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Shedding light on plant development: light signalling in the model plant

Arabidopsis thaliana

Article · June 2016

DOI: 10.4038/cjs.v45i1.7359

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Ceylon Journal of Science 45(1) 2016: 3-13 DOI:
http://dx.doi.org/10.4038/cjs.v45i1.7359

REVIEW ARTICLE

Shedding light on plant development: light signalling in the model plant

Arabidopsis thaliana
V. C. Dilukshi Fernando and Dana F. Schroeder
Department of Biological Sciences, University of Manitoba, Winnipeg, MB R3T 2N2, Canada

Received: 19 April 2016; Accepted: 17 May 2016

Abstract: Light is one of the most important factors hypocotyls (embryonic stems), small folded
regulating plant growth and development. Depending cotyledons (embryonic leaves), and undeveloped
on the availability of light, seedlings undergo two chloroplasts. In contrast, seedling growth in the
different developmental programs namely light (photomorphogenesis) results in short
photomorphogenesis in the presence of light, and
hypocotyls, open cotyledons, and developed
skotomorphogenesis in the absence of light. In the
model plant Arabidopsis thaliana mutants in light chloroplasts (Figure 1a) (Chory 1993). These
signalling path ways have been identified that distinct phenotypes have been used in genetic
misregulate this response. The mechanisms behind studies to examine light signal transduction
light and dark growth have been studied extensively pathways. Mutants have been identified in the
and recent studies have revealed how light signals are model plant Arabidopsis thaliana that show the
perceived and transmitted to downstream components. opposite phenotypes to those exhibited in wild
This review provides insight into light-perceiving type plants. These light signalling mutants are
photoreceptors and other positive and negative broadly divided into two classes, mutants
regulators of light signalling as well as interactions showing light grown phenotypes in the dark and
between these components. Genetic and biochemical
mutants showing dark grown phenotypes in the
evidence for the basis of light signalling mechanisms
are discussed as well as the importance of light light (Figure 1b). These phenotypes are a
signalling in plant development. consequence of defects in either positive or
negative regulators of light signalling (Quail
Keywords:Arabidopsis thaliana, photomorphogenesis, 1991, Chory 1993).
photoreceptors, COP1, DET1, CUL4-DDB1 E3
ligases. Arabidopsis thaliana (family Brassicaceae)
is an excellent model plant to study the genetic
basis of the effects of external environmental
INTRODUCTION factors. It has a small genome (125Mb), the first
plant genome to be fully sequenced. In addition,
Among all the external stimuli affecting plant its small size, rapid growth, and extensive
development, light has an important role in collections of mutants and other molecular
photosynthesis, chloroplast biogenesis, resources make Arabidopsis an excellent model
germination, seedling development, floral plant. Its ability to produce large numbers of
induction, phototropism, and shade avoidance. progeny and ease of Agrobacterium mediated
Thus light acts not only as an energy source but, transformation has also contributed to making
in addition, functions as a trigger for growth and Arabidopsis a popular genetic model
development (Chory 1993, Deng 1994, Dong et (Sivasubramanian et al. 2015).
al. 2015).
Although the major positive and negative
The effect of light on plant development regulators of light signalling in Arabidopsis were
can be clearly detected during seedling growth. discovered more than 20 years ago, direct
Seedling growth in the dark biochemical interactions between these
(skotomorphogenesis) has a developmentally components were revealed only recently.
arrested etiolated phenotype with elongated

*Corresponding Author’s Email: [email protected]

4 Ceylon Journal of Science 45(1) 2016: 3-13

Figure 1: Dark and light grown wild type seedling phenotypes (a) and light signalling mutants (b).

