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ELF-3[edit]
Introduction[edit]
Early flowering 3 (ELF3) is a gene that encodes the ELF3 protein, which is a component of the plant molecular circadian clock, a complex network of interlocked transcriptional feedback loops. It is coupled to LUX and ELF4 to form the evening complex (EC), which controls plant sensitivity of the photoperiod. Mutations in ELF3 can lead to abnormalities in the timing of flowering, hypocotyl growth, and free-running period of the plant in constant light.[1] However, in constant darkness, rhythms continue to persist.[2]
| Gene | |
|---|---|
| Number of Exons | 4 |
| Size | 4.38 kb |
| mRNA | |
| Number of Introns | 2747 bp |
| Protein | |
| Molecular Weight | 77.5 kDa |
| pI | 8.68 |
| Number of Amino Acids | 695 |
| Location in Arabidopsis | |
| Chromosome | 2 |
| Coordinates | 11058944 - 11063324 bp |
| Orientation | forward |
| Identifiers | |
| Organism | Arabidopsis thaliana |
| Symbol | ELF3 |
| Alt symbols | PYK20, Early flowering 3 |
| Entrez | 817134 |
| RefSeq (mRNA) | NM_128153.3 |
| RefSeq (Protein) | NP_180164.1 |
| UniProt | O82804 |
Discovery[edit]
In 1992, at the University of Oregon, Michelle T. Zagotta found ELF3 mutants by screening for Arabidopsis thaliana mutants with altered flowering times. The initial goal of this reverse genetics screen was to identity genes that play a role in the signal and response pathway that leads to reproductive development. Initially, she described these mutants as “early-flowering, photoperiod-insensitive.” [3] Homozygous ELF3 mutants were found to be photoperiod-insensitive. In a study four years later, Zagotta classified the ELF3 gene after analyzing these mutants lines. The loci associated with this mutant was localized to chromosome 2 via linkage analysis, and a novel gene, ELF3, was proposed to reside at this loci. In the same study, ELF3 was determined to play a role in blue-light regulated morphogenesis via double mutant tests with other clock genes. [4]
Gene characteristics[edit]
ELF3 is a gene composed of 4 exons found on chromosome 2 of Arabidopsis thaliana. ELF3 encodes two isoforms. Isoform 1 contains 695 amino acids. Isoform 2 differs from the canonical sequence by the mutation of an asparagine to a lysine at position 339 and the loss of the sequence from position 340-695. Expression of ELF3 is up-regulated by auxin and cytokinin and down-regulated by abscisic acid and temperature stress.[5]
Protein characteristics[edit]
The ELF3 protein localizes to the nucleus and contains domains that are frequently associated with transcriptional regulators: a proline-rich region, an acidic region, and a threonine/glutamine-rich region. ELF3 does not contain a known DNA-binding domain, but is hypothesized to regulate transcription in concert with other factors.[6]
Function[edit]
ELF3 gene encodes a 695-amino acid protein which peaks in a circadian fashion at dusk.[7] ELF3 protein plays a key role in the Arabidopsis repressilator, where ELF3, ELF4, and LUX bind to form the EC that regulates night time expression of clock genes.[8] The EC binds to promoters of genes including ELF4, LUX and PRR9, inhibiting their transcription. Therefore, the EC negatively feeds back on transcription of its own genes. EC inhibition of PRR genes indirectly inhibits CCA1 and LHY (morning complex) expression.[8] Expression of EC genes is in turn inhibited by morning complex (MC) proteins LHY and CCA1. These negative EC and MC feedback loops form the plant repressilator, which is central to the plant circadian clock.[8] Recent models also implicate TOC1, PRR5, and PRR7 in the inhibition of EC expression.[9]
Evidence from mutant plants suggests that ELF3 also plays a role in the light transduction input pathway. When it is absent, the plant is unable to properly translate light into a regulatory signal for its circadian oscillators.[10] Results suggest that ELF3 plays a gating role in the light input pathway, by which ELF3 acts on phytochrome B (phyB) to antagonize light input to the plant’s TOC1 gene.[7][6] However, one study observed an additive effect in phyB-ELF3 double mutant plants, implying that these genes either serve a redundant function, or are involved in separate signaling pathways.[11] The specifics on how ELF3 mechanistically inhibits the light transduction pathway is still unclear.[7]
ELF3 is distinct from the ELF4 gene. Mutations in ELF4 produce early flowering in short days, but unlike ELF3, they show similar flowering times to wild type plants in long days. ELF4 is involved in regulation of CCA1 expression, and maintenance of plant clock accuracy.[11]
Mutations[edit]
