be intimately associated with the CIRCADIAN CLOCK-ASSOCIATED1 (CCA1)/LONG ELONGATED HYPOCOTYL (LHY)-TIMING OF CAB EXPRESSION1 (TOC1) feedback loop because, under free run, ELF4 is required to regulate the expression of CCA1 and TOC1 and, further, ELF4 is locked in the evening phase of this feedback loop. ELF4, therefore, can be considered a component of the central CCA1/LHY-TOC1 feedback loop in the plant circadian clock.

Ferenc Nagy - One of the best experts on this subject based on the ideXlab platform.

  • a reduced function allele reveals that early flowering3 repressive action on the circadian clock is modulated by phytochrome signals in arabidopsis
    The Plant Cell, 2011
    Co-Authors: Elsebeth Kolmos, Ferenc Nagy, Eva Herrero, Nora Bujdoso, Peter Gyula, Andrew J Millar, Reka Toth, Seth J Davis
    Abstract:

    Arabidopsis thaliana EARLY FLOWERING3 (ELF3) is essential for the generation of circadian rhythms. ELF3 has been proposed to restrict light signals to the oscillator through phytochrome photoreceptors, but that has not been explicitly shown. Furthermore, the genetic action of ELF3 within the clock had remained elusive. Here, we report a functional characterization of ELF3 through the analysis of the elf3-12 allele, which encodes an amino acid replacement in a conserved domain. Circadian oscillations persisted, and unlike elf3 null alleles, elf3-12 resulted in a short circadian period only under ambient light. The period shortening effect of elf3-12 was enhanced by the overexpression of phytochromes phyA and phyB. We found that elf3-12 was only modestly perturbed in resetting of the oscillator and in gating light-regulated gene expression. Furthermore, elf3-12 essentially displayed wild-type development. We identified targets of ELF3 transcriptional repression in the oscillator, highlighting the action at the morning gene PSEUDO-RESPONSE REGULATOR9. Taken together, we identified two separable roles for ELF3, one affecting the circadian network and the other affecting light input to the oscillator. This is consistent with a dual function of ELF3 as both an integrator of phytochrome signals and a repressor component of the core oscillator.

  • integrating ELF4 into the circadian system through combined structural and functional studies
    Hfsp Journal, 2009
    Co-Authors: Elsebeth Kolmos, Monika Nowak, Maria Werner, Katrin Fischer, Guenter Schwarz, Sarah Mathews, Heiko Schoof, Ferenc Nagy, Janusz M Bujnicki, Seth J Davis
    Abstract:

    The circadian clock is a timekeeping mechanism that enables anticipation of daily environmental changes. In the plant Arabidopsis thaliana, the circadian system is a multiloop series of interlocked transcription‐translation feedbacks. Several genes have been arranged in these oscillation loops, but the position of the core‐clock gene ELF4 in this network was previously undetermined. ELF4 lacks sequence similarity to known domains, and functional homologs have not yet been identified. Here we show that ELF4 is functionally conserved within a subclade of related sequences, and forms an alpha‐helical homodimer with a likely electrostatic interface that could be structurally modeled. We support this hypothesis by expression analysis of new ELF4 hypomorphic alleles. These weak mutants were found to have expression level phenotypes of both morning and evening clock genes, implicating multiple entry points of ELF4 within the multiloop network. This could be mathematically modeled. Furthermore, morning‐expression...

  • ELF4 is required for oscillatory properties of the circadian clock
    Plant Physiology, 2007
    Co-Authors: Harriet G Mcwatters, Elsebeth Kolmos, Ferenc Nagy, Mark R Doyle, Richard M Amasino, Anthony Hall, Peter Gyula, Andrew J Millar, Seth J Davis
    Abstract:

    Circadian clocks are required to coordinate metabolism and physiology with daily changes in the environment. Such clocks have several distinctive features, including a free-running rhythm of approximately 24 h and the ability to entrain to both light or temperature cycles (zeitgebers). We have previously characterized the EARLY FLOWERING4 (ELF4) locus of Arabidopsis (Arabidopsis thaliana) as being important for robust rhythms. Here, it is shown that ELF4 is necessary for at least two core clock functions: entrainment to an environmental cycle and rhythm sustainability under constant conditions. We show that ELF4 demonstrates clock input defects in light responsiveness and in circadian gating. Rhythmicity in ELF4 could be driven by an environmental cycle, but an increased sensitivity to light means the circadian system of ELF4 plants does not entrain normally. Expression of putative core clock genes and outputs were characterized in various ELF4 backgrounds to establish the molecular network of action. ELF4 was found to be intimately associated with the CIRCADIAN CLOCK-ASSOCIATED1 (CCA1)/LONG ELONGATED HYPOCOTYL (LHY)-TIMING OF CAB EXPRESSION1 (TOC1) feedback loop because, under free run, ELF4 is required to regulate the expression of CCA1 and TOC1 and, further, ELF4 is locked in the evening phase of this feedback loop. ELF4, therefore, can be considered a component of the central CCA1/LHY-TOC1 feedback loop in the plant circadian clock.

  • the ELF4 gene controls circadian rhythms and flowering time in arabidopsis thaliana
    Nature, 2002
    Co-Authors: Mark R Doyle, Ferenc Nagy, Seth J Davis, Harriet G Mcwatters, Andrew J Millar, Ruth Bastow, Laszlo Kozmabognar, Richard M Amasino
    Abstract:

    Many plants use day length as an environmental cue to ensure proper timing of the switch from vegetative to reproductive growth. Day-length sensing involves an interaction between the relative length of day and night, and endogenous rhythms that are controlled by the plant circadian clock. Thus, plants with defects in circadian regulation cannot properly regulate the timing of the floral transition. Here we describe the gene EARLY FLOWERING 4 (ELF4), which is involved in photoperiod perception and circadian regulation. ELF4 promotes clock accuracy and is required for sustained rhythms in the absence of daily light/dark cycles. ELF4 mutants show attenuated expression of CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), a gene that is thought to function as a central oscillator component. In addition, ELF4 plants transiently show output rhythms with highly variable period lengths before becoming arrhythmic. Mutations in ELF4 result in early flowering in non-inductive photoperiods, which is probably caused by elevated amounts of CONSTANS (CO), a gene that promotes floral induction.