This review focuses on recent advances in our mediated by phyA, while phyB-E initiate red
understanding of light signalling in Arabidopsis light signalling, with phyB acting predominantly
thaliana, with emphasis on interactions between (Wang and Wang 2015). Phytochromes occur in
key regulatory components of light signalling. a biologically active Pfr form and an inactive Pr
form. Pfr and Pr are photoconvertible, where Pr
POSITIVE REGULATORS OF LIGHT is transformed into Pfr upon red light (R)
SIGNALLING absorption and Pfr transformed into Pr upon far-
red (FR) light absorption. This conformational
When a component of the light signalling change in phytochromes is an important
pathway that is involved in perception of the regulatory switch that mediates transduction of
light signal or transduction of the light signal to light signals to downstream components (Furuya
downstream components is compromised, such 1993). For phyB, conversion to the Pfr form
mutants will exhibit a seedling phenotype that is reveals a masked nuclear localization signal that
insensitive, or exhibits reduced response, to light. results in nuclear import in the presence of light.
That is, these seedlings will show an etiolated PhyA nuclear localization requires FHY1 (FAR
phenotype in the light, with elongated hypocotyls RED ELONGATED HYPOCOTYL 1) and FHL
and reduced cotyledon expansion (Figure 1b). (FHY1 LIKE) (Wang and Wang 2015). Phys are
This group of mutants can be categorized into homodimeric chromoprotein complexes that
photoreceptor mutants and mutants in contain a phytochromobilin (PɸB) chromophore.
photomorphogenesis-promoting transcription Phys consist of chromophore binding,
factors. dimerization and kinase domains (Burgie et al.
Photoreceptors 2014). Pr to Pfr conversion occurs after light
activates the bilin chromophore, which
Initiation of light signalling occurs via perception undergoes isomerization and thereby a
of light by photoreceptors. Plants have evolved confirmation change in hairpin and helical spine
several photoreceptors to sense and respond to a structure, which stabilizes the Pfr form (Burgie et
broad range of light frequencies in the al. 2016).
environment. The major photoreceptors are the
far-red and red light detecting phytochromes, Cryptochromes are involved in blue light
blue/UV-A light sensing cryptochromes and mediated regulation of seedling development and
phototropins, and UV-B detecting receptors, photoperiodic initiation of flowering. Analysis of
such as UVR8 (Galvão and Fankhauser 2015). cryptochrome 1 and 2 (cry1 cry2) mutants has
shown that CRY1 and CRY2 have both unique
Arabidopsis has five phytochrome and overlapping functions in these responses.
isoforms (phyA-E). Far red perception is CRY2 is always nuclear localized while CRY1 is
V.C.D. Fernando and D.F. Schroeder 5

either nuclear or cytoplasmic. Upon blue light transcription. HY5 also activates its own gene
absorption, the main chromophore in CRYs is expression. Therefore both HY5 and CAM7
rapidly photo reduced, resulting in positively regulate HY5 transcription (Abbas et
conformational changes that facilitate al. 2014).
interactions with downstream signalling
components (Galvão and Fankhauser 2015, Liu Other positive regulators of
et al. 2016). photomorphogenesis include HY5 HOMOLOG
(HYH), a G-box binding bZIP transcription
Photomorphogenesis-promoting transcription factor which shows functional redundancy with
factors HY5. Unlike hy5, hyh mutants exhibit resistance
to inhibition of hypocotyl elongation only in blue
LONG HYPOCOTYL 5 (HY5) was one of the light thus HYH acts as the main positive
first positive regulators of photomorphogenesis regulator of blue light signalling mediated by
to be characterized. The hy5 mutants were CRY1 and CRY2. HYH protein levels were
initially identified in a screen for insensitivity to significantly lower in hy5 mutants indicating that
light inhibition of hypocotyl elongation (Figure. HY5 is essential for HYH protein accumulation.
1b) (Koornneef et al. 1980). hy5 mutants are hyh mutants flower earlier than wild type but hy5
deficient in red, far-red, and blue light responses hyh double mutants did not show an additive
and act downstream from the photoreceptors effect on flowering time phenotypes (Holm et al.
(Chory 1992, Ang and Deng 1994). In addition, 2002).
hy5 mutants have defects in chlorophyll
accumulation and lateral root formation (Pepper HFR1, a bHLH transcription factor, is
and Chory 1997, Oyama et al. 1997). another positive regulator of
photomorphogenesis. The hfr1 mutant has
HY5 encodes a nuclear localized basic elongated hypocotyls in FR light. HFR1 is
leucine zipper transcription factor that promotes responsible for phyA mediated FR and CRY1
photomorphogenesis in a broad range of mediated blue light signalling (Jang et al. 2005,
wavelengths (Oyama et al. 1997). Studies of Yang et al. 2005, Casal et al. 2014).
photoreceptor mutants and overexpression lines
have shown that both phytochromes and LAF1, a Myb transcriptional activator, is
cryptochromes promote HY5 accumulation in involved in transmitting phyA signals to
the nucleus. The key photoreceptor responsible downstream signalling components. Interestingly
for HY5 accumulation in R light is phyB while HY5, HFR1, and LAF1 have the ability to bind
phyA plays a more important role in FR light. with each other and decrease degradation of each
CRY1 and CRY2 are involved in HY5 other (Casal et al. 2014).
accumulation under blue light conditions
(Osterlund et al. 2000). NEGATIVE REGULATORS OF LIGHT
SIGNALLING
Chromatin immuno-precipitation and
whole genome expression analysis have shown In Arabidopsis mutants have been identified that
that HY5 specifically binds to the promoters of a resemble light grown plants even when grown in
large number of genes of which 10% encode the dark, that is, exhibit short hypocotyls, open
transcription factors. In addition, 24% of light cotyledons, and light regulated gene expression
regulated genes are HY5 targets, including both (Figure 1b) (Chory et al. 1989). These mutants
light induced and light repressed genes, are referred to as constitutive photomorphogenic
indicating that HY5 has a dual role in (cop), de-etiolated (det), or fusca (fus).
transcriptional regulation of light signalling as an Subsequent cloning of the genes associated with
activator as well as a repressor (Lee et al. 2007). these loci revealed the identity of these central
repressors of photomorphogenesis. The
CALMODULIN 7 (CAM7) has a critical COP/DET/FUS proteins are components of three
role in transcriptional regulation of HY5 during distinct protein complexes: (i) the COP1-SPA
seedling development in a broad spectrum of complex, (ii) the COP9 signalosome (CSN) and
light conditions. CAM7 directly interacts with (iii) the COP10-DET1-DDB1 (CDD) complex
the HY5 promoter and upregulates HY5 (Lau and Deng 2012).
6 Ceylon Journal of Science 45(1) 2016: 3-13