Flowering time[edit]
The timing of flowering in plants with mutations in ELF3 is shifted earlier compared to wild-type plants. Since plants with ELF3 mutations lack normal photoperiod sensitivity, this early induction of flowering occurs at the same time, regardless of whether it is placed in short or long day conditions.[6] In wild-type Arabidopsis plants, induction of flowering tends to occur earlier in long days than in short days. [6]
Premature aging[edit]
Mutations in ELF3 have also been associated with the speed of plant aging, or plant senescence. ELF3, ELF4, and LUX inhibit the evening transcription of phytochrome-interacting factor 4 and 5 (PIF4 and PIF5.)[10] This prevents the process of leaf yellowing, an indicator of plant aging. In plants with ELF3 mutations, leaf yellowing occurred at a faster rate than wild type plants.[10] However, ELF3’s regulation pathway for senescence has not been fully established. [10]
Hypocotyl elongation[edit]
Mutations in ELF3 in Arabidopsis cause the growth of long hypocotyls, a characteristic feature of plants that do not receive proper light or have defects in light signal transduction. Defects persist in both red-light and blue-light conditions, although they are less severe when the plants are grown in constant white light.[3][4] Studies have shown that ELF3 mutations have additive effects on hypocotyl elongation (in interaction with phyB mutations).[3][4]
Chlorophyll a and chlorophyll b (cab) arrhythmia[edit]
Mutations in ELF3 cause arrhythmia in cab transcription, which is normally rhythmic in producing CAB proteins. When the transgenic reporter construct cab2-luc was introduced into a mutated elf3-1 background, circadian rhythm of cab2-luc was abolished. By contrast, wild-type seedlings showed rhythms that were three to four times stronger. Arrhythmia has been observed in red-light and blue-light conditions, although the effects are less severe in blue-light conditions.[3][4]
See also[edit]
References[edit]
- ^ Oakenfull, Rachael J.; Davis, Seth J. (September 28, 2017). "Shining a light on the Arabidopsis circadian clock". Plant, Cell & Environment. 40 (11): 2571–2585. doi:10.1111/pce.13033. ISSN 1365-3040. PMID 28732105.
- ^ Caldana, Camila; Akiko Satake; Seki, Motohide; Webb, Alex A. R. (2019-02-01). "Continuous dynamic adjustment of the plant circadian oscillator". Nature Communications. 10 (1): 550. doi:10.1038/s41467-019-08398-5. ISSN 2041-1723.
- ^ a b c d Yanovsky, M. J.; Kay, S. A. (October 2001). "Signaling networks in the plant circadian system". Current Opinion in Plant Biology. 4 (5): 429–435. ISSN 1369-5266. PMID 11597501.
- ^ a b c d Ahn, Ji Hoon; Nasim, Zeeshan; Susila, Hendry (October 2018). "Ambient Temperature-Responsive Mechanisms Coordinate Regulation of Flowering Time". International Journal of Molecular Sciences. 19 (10): 3196. doi:10.3390/ijms19103196.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ "ELF3 - Protein EARLY FLOWERING 3 - Arabidopsis thaliana (Mouse-ear cress) - ELF3 gene & protein". www.uniprot.org. Retrieved 2019-04-25.
- ^ a b c d Steve A. Kay; Yanovsky, Marcelo J. (April 2003). "Living by the calendar: how plants know when to flower". Nature Reviews Molecular Cell Biology. 4 (4): 265–276. doi:10.1038/nrm1077. ISSN 1471-0080.
- ^ a b c Boss, Paul K.; Bastow, Ruth M.; Mylne, Joshua S.; Dean, Caroline (June 2004). "Multiple pathways in the decision to flower: enabling, promoting, and resetting". The Plant Cell. 16 Suppl: S18–31. doi:10.1105/tpc.015958. ISSN 1040-4651. PMC 2643402. PMID 15037730.
- ^ a b c Millar, Andrew J.; Halliday, Karen J.; Southern, Megan M.; Edwards, Kieron D.; Fernández, Aurora Piñas; Pokhilko, Alexandra (2012-01-01). "The clock gene circuit in Arabidopsis includes a repressilator with additional feedback loops". Molecular Systems Biology. 8 (1): 574. doi:10.1038/msb.2012.6. ISSN 1744-4292. PMID 22395476.
- ^ McClung, C. Robertson (2014-01-02). "Wheels within wheels: new transcriptional feedback loops in the Arabidopsis circadian clock". F1000Prime Reports. 6. doi:10.12703/P6-2. ISSN 2051-7599. PMC 3883422. PMID 24592314.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b c d Kuai, Benke; Qiu, Kai; Chen, Junyi; Zhu, Xiaoyu (2017). "Phytohormone and Light Regulation of Chlorophyll Degradation". Frontiers in Plant Science. 8. doi:10.3389/fpls.2017.01911. ISSN 1664-462X.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Mas, Paloma (2004-09-01). "Circadian clock signaling in Arabidopsis thaliana: from gene expression to physiology and development". International Journal of Developmental Biology. 49 (5–6): 491–500. doi:10.1387/ijdb.041968pm. ISSN 0214-6282. PMID 16096959.