Figure 2: COP1 regulation of HY5 levels in (a) dark and (b) light. In the dark, nuclear localized COP1-SPA targets HY5 for
degradation via the 26S proteasome and prevents photomorphogenesis. In the light, the active Pfr form of phytochrome
enters the nucleus and inhibits COP1-SPA interaction. In addition, COP1 is slowly exported from the nucleus. This results in
HY5 accumulation, expression of HY5 target genes and light growth.

In addition to the COP/DET/FUS genes, a photoreceptors. Two mechanisms appear to

group of phytochrome interacting basic helix- contribute to repression of COP1 in the light.
loop-helix (bHLH) transcription factors were One is the slow translocation of COP1 from the
later identified as another class of negative nucleus to the cytosol and the other is rapid
regulators of light signalling. These transcription inhibition of COP1 by the photoreceptors (Casal
factors are called PHYTOCHROME et al. 2014, Lu et al. 2015). Recent studies have
INTERACTING FACTORS (PIFs) (Leivar et al. shown that both phyA and phyB co-localize with
2008, Leivar and Monte 2014). SPA1 in the nucleus. Photoactive phyA and
phyB interact with SPA1 in a light dependent
COP1 manner and prevent COP1-SPA interaction and
thereby formation of the active COP1-SPA
COP1 is a 76 kDa protein that targets positive complex (Figure 2) (Lu et al. 2015, Sheerin et al.
regulators of light signalling for degradation. 2015). In addition, both CRY1 and CRY2
Ubiquitination is a mechanism whereby ubiquitin regulate COP1 activity in blue light by
(Ub) tags are added to proteins, targeting them interacting with SPA1 and preventing COP1-
for subsequent proteolytic degradation via the SPA E3 ligase function (Lau and Deng 2012, Liu
26S proteasome pathway. COP1 interacts with et al. 2016).
SUPPRESSOR OF PHYA-105 (SPA) proteins to
form a RING E3 ubiquitin ligase which, in the Another recently identified COP1
dark, targets photomorphogenesis promoting repressor, COP1 SUPPRESSOR 2 (CSU2),
transcription factors such as HY5, HYH, HFR1, directly interacts with COP1 and inhibits its E3
and LAF1 for degradation via the 26S ligase activity. CSU2 loss of function suppresses
proteasome system, leading to the cop1 mutant phenotype (Xu et al. 2015).
skotomorphogenesis (Casal et al. 2014).
In contrast to its negative regulatory role in
COP1 has 3 distinct domains that facilitate visible light signalling, COP1 acts as a positive
interaction with other proteins, namely a RING regulator in UV-B signalling. Upon exposure to
finger domain, a coiled–coil domain, and WD-40 UV-B, the UV photoreceptor UVR8 undergoes a
repeat domain. COP1 interacts with most of its conformational change enabling interaction with
substrates via the WD-40 domain (Yi and Deng COP1. As a result HY5 expression is increased,
2005). COP1 is capable of auto-ubiquitination which leads to activation of UV-B induced
and SPA1 has no specific role for this self- genes. Thus, COP1 has a role in plant UV-B
ubiquitination. However COP1 E3 ligase activity tolerance (Lau and Deng 2012, Kong and
is strictly impaired in spa1 mutants and thus, Okajima 2016).
SPA1 is required for ubiquitination of other
substrates (Seo et al., 2003). The COP9 signalosome

COP1 interacts with phyA, phyB, CRY1, The COP9 signalosome (CSN) consists of eight
and CRY2 in response to photoperception by the subunits, six of which were identified as
V.C.D. Fernando and D.F. Schroeder 7

cop/det/fus mutants. The CSN regulates the grown adult det1 plants are small with increased
activity of CULLIN RING E3 ligases and number of inflorescence stems as well as reduced
thereby plays an important role in regulation of fertility (Chory et al. 1989, Pepper et al. 1994).
ubiquitin/proteasome mediated protein DET1 is also involved in spatial patterning of
degradation. The CSN removes the ubiquitin-like light regulated gene expression and chloroplast
modifier Nedd8 from CUL based E3 ligases development (Chory and Peto 1990). In addition,
(Lau and Deng 2012, Dong et al. 2015). Loss of pleiotropic defects in det1 mutants, including
function csn mutants shows a constitutive morphological defects and abnormal gene
photomorphogenic phenotype because the CSN expression in the dark and light, can be restored
is essential for COP1 activity. Thus, a number of by increased peroxisome function. TED3 is the
genes including light regulated genes are mis- Arabidopsis homologue of the yeast and
regulated in csn mutants (Chamovitz 2009, Wang mammalian peroxisomal protein PEX2 and ted3
et al. 2009). gain of function mutants can rescue det1
phenotypes. This indicates that both DET1 and
The COP10/DET1/DDB1 (CDD) complex peroxisomes play important roles in
photomorphogenesis (Hu et al. 2002).
In the CDD complex, COP10 and DET1 form a
complex with CUL4 via DAMAGED DNA hy5 mutants suppress det1 dark grown
BINDING protein 1 (DDB1). seedling phenotypes as well as det1 light grown
adult phenotypes such as size, flowering, apical
COP10 dominance, and fertility phenotypes. This
COP10 is an ubiquitin conjugating enzyme (E2) suggests that HY5 acts downstream from DET1,
variant (Suzuki et al. 2002). COP10 is also consistent with the lack of HY5 degradation in
required for COP1 mediated degradation of HY5 det1 mutants (Chory 1992, Pepper and Chory
(Osterlund et al., 2000). COP10 directly interacts 1997, Osterlund et al. 2000, Fernando and
with COP1, the CSN, and proteasome subunits Schroeder 2015). DET1 represses
and forms a stable complex with DDB1 and CHLOROPHYLL A/B BINDING PROTEIN 2
DET1 (CDD complex). The CDD complex (CAB2) gene expression in the dark but activates
promotes ubiquitin chain formation and enhances it in the light. DET1 regulation of CAB2
E2 activity. COP10 itself has no E2 activity but expression was found to be via HY5 and the
can enhance the activity of other E2s in the circadian regulator CIRCADIAN CLOCK
presence or absence of the CDD complex ASSOCIATED 1 (CCA1) (Maxwell et al. 2003).
(Yanagawa et al. 2004). The CDD complex DET1 is nuclear localized and interacts
interacts with CUL4 and shows E3 ligase directly or indirectly with a number of other
activity, however the target proteins were proteins. DET1 interacts physically and
unknown until recently. The only known direct genetically with DAMAGED DNA BINDING
target of the CDD complex is HFR1 (Chen et al. PROTEIN 1 A/B (DDB1A/B) and COP10 to
2006, Shi et al. 2015). form the CDD complex (Pepper et al. 1994,
DET1 Schroeder et al. 2002, Yanagawa et al. 2004,
Ganpudi and Schroeder 2013). The CDD
De-etiolation refers to inhibition of hypocotyl complex in turn interacts with CUL4 to form an
elongation and induction of leaf expansion and active E3 Ub ligase. However, a direct target of
differentiation. The de-etiolated mutants in the complex was not known until the recent
Arabidopsis, such as det1, resemble light grown discovery that HFR1 degradation mediated by
plants when grown in complete darkness. Hence the CUL4-CDD complex (Chen et al. 2006, Shi
det1 mutants exhibit short hypocotyls, expanded et al. 2015). In addition, COP1 nuclear retention
cotyledons with noticeable leaf primordia and and HY5 degradation require the activity of the
initiation of chloroplast development in the dark. CDD and CSN complexes (von Arnim et al.
In addition, det1 mutants express light regulated 1997, Osterlund et al. 2000, Wang et al. 2009).
genes in the dark, such as photosynthesis related Thus, det1 mutants have increased levels of HY5
genes. Thus, DET1 acts as a negative regulator protein but DET1 does not appear to directly
of seedling de-etiolation response. det1 mutants interact with HY5 (Osterlund et al. 2000, Lau et
can continue to grow for extended periods in the al. 2011). Also there is no evidence of direct
dark, developing leaves and flowers. Light interaction between COP1 and DET1, therefore
8 Ceylon Journal of Science 45(1) 2016: 3-13

the basis of this mechanism is still not clear E3 ligase associates with POLYCOMB
(Chen et al. 2010). REPRESSIVE COMPLEX 2 containing histone
methyltransferase CLF (CLF-PCR2) and
In contrast, DET1 was found to directly represses FLC expression. det1 exhibits altered
interact with the SINAT5 E3 ligase and block FLC promoter methylation and expression
degradation of LATE ELONGATED (Pazhouhandeh et al. 2011, Kang et al. 2015).
HYPOCOTYL (LHY), a component of the
Arabidopsis circadian clock. SINAT5 interacts A recent study showed that DET1
with both LHY1 and DET1 but ubiquitinates suppresses accumulation of DELLA proteins,
only LHY. Thus, DET1 may influence flowering which are negative regulators of Gibberellic acid
time in Arabidopsis by affecting protein (GA) signalling. Light and GA antagonistically
abundance of LHY via inhibition of the SINAT5 regulate seedling growth and DELLAs play a
E3 ligase (Song and Carré 2005, Park et al. role in promoting skotomorphogenesis in the
2010). dark. Therefore, DET1’s role in repression of
photomorphogenesis may be partly through
In addition to its role in E3 ligase negative regulation of DELLA protein levels in
complexes, DET1 has been shown to be involved the dark (Li et al. 2015). DELLAs inhibit another
in transcriptional regulation (Lau et al. 2011, negative regulator of photomorphogenesis, PIFs
Huang et al. 2014). DET1 acts as a (discussed below) (Davière and Achard 2016).
transcriptional co-repressor of the Arabidopsis
circadian clock. CIRCADIAN CLOCK Other roles of DET1 include the recent
ASSOCIATED 1 (CCA1) and LHY1 are MYB discovery that DET1 is involved in stabilization
transcription factors with partially overlapping of PHYTOCHROME INTERACTING
functions that act as transcriptional repressors in FACTORS (PIFs), which will be discussed later
the morning phase of the central loop of in this review, and mediating degradation of
circadian clock. DET1 directly interacts with HFR1 (Dong et al. 2014, Shi et al. 2015). DET1
CCA1 and LHY1 to repress CCA1/LHY1 target directly regulates both positive (HFR1) and
genes. DET1 is essential for CCA1 negative (PIF1) regulators of seed germination.
transcriptional repression activity and for In the dark, DET1 degrades HFR1 and stabilizes
functioning of the plant circadian clock (Lau et PIF1, repressing seed germination. In the light
al. 2011). Moreover, DET1 has a possible role in DET1 is somehow inactivated, resulting in
chromatin remodelling via binding to non- increased HFR1 and decreased PIF1, inducing
acetylated histone 2B (H2B) tails in nucleosomes seed germination (Shi et al. 2015). Therefore,
(Benvenuto et al. 2002). DET1 is not only a central repressor of
photomorphogenesis but also a central repressor
DET1 not only represses of seed germination and flowering time.
photomorphogenesis but also represses flowering
by altering the photoperiod and autonomous CUL4 / DDB1A/B E3 ligase complexes in light
pathways. DET1 delays flowering particularly signaling
under short day conditions. Flowering is
controlled by multiple signalling components Cullin proteins are the scaffolding subunits
including GIGANTIA (GI) and FLOWERING of E3 ligase complexes, where the N-terminus of
LOCUS T (FT). GI functions as a flowering the cullin binds to an adaptor protein and the C-
inducer and activates FT transcription. DET1 terminus binds to the RING finger protein
directly interacts with GI and delays flowering RBX1. The adaptor protein functions to connect
by inhibiting the interaction between GI and the the cullin to specific substrate receptors that
FT promoter. Thus, DET1 does not affect GI enable interaction with the substrate to be
protein stability but functions as a repressor of targeted for ubiquitination. For instance, in
FT transcription (Kang et al. 2015). In addition, CUL4 E3 ligases, DDB1 acts as the adaptor and
DET1 binds directly to MULTICOPY interacts with a number of different substrate
SUPPRESSOR OF IRA1 4 (MSI4), which is part receptors. These substrate receptors commonly
of a CUL4-DDB1 complex that alters the have roughly seven WD40 domains thus are
expression of FLOWERING LOCUS C (FLC). called DWD (DDB1 binding WD40) proteins or
FLC inhibits floral transition by suppression of DDB1 CUL4 ASSOCIATED FACTORS
floral inducers like FT. The CUL4-DDB1-MSI4 (DCAFs). There are certain proteins, such as
DET1 and COP10, which lack a WD40 domain
V.C.D. Fernando and D.F. Schroeder 9

but still interact with DDB1. CUL4-DDB1- interact directly with PIFs. Phytochromes then
DCAF complexes are involved in a wide array of phosphorylate the PIFs, targeting them for
functions in plants including repression of ubiquitination and degradation via the
photomorphogenesis, facilitating damaged DNA proteasome (Figure 3). While there is
repair, and response to abiotic stress redundancy among the PIFs, pif3 mutants have
(Biedermann and Hellmann 2011). short hypocotyls in red light while PIF4 and PIF5
are also involved in negative regulation of light
DDB1 was first identified in mammals as signalling. PIF1 regulates seed germination and
part of the DDB1-DDB2 complex that binds to hypocotyl elongation. Furthermore, pifq (which
UV damaged DNA and is involved in nucleotide lacks PIF1, PIF3, PIF4 and PIF5) shows a
excision repair of damaged DNA. DDB1 is a constitutive photomorphogenic phenotype
highly conserved protein in eukaryotes. In (Leivar and Monte 2014).
Arabidopsis DDB1 exists as two homologues,
DDB1A and DDB1B, which exhibit 91% amino Microarray expression profile analysis
acid identity with each other. Although the two indicated that DET1 represses
proteins are not biochemically different, DDB1A photomorphogenesis by regulating a number of
and DDB1B show distinct functions in the light transcription factors including PIFs. Thus, lack
and dark and the double mutant is embryonic of PIF3 enhances the det1 de-etiolated phenotype
lethal (Schroeder et al. 2002, Bernhardt et al. while overexpression can partially restore
2010, Ganpudi and Schroeder 2013). seedling de-etiolation in the dark. In addition,
DET1 and other components of the CDD
Distinct DDB1 complexes appear to complex affect the protein stability of PIFs at the
interact with each other genetically and post-transcriptional level. DET1 positively
biochemically. DDB2 is mainly involved in the regulates only PIF3 at the gene expression level
global genomic repair pathway as a substrate but positively regulate all the PIFs at the post-
receptor for CUL4-DDB1 (Ganpudi and translational level. Moreover, both det1 and cop1
Schroeder 2011). In Arabidopsis however DDB2 mutants have significantly reduced PIF3 protein
also genetically interacts with DDB1A and levels, suggesting that the DET/COP/FUS group
DET1. DDB2 interactions with DET1 were of genes repress photomorphogenesis in part by
shown to be DDB1A independent for some adult mediating protein stability of PIFs and
phenotypes while in some dark grown seedling upregulating the function of PIF3 in the dark
phenotypes the interactions were DDB1A (Lau and Deng 2012, Dong et al. 2014, Dong et
dependent (Al Khateeb and Schroeder 2007). In al. 2015, Shi et al. 2015).
addition, DET1 is essential for the degradation of
DDB2 via the CUL4-DDB1 E3 ligase during UV Interactions between the two main classes
damage repair. Removal of DDB2 after damaged of repressors of photomorphogenesis,
DNA lesion recognition is an important step, COP/DET/FUS and PIFs, are just beginning to
allowing the repair machinery to access the unravel. COP1 and PIFs have additive roles in
damaged lesions. Thus DET1 and DDB2 work the dark. PIFs enhance the substrate recruitment
together in UV damaged DNA repair (Castells et and ubiquitination functions of COP1 and PIF1
al. 2011). interacts with COP1, SPA1 and HY5. Basically
PIF1 functions in COP1 mediated HY5
Phytochrome Interacting Factors (PIFS) degradation by enhancing COP1 affinity to HY5,
promoting auto-ubiquitination of COP1 then
The bHLH type transcription factors facilitating transubiquitination of HY5 by COP1.
PHYTOCHROME INTERACTING FACTORs Thus, negative regulation of photomorphogenesis
(PIFs) act directly downstream of phytochromes by PIFs is not an independent mechanism but
to negatively regulate photomorphogenes is and acts by affecting the protein stability of HY5 via
promote skotomorphogenesis. PIFs (PIF1/PIF3- regulation of COP1-SPA E3 ligase activity.
LIKE 5, PIF3, PIF4, PIF5/PIL6, PIF6/PIL2, Therefore, PIF1 and COP act as cofactors and
PIF7, and PIF8) accumulate in the dark to synergistically repress light growth in the dark
promote dark growth. In the presence of light, (Xu et al. 2014).
activated phytochromes, in the nuclear Pfr form,
10 Ceylon Journal of Science 45(1) 2016: 3-13

Figure 3: Interaction between light and PIFs in light signalling (a) In the dark phytochromes are in the biologically inactive
Pr form and are localized in the cytosol. Homo and heterodimers of PIFs bind to light regulated genes, preventing their
expression and repressing photomorphogenesis. (b) In the light, the active Pfr form of phytochromes move to the nucleus to
bind and rapidly phosphorylates PIFs. The phosphorylated PIFs are degraded via the 26S proteasome. As a result
photomorphogenesis occurs.
COP1 degradation of HY5 and other
LIGHT SIGNALLING OVERVIEW photomorphogenesis promoting transcription
factors. Thus in the dark the negative regulators
In summary, different wavelengths of light are promote skotomorphogenesis and inhibit
perceived by photoreceptors, with phyA photomorphogenesis, while the light inactivation
mediating FR perception, phyB red light, and of the negative regulators by the photoreceptors
CRY1 and CRY2 blue (Figure. 4). In general allows light development to proceed (Huang et
light absorption results in changes in al., 2014; Dong et al., 2015). Light influences
photoreceptor conformation and/or localization, nearly all aspects of growth and development in
which facilitates interactions between the plants and our understanding of this critical
photoreceptors and downstream negative process is finally becoming illuminated. The
regulators. The photoreceptors then inhibit the knowledge gained through genetic and
negative regulators, resulting in disruption of biochemical studies in the model plant
COP1 activity and degradation of the PIFs. In the Arabidopsis can be transferred to agriculturally
absence of light the negative regulators more important crops, allowing us to optimize
positively reinforce each other, with DET1 light use during crop production.
stabilizing the PIFs and the PIFs promoting

Figure 4: Light perception and signalling pathways (arrows indicate positive regulation and T-bars indicate
negative regulation).
11 Ceylon Journal of Science 45(1) 2016: 3-13

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